27 results on '"Yueyong Li"'
Search Results
2. Study on torrential rain comprehensive disaster-causing index and its threshold based on Dominance Analysis Method: A case of insurance industry in Zhangjiajie City
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Yueyong LI, Wei ZHOU, Hao LI, and Ke LIANG
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torrential rain ,property and cargo insurance ,dominance analysis method ,disaster threshold ,Meteorology. Climatology ,QC851-999 - Abstract
First, based on the precipitation data and torrential rain disaster data in Zhangjiajie City of Hunan Province from 2016 to 2020, taking the claim cases of the property and cargo insurance (hereinafter referred to as "property and cargo insurance") from Hunan Branch of the People's Insurance Company of China as the research sample, the Dominance Analysis Method was used to determine the influence weights of disaster-causing factors to establish a comprehensive disaster-causing index (I) model of torrential rain. Second, an exponential function is used to fit the relationship between the number of town or street which filed claims of property and cargo insurance and I, then to determine the threshold of I corresponding to different accident levels. Finally, the claim case caused by torrential rain disaster in Zhangjiajie in the flood season of 2021 were selected to verify the I and its threshold. The results show that the number of property and cargo insurance accidents caused by torrential rain in Zhangjiajie is generally low in east and west but high in middle areas. Among the disaster-causing factors, the weight of the 96-hour accumulated precipitation on the scope of accident is the largest, reaching 28.6%. The simulated grades of the scope of accident, the amount of claim and the number of accidents of property and cargo insurance have a high correlation with the grades of actual disasters, and all passed the test at the 0.01 significance level. The threshold test results show that the consistency rate or accuracy between the predicted level and the actual level of torrential rain disaster-causing cases is 71.4%, in which the predicted values of accuracy for the mild, moderate and severe disaster levels are 70%, 70% and 100%, respectively. Therefore, the threshold of I established in this study can be used for the industrial meteorological services related to the property and cargo insurance in Zhangjiajie.
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- 2022
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- View/download PDF
3. Human papillomavirus infection can alter the level of tumour stemness and T cell infiltration in patients with head and neck squamous cell carcinoma
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Lingzhang Meng, Heming Lu, Yueyong Li, Jingjie Zhao, Siyuan He, Zechen Wang, Jiajia Shen, Huixian Huang, Jinru Xiao, Suren Rao Sooranna, and Jian Song
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human papillomavirus ,single cell transcriptomic ,head and neck squamous cell carcinoma ,tumour stemness ,tumour infiltrating immune cells ,immune checkpoint genes ,Immunologic diseases. Allergy ,RC581-607 - Abstract
Head and neck squamous cell carcinoma (HNSCC) usually has a poor prognosis and is associated with a high mortality rate. Its etiology is mainly the result from long-term exposure to either alcohol, tobacco or human papillomavirus (HPV) infection or a combination of these insults. However, HNSCC patients with HPV have been found to show a survival advantage over those without the virus, but the mechanism that confers this advantage is unclear. Due to the large number of HPV-independent HNSCC cases, there is a possibility that the difference in prognosis between HPV-positive (HPV+) and negative (HPV-) patients is due to different carcinogens. To clarify this, we used scRNA data and viral tracking methods in order to identify HPV+ and HPV- cells in the tumour tissues of patients infected with HPV. By comparing HPV+ and HPV- malignant cells, we found a higher level of tumour stemness in HPV- tumour cells. Using tumour stemness-related genes, we established a six-gene prognostic signature that was used to divide the patients into low- and high-risk groups. It was found that HPV patients who were at low-risk of contracting HNSCC had a higher number of CD8+ T-cells as well as a higher expression of immune checkpoint molecules. Correspondingly, we found that HPV+ tumour cells expressed higher levels of CCL4, and these were highly correlated with CD8+ T cells infiltration and immune checkpoint molecules. These data suggest that the stemness features of tumour cells are not only associated with the prognostic risk, but that it could also affect the immune cell interactions and associated signalling pathways.
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- 2022
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4. circRNA circARNT2 Suppressed the Sensitivity of Hepatocellular Carcinoma Cells to Cisplatin by Targeting the miR-155-5p/PDK1 Axis
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Yueyong Li, Yingjun Zhang, Shuai Zhang, Deyou Huang, Baosheng Li, Gencheng Liang, Yingning Wu, Qiulan Jiang, Longhua Li, Cheng Lin, Zhonghen Wei, and Lingzhang Meng
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circARNT2 ,circRNA ,HCC ,chemoresistance ,cisplatin ,ceRNA ,Therapeutics. Pharmacology ,RM1-950 - Abstract
Circular RNA (circRNA) is a novel subclass of noncoding-RNA molecules that participate in development and progression of a variety of human diseases via sponging microRNAs (miRNAs). Until now, the contributions of circRNAs in chemoresistance of hepatocellular carcinoma (HCC) remain largely unknown. In the present study, we aimed to investigate the role of circRNA in cisplatin resistance of HCC. We investigated the expression of circRNAs in 5 paired cisplatin-sensitive and cisplatin-resistant HCC tissues by microarray analysis. The qRT-PCR analysis was to investigate the expression pattern of circARNT2 in HCC patient tissues and cell lines. Then, the effects of circARNT2 on cisplatin resistance, cell proliferation, and apoptosis were assessed in HCC in vitro and in vivo. circARNT2 was significantly upregulated in HCC tissues and cell lines. Overexpression of circARNT2 in HCC was significantly correlated with aggressive characteristics and served as an independent risk factor for overall survival in patients with HCC. In vitro experiments showed that knockdown of circARNT2 inhibited cell proliferation and enhances the cisplatin sensitivity of HCC cells. Furthermore, circARNT2 facilitates HCC progression in vivo. We demonstrated that circARNT2 acts as a sponge for miR-155-5p and verified that PDK1 is a novel target of miR-155-5p. In summary, our study demonstrated that circARNT2 modulates cisplatin resistance through miR-155-5p/PDK1 pathway. Our findings indicated that circARNT2 may serve as a promising therapeutic target for overcoming cisplatin resistance for HCC.
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- 2021
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5. Long noncoding RNA LINC00511 contributes to breast cancer tumourigenesis and stemness by inducing the miR-185-3p/E2F1/Nanog axis
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Guanming Lu, Yueyong Li, Yanfei Ma, Jinlan Lu, Yongcheng Chen, Qiulan Jiang, Qiang Qin, Lifeng Zhao, Qianfang Huang, Zhizhai Luo, Shiqing Huang, and Zhongheng Wei
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Breast cancer stem cells ,LINC00511 ,E2F1 ,Nanog ,miR-185-3p ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Abstract Background Emerging evidence have illustrated the vital role of long noncoding RNAs (lncRNAs) long intergenic non-protein coding RNA 00511 (LINC00511) on the human cancer progression and tumorigenesis. However, the role of LINC00511 in breast cancer tumourigenesis is still unknown. This research puts emphasis on the function of LINC00511 on the breast cancer tumourigenesis and stemness, and investigates the in-depth mechanism. Methods The lncRNA and RNA expression were measured using RT-PCR. Protein levels were measured using western blotting analysis. CCK-8, colony formation assays and transwell assay were performed to evaluate the cell proliferation ability and invasion. Sphere-formation assay was also performed for the stemness. Bioinformatic analysis, chromatin immunoprecipitation (ChIP) and luciferase reporter assays were carried to confirm the molecular binding. Results LINC00511 was measured to be highly expressed in the breast cancer specimens and the high-expression was correlated with the poor prognosis. Functionally, the gain and loss-of-functional experiments revealed that LINC00511 promoted the proliferation, sphere-formation ability, stem factors (Oct4, Nanog, SOX2) expression and tumor growth in breast cancer cells. Mechanically, LINC00511 functioned as competing endogenous RNA (ceRNA) for miR-185-3p to positively recover E2F1 protein. Furthermore, transcription factor E2F1 bind with the promoter region of Nanog gene to promote it transcription. Conclusion In conclusion, our data concludes that LINC00511/miR-185-3p/E2F1/Nanog axis facilitates the breast cancer stemness and tumorigenesis, providing a vital insight for them.
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- 2018
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6. Genes Induced by Panax Notoginseng in a Rodent Model of Ischemia-Reperfusion Injury
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Lanqing Meng, Qing Huang, Xuebin Li, Ping Liang, Yueyong Li, Xiaohua Huang, Jingjie Zhao, Qiuping Chen, Rong Qiu, Lan Li, Chongdong Jian, Hongfei Yao, Jianmin Huang, Xionglin Tang, Zechen Wang, Zhongheng Wei, Jun Wu, Liuzhi Wei, Qiuju Wei, Qianli Tang, Lu Huang, Jihua Wei, Dinggui Lu, Qunqiang Luo, Kegong Xie, Yang Ouyang, Jian Chen, Genliang Li, Linxue Luo, Linbo He, Chenyi Zhuo, Anding Xu, and Lingzhang Meng
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Immunologic diseases. Allergy ,RC581-607 - Abstract
Stroke is a cerebrovascular disease that results in decreased blood flow. Although Panax notoginseng (PN), a Chinese herbal medicine, has been proven to promote stroke recovery, its molecular mechanism remains unclear. In this study, middle cerebral artery occlusion (MCAO) was induced in rats with thrombi generated by thread and subsequently treated with PN. After that, staining with 2,3,5-triphenyltetrazolium chloride was employed to evaluate the infarcted area, and electron microscopy was used to assess ultrastructural changes of the neurovascular unit. RNA-Seq was performed to determine the differential expressed genes (DEGs) which were then verified by qPCR. In total, 817 DEGs were identified to be related to the therapeutic effect of PN on stroke recovery. Further analysis by Gene Oncology analysis and Kyoto Encyclopedia of Genes and Genomes revealed that most of these genes were involved in the biological function of nerves and blood vessels through the regulation of neuroactive live receptor interactions of PI3K-Akt, Rap1, cAMP, and cGMP-PKG signaling, which included in the 18 pathways identified in our research, of which, 9 were reported firstly that related to PN’s neuroprotective effect. This research sheds light on the potential molecular mechanisms underlying the effects of PN on stroke recovery.
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- 2020
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7. Effect of SIS3 on Extracellular Matrix Remodeling and Repair in a Lipopolysaccharide-Induced ARDS Rat Model
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Qiong Liang, Qiqing Lin, Yueyong Li, Weigui Luo, Xia Huang, Yujie Jiang, Chunyan Qin, Jin Nong, Xiang Chen, Suren Rao Sooranna, and Liao Pinhu
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Immunologic diseases. Allergy ,RC581-607 - Abstract
The remodeling of the extracellular matrix (ECM) in the parenchyma plays an important role in the development of acute respiratory distress syndrome (ARDS), a disease characterized by lung injury. Although it is clear that TGF-β1 can modulate the expression of the extracellular matrix (ECM) through intracellular signaling molecules such as Smad3, its role as a therapeutic target against ARDS remains unknown. In this study, a rat model was established to mimic ARDS via intratracheal instillation of lipopolysaccharide (LPS). A selective inhibitor of Smad3 (SIS3) was intraperitoneally injected into the disease model, while phosphate-buffered saline (PBS) was used in the control group. Animal tissues were then evaluated using histological analysis, immunohistochemistry, RT-qPCR, ELISA, and western blotting. LPS was found to stimulate the expression of RAGE, TGF-β1, MMP2, and MMP9 in the rat model. Moreover, treatment with SIS3 was observed to reverse the expression of these molecules. In addition, pretreatment with SIS3 was shown to partially inhibit the phosphorylation of Smad3 and alleviate symptoms including lung injury and pulmonary edema. These findings indicate that SIS3, or the blocking of TGF-β/Smad3 pathways, could influence remodeling of the ECM and this may serve as a therapeutic strategy against ARDS.
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- 2020
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8. RETRACTED ARTICLE: Isoginkgetin attenuates endoplasmic reticulum stress-induced autophagy of brain after ischemic reperfusion injury
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Lingzhang Meng, Dong Li, Yingning Wu, Xuebin Li, Xiaohua Huang, Baosheng Li, Yueyong Li, Cheng Lin, Shaocai Qiu, Deyou Huang, and Zhongheng Wei
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Kinase ,Chemistry ,ATF6 ,Endoplasmic reticulum ,Autophagy ,Ischemia ,Bioengineering ,General Medicine ,Tunicamycin ,Pharmacology ,medicine.disease ,Applied Microbiology and Biotechnology ,chemistry.chemical_compound ,Unfolded protein response ,medicine ,Protein kinase A ,Biotechnology - Abstract
Isoginkgetin is characterized by properties of potent anticancer and anti-inflammation. To explore its effect on ischemic stroke, a rat model of ischemia/reperfusion (I/R) injury was established and induced by transient middle cerebral artery occlusion/reperfusion (MCAO/R). Different doses of isoginkgetin were intraperitoneally injected into each rat. Expressions of ER stress activation-related makers including phosphorylated inositol-requiring enzyme 1 (IRE1), phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (p-PERK), activating transcription factor-6 (ATF6), and two autophagy markers (ratio of LC3II/I and Beclin-1) were detected by western blot. Infarct volume, neurological deficits, and brain water content were detected. The results showed that ER stress and autophagy were activated by cerebral (I/R) injury, which could be effectively attenuated following pre-ischemia isoginkgetin administration. Moreover, autophagy induced by ER stress was triggered by the activation of PERK and IRE1 pathways. ER stress inhibitor (4-PBA) and ER related signaling inhibitors including PERK, GSK, IRE1, and DBSA markedly inhibited ER stress and autophagy induced by I/R. In addition, isoginkgetin markedly mitigated cerebral infarction, edema, neuronal apoptosis as well as neurological impairment induced by I/R injury, while tunicamycin (ER stress activator TM) and rapamycin (autophagy activator RAPA) could eliminate these lesions. This research identified a novel therapeutic agent isoginkgetin, which could effectively attenuate I/R injury by blocking autophagy induced by ER stress.
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- 2022
9. Nanoparticles in the Treatment of Alzheimer’s Disease with Magnetic Resonance
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Wubing Mao, Yueyong Li, Yingjun Zhang, Ning Zhu, Ting Nie, Huacheng Fu, Mingshan Zhu, Haichen Guan, Wenzhong Yi, and Min Feng
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Nuclear magnetic resonance ,Materials science ,medicine.diagnostic_test ,medicine ,Nanoparticle ,General Materials Science ,Magnetic resonance imaging - Abstract
This study was to explore the effect of nanoparticles on the cognitive function, learning and memory ability (LMA) of Alzheimer’s disease (AD) rats, and to analyze the changes on magnetic resonance (MR) image. Specifically, the TGN nanoparticles loading H102 (TGN-NP-H102) were prepared, and characterized first. The sprague-dawley (SD) rats were selected as the research subjects, and the AD model was constructed. They were divided into a Sham group (normal SD rats, group A), an AD model group (group B), an H102 group (treated with H102 drugs based on AD model, group C), and a TGN-NP-H102 group (treated with TGN-NP-H102 nanoparticles based on AD model, group D). The changes in T2 value in hippocampal CA1 area (T2-CA1) were analyzed, and the changes in cognitive function and LMA were tested with the Morris water maze experiment (Morris experiment). The results revealed that, the average PS (APS) of TGN-NP-H102 nanoparticles was 122.9±2.8 nm, and its average Zeta potential (AZP) was -28.8±0.2 mV. In group A, the TGN-NP-H102 nanoparticles still remained in the brain tissue homogenate by 74.3 ±4.8% after 10 hours, and the drug-release rate was 53.2 ± 3.2%. After 30 days of treatment, the T2-CA1 value of group D was lower (P P < 0.05). It indicated that, the brain-targeted TGN-NP-H102 nanoparticles prepared could act on the hippocampus of AD rats, and improve their LMA.
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- 2021
10. Efficacy of dexmedetomidine on myocardial ischemia/reperfusion injury in patients undergoing cardiac surgery with cardiopulmonary bypass: A protocol for systematic review and meta-analysis
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Gencheng Liang, Yueyong Li, Sheng Li, and Zhaohe Huang
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General Medicine - Published
- 2023
11. circRNA circARNT2 Suppressed the Sensitivity of Hepatocellular Carcinoma Cells to Cisplatin by Targeting the miR-155-5p/PDK1 Axis
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Zhonghen Wei, Baosheng Li, Yingning Wu, Cheng Lin, Deyou Huang, Gencheng Liang, Qiulan Jiang, Yueyong Li, Lingzhang Meng, Shuai Zhang, Yingjun Zhang, and Longhua Li
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0301 basic medicine ,cisplatin ,Biology ,circARNT2 ,miR-155 ,03 medical and health sciences ,0302 clinical medicine ,Downregulation and upregulation ,Drug Discovery ,microRNA ,medicine ,circRNA ,miR-155-5p ,HCC ,neoplasms ,Cisplatin ,Gene knockdown ,Cell growth ,Microarray analysis techniques ,Competing endogenous RNA ,lcsh:RM1-950 ,chemoresistance ,ceRNA ,digestive system diseases ,030104 developmental biology ,lcsh:Therapeutics. Pharmacology ,030220 oncology & carcinogenesis ,Cancer research ,Molecular Medicine ,Original Article ,medicine.drug - Abstract
Circular RNA (circRNA) is a novel subclass of noncoding-RNA molecules that participate in development and progression of a variety of human diseases via sponging microRNAs (miRNAs). Until now, the contributions of circRNAs in chemoresistance of hepatocellular carcinoma (HCC) remain largely unknown. In the present study, we aimed to investigate the role of circRNA in cisplatin resistance of HCC. We investigated the expression of circRNAs in 5 paired cisplatin-sensitive and cisplatin-resistant HCC tissues by microarray analysis. The qRT-PCR analysis was to investigate the expression pattern of circARNT2 in HCC patient tissues and cell lines. Then, the effects of circARNT2 on cisplatin resistance, cell proliferation, and apoptosis were assessed in HCC in vitro and in vivo. circARNT2 was significantly upregulated in HCC tissues and cell lines. Overexpression of circARNT2 in HCC was significantly correlated with aggressive characteristics and served as an independent risk factor for overall survival in patients with HCC. In vitro experiments showed that knockdown of circARNT2 inhibited cell proliferation and enhances the cisplatin sensitivity of HCC cells. Furthermore, circARNT2 facilitates HCC progression in vivo. We demonstrated that circARNT2 acts as a sponge for miR-155-5p and verified that PDK1 is a novel target of miR-155-5p. In summary, our study demonstrated that circARNT2 modulates cisplatin resistance through miR-155-5p/PDK1 pathway. Our findings indicated that circARNT2 may serve as a promising therapeutic target for overcoming cisplatin resistance for HCC., Graphical Abstract, Li et al. found that circARNT2 modulates cisplatin resistance through miR-155-5p/PDK1 pathway. Our findings indicated that circARNT2 may serve as a promising therapeutic target for overcoming cisplatin resistance for HCC.
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- 2021
12. Apelin Alleviates Meniscus Endothelial Cell Apoptosis in Osteoarthritis
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Dinggui Lu, Jihua Wei, Jian Chen, Jingjie Zhao, Jiajia Wang, Yuanxun Gong, Liuzhi Wei, Qiuju Wei, Huadeng Ban, Yueyong Li, Zechen Wang, Changtai Luo, Haidong Zhou, Jiajia Shen, Qiujiao Liao, Siyuan He, Weiyang Zhang, Qunqiang Luo, Kegong Xie, Jian Song, and Lingzhang Meng
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Medicine (General) ,Article Subject ,Biochemistry (medical) ,Clinical Biochemistry ,Endothelial Cells ,Apoptosis ,General Medicine ,R5-920 ,Osteoarthritis ,Genetics ,Apelin ,Humans ,Meniscus ,Molecular Biology ,Research Article - Abstract
Osteoarthritis (OA) is a degenerative disease characterized by articular cartilage and/or chondrocyte destruction, and although it has long been considered as a primary disease, the importance of meniscus endothelial cell modulation in the subchondral microenvironment has recently drawn attention. Previous studies have shown that apelin could potentially inhibit cellular apoptosis; however, it remains unclear whether apelin could play a protective role in protecting the endothelium in the OA meniscus. In this study, with the advantages of single-cell RNA sequencing (scRNA-seq) data, in combination with flow cytometry, we identified two endothelial subclusters in the meniscus, featured by high expression of Homeobox A13 (HOXA13) and Ras Protein-Specific Guanine Nucleotide Releasing Factor 2 (RASGRF2), respectively. Compared with control patients, both subclusters decreased in absolute cell numbers and exhibited downregulated APJ endogenous ligand (APLN, coding for apelin) and upregulated apelin receptor (APLNR, coding apelin receptor). Furthermore, we confirmed that in OA, decreased endothelial cell numbers, including both subclusters, were related to intrinsic apoptosis factors: one more relevant to caspase 3 (CASP3) and the other to BH3-Interacting Domain Death agonist (BID). In vitro culturing of meniscal endothelial cells purified from patients proved that apelin could significantly inhibit apoptosis by downregulating these two factors in endothelial cell subclusters, suggesting that apelin could potentially serve as a therapeutic target for patients with OA.
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- 2022
13. Isoginkgetin attenuates endoplasmic reticulum stress-induced autophagy of brain after ischemic reperfusion injury
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Yueyong Li, Lingzhang Meng, Baosheng Li, Deyou Huang, Xiaohua Huang, Cheng Lin, Dong Li, Shaocai Qiu, Yingning Wu, Zhongheng Wei, and Xuebin Li
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autophagy ,isoginkgetin ,ischemia/reperfusion (i/r) ,er stress ,TP248.13-248.65 ,Biotechnology - Abstract
Isoginkgetin is characterized by properties of potent anticancer and anti-inflammation. To explore its effect on ischemic stroke, a rat model of ischemia/reperfusion (I/R) injury was established and induced by transient middle cerebral artery occlusion/reperfusion (MCAO/R). Different doses of isoginkgetin were intraperitoneally injected into each rat. Expressions of ER stress activation-related makers including phosphorylated inositol-requiring enzyme 1 (IRE1), phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (p-PERK), activating transcription factor-6 (ATF6), and two autophagy markers (ratio of LC3II/I and Beclin-1) were detected by western blot. Infarct volume, neurological deficits, and brain water content were detected. The results showed that ER stress and autophagy were activated by cerebral (I/R) injury, which could be effectively attenuated following pre-ischemia isoginkgetin administration. Moreover, autophagy induced by ER stress was triggered by the activation of PERK and IRE1 pathways. ER stress inhibitor (4-PBA) and ER related signaling inhibitors including PERK, GSK, IRE1, and DBSA markedly inhibited ER stress and autophagy induced by I/R. In addition, isoginkgetin markedly mitigated cerebral infarction, edema, neuronal apoptosis as well as neurological impairment induced by I/R injury, while tunicamycin (ER stress activator TM) and rapamycin (autophagy activator RAPA) could eliminate these lesions. This research identified a novel therapeutic agent isoginkgetin, which could effectively attenuate I/R injury by blocking autophagy induced by ER stress.
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- 2021
14. Study on Torrential Rain Disaster Index and Threshold in Zhangjiajie City.
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Yueyong LI, Wei ZHOU, Hao LI, and Ke LIANG
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RAINFALL , *MARINE insurance , *METEOROLOGICAL services , *ACCIDENT insurance , *INSURANCE companies , *EMERGENCY management , *NATURAL disasters - Abstract
Based on the precipitation data and torrential rain disaster data in Zhangjiajie City of Hunan Province from 2Û16 to 2020, taking the claim cases of the property and cargo insurance (hereinafter referred to as "property and cargo insurance") from Hunan Branch of the People's Insurance Company of China as the research sample, the Dominance Analysis Method was used to determine the influence weights of disaster-causing factors to establish a Comprehensive disaster-causing index (I) model of torrential rain. Second, an exponential function was used to fit the relationship between the number of town or street which filed claims of property and cargo insurance and I, then to determine the threshold of I corresponding to different accident levels. The claim cases caused by torrential rain disaster in Zhangjiajie in the flood season of 2021 were selected to verify the I and its threshold. The results showed that the number of property and cargo insurance accidents caused by torrential rain in Zhangjiajie was generally low in east and west but high in middle areas. Among the disaster-causing factors, the weight of the 96-h accumulated precipitation on the scope of accident was the largest, reaching 28. 6%. The simulated grades of the scope of accident, the amount of claim and the number of accidents of property and cargo insurance had a high correlation with the grades of actual disasters, and all passed the test at the 0.01 significance level. The threshold test results showed that the consistency rate or accuracy between the predicted level and the actual level of torrential rain disaster-causing cases was 71.4%, in which the predicted values of accuracy for the mild, moderate and severe disaster levels were 70%, 70% and 100%, respectively. Therefore, the threshold of I established in this study can be used for the industrial meteorological services related to the property and cargo insurance in Zhangjiajie. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
15. Hes1 Knockdown Exacerbates Ischemic Stroke Following tMCAO by Increasing ER Stress-Dependent Apoptosis via the PERK/eIF2α/ATF4/CHOP Signaling Pathway
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Huatuo Huang, Zhongheng Wei, Huadong Huang, Yingjun Zhang, Yingning Wu, Qifeng Lu, Huangde Fu, Yueyong Li, Pinhu Liao, Houji Qin, and Guizhen Mao
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Male ,0301 basic medicine ,congenital, hereditary, and neonatal diseases and abnormalities ,endocrine system ,Indoles ,Physiology ,Eukaryotic Initiation Factor-2 ,Apoptosis ,Brain damage ,CHOP ,Mice ,eIF-2 Kinase ,03 medical and health sciences ,0302 clinical medicine ,medicine ,Animals ,Gene knockdown ,Cerebral infarction ,business.industry ,Adenine ,General Neuroscience ,ATF4 ,Brain ,Infarction, Middle Cerebral Artery ,General Medicine ,Endoplasmic Reticulum Stress ,medicine.disease ,Activating Transcription Factor 4 ,Mice, Inbred C57BL ,Stroke ,030104 developmental biology ,embryonic structures ,Unfolded protein response ,Cancer research ,Transcription Factor HES-1 ,Original Article ,medicine.symptom ,Signal transduction ,business ,Transcription Factor CHOP ,030217 neurology & neurosurgery ,Signal Transduction - Abstract
Apoptosis induced by endoplasmic reticulum (ER) stress plays a crucial role in mediating brain damage after ischemic stroke. Recently, Hes1 (hairy and enhancer of split 1) has been implicated in the regulation of ER stress, but whether it plays a functional role after ischemic stroke and the underlying mechanism remain unclear. In this study, using a mouse model of ischemic stroke via transient middle cerebral artery occlusion (tMCAO), we found that Hes1 was induced following brain injury, and that siRNA-mediated knockdown of Hes1 increased the cerebral infarction and worsened the neurological outcome, suggesting that Hes1 knockdown exacerbates ischemic stroke. In addition, mechanistically, Hes1 knockdown promoted apoptosis and activated the PERK/eIF2α/ATF4/CHOP signaling pathway after tMCAO. These results suggest that Hes1 knockdown promotes ER stress-induced apoptosis. Furthermore, inhibition of PERK with the specific inhibitor GSK2606414 markedly attenuated the Hes1 knockdown-induced apoptosis and the increased cerebral infarction as well as the worsened neurological outcome following tMCAO, implying that the protection of Hes1 against ischemic stroke is associated with the amelioration of ER stress via modulating the PERK/eIF2α/ATF4/CHOP signaling pathway. Taken together, these results unveil the detrimental role of Hes1 knockdown after ischemic stroke and further relate it to the regulation of ER stress-induced apoptosis, thus highlighting the importance of targeting ER stress in the treatment of ischemic stroke.
- Published
- 2019
16. Genetic variants in IL-33/ST2 pathway with the susceptibility to hepatocellular carcinoma in a Chinese population
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Zhongheng Wei, Zhong-Qiu Tan, Yueyong Li, and Shi-Qing Huang
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Male ,0301 basic medicine ,Oncology ,medicine.medical_specialty ,Carcinoma, Hepatocellular ,Genotype ,Angiogenesis ,Immunology ,medicine.disease_cause ,Polymorphism, Single Nucleotide ,Biochemistry ,Metastasis ,03 medical and health sciences ,0302 clinical medicine ,Asian People ,Gene Frequency ,Internal medicine ,Tumor Microenvironment ,medicine ,Humans ,Immunology and Allergy ,Genetic Predisposition to Disease ,Molecular Biology ,Genotyping ,Alleles ,Genetic Association Studies ,Tumor microenvironment ,business.industry ,Liver Neoplasms ,Interleukin ,Hematology ,Middle Aged ,Interleukin-33 ,medicine.disease ,Interleukin-1 Receptor-Like 1 Protein ,030104 developmental biology ,Case-Control Studies ,030220 oncology & carcinogenesis ,Hepatocellular carcinoma ,Female ,business ,Carcinogenesis ,Signal Transduction - Abstract
Interleukin (IL)-33/ST2 pathway plays a pivotal role in tumorigenesis through influencing cancer stemness, tumor growth, metastasis, angiogenesis, and accumulation of regulatory T cells in tumor microenvironments. The aim of this study was to investigate the association of IL-33 rs7025417 and ST2 rs3821204 with the risk of hepatocellular carcinoma (HCC). Genotyping of IL-33 rs7025417 and ST2 rs3821204 was carried out using a Taqman assay. IL-33 and ST2 mRNA was examined using real-time PCR and plasma IL-33 and sST2 levels were measured using enzyme-linked immunosorbent assay. The ST2 rs3821204 CC genotype was associated with a significantly increased risk of HCC (CC vs. GG: adjusted OR = 2.29, 95% CI, 1.39-3.78; dominant model: adjusted OR = 1.58, 95% CI, 1.12-2.23; recessive model: adjusted OR = 1.88, 95% CI, 1.21-2.93; C vs. G: adjusted OR = 1.53, 95% CI, 1.20-1.95). Gene-environment interaction analysis showed that the risk effect of rs3821204 CG/CC genotypes was more evident in smokers (adjusted OR = 1.70, 95% CI, 1.13-2.55) and drinkers (adjusted OR = 1.57, 95% CI, 1.04-2.37). The increased risk was also observed in combined analysis. Moreover, HCC patients with ST2 rs3821204 CC genotype had higher levels of mRNA and protein expression (P 0.05). These findings suggest that ST2 rs3821204 CC genotype may contribute to hepatocarcinogenesis by enhancing ST2 production at the transcriptional and translational level.
- Published
- 2019
17. CircANKRD36 Knockdown Suppressed Cell Viability and Migration of LPS-Stimulated RAW264.7 Cells by Sponging MiR-330
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Qiong Liang, Yueyong Li, Qiqing Lin, and Chunyan Qin
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0301 basic medicine ,Lipopolysaccharides ,ARDS ,Cell Survival ,Immunology ,Cell ,Inflammation ,Lung injury ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Cell Movement ,medicine ,Immunology and Allergy ,Animals ,Humans ,ROCK1 ,Viability assay ,Gene knockdown ,Respiratory Distress Syndrome ,business.industry ,Macrophages ,Nuclear Proteins ,Cell migration ,medicine.disease ,MicroRNAs ,030104 developmental biology ,medicine.anatomical_structure ,RAW 264.7 Cells ,030220 oncology & carcinogenesis ,Gene Knockdown Techniques ,Cancer research ,medicine.symptom ,business - Abstract
Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is an independent risk factor for mortality in patients with sepsis. In this study, we attempt to investigate the molecular mechanism of circANKRD36 underlying sepsis-induced ALI/ARDS in vitro. We first detected the altered circRNAs in serums of patients with sepsis-induced ARDS using circRNAs microarray. CircANKRD36 expression in serums and LPS-stimulated RAW264.7 cells was measured using qRT-PCR. CCK-8, cell migration, ELISA, and qRT-PCR were applied to the evaluation of cell biological behavior and inflammation reaction. The results showed that circANKRD36 expression was significantly elevated in serum of patients with sepsis-induced ARDS. Knockdown of circANKRD36 inhibited cell viability and migration and alleviated inflammation of lipopolysaccharide-stimulated (LPS-stimulated) RAW264.7 cells. Bioinformatic analysis demonstrated that circANKRD36 serves as a sponge for miR-330 and ROCK1 was directly targeted by miR-330. Furthermore, knockdown of circANKRD36 repressed ROCK1 expression by targeting miR-330. In short, circANKRD36 knockdown suppressed cell viability and migration of LPS-stimulated RAW264.7 cells in vitro via sponging miR-330, which may provide new ideas for the treatment of sepsis-induced ARDS.
- Published
- 2021
18. Effect of SIS3 on Extracellular Matrix Remodeling and Repair in a Lipopolysaccharide-Induced ARDS Rat Model
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Xiang Chen, Liao Pinhu, Yujie Jiang, Chunyan Qin, Qiong Liang, Xia Huang, Weigui Luo, Yueyong Li, Suren R. Sooranna, Jin Nong, and Qiqing Lin
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Lipopolysaccharides ,ARDS ,MMP2 ,Article Subject ,Lipopolysaccharide ,Neutrophils ,Pyridines ,Immunology ,Receptor for Advanced Glycation End Products ,Gene Expression ,Lung injury ,Pharmacology ,MMP9 ,Extracellular matrix ,Transforming Growth Factor beta1 ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,medicine ,Immunology and Allergy ,Animals ,Pyrroles ,Smad3 Protein ,030304 developmental biology ,0303 health sciences ,Respiratory Distress Syndrome ,Chemistry ,General Medicine ,RC581-607 ,Pulmonary edema ,medicine.disease ,Isoquinolines ,Extracellular Matrix ,Rats ,Disease Models, Animal ,030228 respiratory system ,Matrix Metalloproteinase 9 ,Matrix Metalloproteinase 2 ,Collagen ,Immunologic diseases. Allergy ,Intracellular ,Biomarkers ,Research Article - Abstract
The remodeling of the extracellular matrix (ECM) in the parenchyma plays an important role in the development of acute respiratory distress syndrome (ARDS), a disease characterized by lung injury. Although it is clear that TGF-β1 can modulate the expression of the extracellular matrix (ECM) through intracellular signaling molecules such as Smad3, its role as a therapeutic target against ARDS remains unknown. In this study, a rat model was established to mimic ARDS via intratracheal instillation of lipopolysaccharide (LPS). A selective inhibitor of Smad3 (SIS3) was intraperitoneally injected into the disease model, while phosphate-buffered saline (PBS) was used in the control group. Animal tissues were then evaluated using histological analysis, immunohistochemistry, RT-qPCR, ELISA, and western blotting. LPS was found to stimulate the expression of RAGE, TGF-β1, MMP2, and MMP9 in the rat model. Moreover, treatment with SIS3 was observed to reverse the expression of these molecules. In addition, pretreatment with SIS3 was shown to partially inhibit the phosphorylation of Smad3 and alleviate symptoms including lung injury and pulmonary edema. These findings indicate that SIS3, or the blocking of TGF-β/Smad3 pathways, could influence remodeling of the ECM and this may serve as a therapeutic strategy against ARDS.
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- 2020
19. AKR1C1 Contributes to Cervical Cancer Progression via Regulating TWIST1 Expression
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Cheng Lin, Zhongheng Wei, Yueyong Li, Xing Wei, and Zhong-Qiu Tan
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0301 basic medicine ,AKR1C1 ,medicine.medical_treatment ,Uterine Cervical Neoplasms ,Reductase ,Biology ,Biochemistry ,Targeted therapy ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Genetics ,medicine ,Humans ,Molecular Biology ,20-Hydroxysteroid Dehydrogenases ,Ecology, Evolution, Behavior and Systematics ,PI3K/AKT/mTOR pathway ,Cervical cancer ,Aldosterone ,Twist-Related Protein 1 ,Nuclear Proteins ,General Medicine ,medicine.disease ,Human genetics ,In vitro ,Neoplasm Proteins ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,chemistry ,030220 oncology & carcinogenesis ,Cancer research ,Female ,HeLa Cells - Abstract
Cervical cancer (CC) is a common gynecological malignancy, accounting for 10% of all gynecological cancers. Recently, targeted therapy for CC has shown unprecedented advantages. To improve CC patients' prognosis, there are still urgent needs to develop more promising therapeutic targets. Aldo-keto reductase 1 family member C1 (AKR1C1) is a type of aldosterone reductase and plays a regulatory role in a variety of key metabolic pathways. Several studies indicated that AKR1C1 was highly expressed in a series of tumors, and participated in the progression of these tumors. However, the possible effects of AKR1C1 on CC progression remain unclear. Herein, we revealed AKR1C1 was highly expressed in human CC tissues and correlated with the clinical characteristics of patients with CC. AKR1C1 could regulate the proliferation and invasion of cervical cancer cells in vitro. Further experiments showed that AKR1C1 could regulate TWIST1 expression and AKT pathway. In summary, we confirmed the involvement of AKR1C1 in CC progression, and therefore AKR1C1 may have the potential to be a molecular target for CC treatment.
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- 2020
20. Genes Induced by Panax Notoginseng in a Rodent Model of Ischemia-Reperfusion Injury
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Zechen Wang, Genliang Li, Liuzhi Wei, Xionglin Tang, Qing Huang, Kegong Xie, Chongdong Jian, Jingjie Zhao, Qianli Tang, Jianmin Huang, Xiaohua Huang, Lu Huang, Xuebin Li, Lanqing Meng, Qiuping Chen, Lan Li, Linbo He, Lingzhang Meng, Jihua Wei, Rong Qiu, Dinggui Lu, Jian Chen, Chenyi Zhuo, Qiuju Wei, Qunqiang Luo, Ping Liang, Yang Ouyang, Hongfei Yao, Jun Wu, Anding Xu, Yueyong Li, Linxue Luo, and Zhongheng Wei
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Article Subject ,Biopsy ,medicine.medical_treatment ,Immunology ,Ischemia ,Panax notoginseng ,Rodentia ,Pharmacology ,Neuroprotection ,03 medical and health sciences ,0302 clinical medicine ,Animals ,Immunology and Allergy ,Medicine ,cardiovascular diseases ,KEGG ,Receptor ,Stroke ,030304 developmental biology ,0303 health sciences ,biology ,business.industry ,Gene Expression Profiling ,Computational Biology ,General Medicine ,RC581-607 ,medicine.disease ,biology.organism_classification ,Rats ,Disease Models, Animal ,Gene Ontology ,Gene Expression Regulation ,Reperfusion Injury ,cardiovascular system ,Female ,Immunologic diseases. Allergy ,Transcriptome ,business ,Stroke recovery ,Reperfusion injury ,Biomarkers ,030217 neurology & neurosurgery ,Drugs, Chinese Herbal ,Signal Transduction ,Research Article - Abstract
Stroke is a cerebrovascular disease that results in decreased blood flow. Although Panax notoginseng (PN), a Chinese herbal medicine, has been proven to promote stroke recovery, its molecular mechanism remains unclear. In this study, middle cerebral artery occlusion (MCAO) was induced in rats with thrombi generated by thread and subsequently treated with PN. After that, staining with 2,3,5-triphenyltetrazolium chloride was employed to evaluate the infarcted area, and electron microscopy was used to assess ultrastructural changes of the neurovascular unit. RNA-Seq was performed to determine the differential expressed genes (DEGs) which were then verified by qPCR. In total, 817 DEGs were identified to be related to the therapeutic effect of PN on stroke recovery. Further analysis by Gene Oncology analysis and Kyoto Encyclopedia of Genes and Genomes revealed that most of these genes were involved in the biological function of nerves and blood vessels through the regulation of neuroactive live receptor interactions of PI3K-Akt, Rap1, cAMP, and cGMP-PKG signaling, which included in the 18 pathways identified in our research, of which, 9 were reported firstly that related to PN’s neuroprotective effect. This research sheds light on the potential molecular mechanisms underlying the effects of PN on stroke recovery.
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- 2020
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21. Long noncoding RNA LINC00511 contributes to breast cancer tumourigenesis and stemness by inducing the miR-185-3p/E2F1/Nanog axis
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Zhi-Zhai Luo, Guanming Lu, Yan-Fei Ma, Lifeng Zhao, Jinlan Lu, Qiulan Jiang, Yongcheng Chen, Shi-Qing Huang, Qianfang Huang, Yueyong Li, Qiang Qin, and Zhongheng Wei
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0301 basic medicine ,Homeobox protein NANOG ,Cancer Research ,Carcinogenesis ,Breast Neoplasms ,Biology ,Transfection ,medicine.disease_cause ,lcsh:RC254-282 ,Nanog ,Mice ,03 medical and health sciences ,0302 clinical medicine ,SOX2 ,Transcription (biology) ,Cell Line, Tumor ,LINC00511 ,medicine ,Animals ,Humans ,E2F1 ,Competing endogenous RNA ,Research ,RNA ,Nanog Homeobox Protein ,miR-185-3p ,Middle Aged ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,Breast cancer stem cells ,Long non-coding RNA ,MicroRNAs ,030104 developmental biology ,Oncology ,030220 oncology & carcinogenesis ,MCF-7 Cells ,Neoplastic Stem Cells ,Cancer research ,Heterografts ,Female ,RNA, Long Noncoding ,E2F1 Transcription Factor - Abstract
Background Emerging evidence have illustrated the vital role of long noncoding RNAs (lncRNAs) long intergenic non-protein coding RNA 00511 (LINC00511) on the human cancer progression and tumorigenesis. However, the role of LINC00511 in breast cancer tumourigenesis is still unknown. This research puts emphasis on the function of LINC00511 on the breast cancer tumourigenesis and stemness, and investigates the in-depth mechanism. Methods The lncRNA and RNA expression were measured using RT-PCR. Protein levels were measured using western blotting analysis. CCK-8, colony formation assays and transwell assay were performed to evaluate the cell proliferation ability and invasion. Sphere-formation assay was also performed for the stemness. Bioinformatic analysis, chromatin immunoprecipitation (ChIP) and luciferase reporter assays were carried to confirm the molecular binding. Results LINC00511 was measured to be highly expressed in the breast cancer specimens and the high-expression was correlated with the poor prognosis. Functionally, the gain and loss-of-functional experiments revealed that LINC00511 promoted the proliferation, sphere-formation ability, stem factors (Oct4, Nanog, SOX2) expression and tumor growth in breast cancer cells. Mechanically, LINC00511 functioned as competing endogenous RNA (ceRNA) for miR-185-3p to positively recover E2F1 protein. Furthermore, transcription factor E2F1 bind with the promoter region of Nanog gene to promote it transcription. Conclusion In conclusion, our data concludes that LINC00511/miR-185-3p/E2F1/Nanog axis facilitates the breast cancer stemness and tumorigenesis, providing a vital insight for them. Electronic supplementary material The online version of this article (10.1186/s13046-018-0945-6) contains supplementary material, which is available to authorized users.
- Published
- 2018
22. Additional file 2: of Long noncoding RNA LINC00511 contributes to breast cancer tumourigenesis and stemness by inducing the miR-185-3p/E2F1/Nanog axis
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Guanming Lu, Yueyong Li, Yanfei Ma, Jinlan Lu, Yongcheng Chen, Qiulan Jiang, Qin, Qiang, Lifeng Zhao, Qianfang Huang, Zhizhai Luo, Shiqing Huang, and Zhongheng Wei
- Abstract
Table S2. Primers sequences for ChIP. (DOCX 16Â kb)
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- 2018
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23. Additional file 3: of Long noncoding RNA LINC00511 contributes to breast cancer tumourigenesis and stemness by inducing the miR-185-3p/E2F1/Nanog axis
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Guanming Lu, Yueyong Li, Yanfei Ma, Jinlan Lu, Yongcheng Chen, Qiulan Jiang, Qin, Qiang, Lifeng Zhao, Qianfang Huang, Zhizhai Luo, Shiqing Huang, and Zhongheng Wei
- Abstract
Table S3. Nanog promoter region. (DOCX 16 kb)
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- 2018
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24. Xingbi Gel Ameliorates Allergic Rhinitis by Regulating IFN-γ Gene Promoter Methylation in CD4+ T Cells via the ERK-DNMT Pathway
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Si Ai, Yueyong Lin, Jian Zheng, and Xiangli Zhuang
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allergic rhinitis ,Xingbi gel ,methylation ,ERK signaling pathway ,CD4+ T cells ,Surgery ,RD1-811 - Abstract
Allergic rhinitis (AR) is a common, non-infectious, chronic nasal mucosal disease primarily mediated by immunoglobulin E (IgE) following allergen exposure. Currently, studies on AR mainly focus on cytokines, IgE and its receptors, basophils, eosinophils, mast cells, and related genes. Among these, an imbalance between T helper (Th) 1 and Th2 cells is considered an important mechanism underlying AR pathogenesis. The most important cytokines in AR are interleukin (Il)-4 and interferon gamma (IFN-γ) which are secreted by Th2 and Th1 cells, respectively. Il-4 and IFN-γ are antagonistic to each other in regulating IgE synthesis. In this study, the expression of extracellular signal-regulated protein kinase (ERK) 1/2 and its phosphorylation from p-ERK1/2, were significantly increased in a cluster of differentiation of 4+ T cells of AR mice, suggesting that the ERK signaling pathway in these cells is involved in the occurrence and development of AR. This result also implies an enhanced expression of deoxyribonucleic acid methyltransferases (DNMTs). To verify the relationship between ERK signaling and DNMT expression, AR mice were treated with PD98059, a specific inhibitor of the ERK1/2 signaling pathway. The results revealed that perturbations in ERK signaling were significantly positively correlated with the downregulation of DNMT1 expression. Pharmacological intervention is key to treating AR. This study demonstrated that Xingbi gel intervention affected both serum IgE levels and AR behavior scores in mice. Based on its effects on IFN-γ gene expression, the regulation of Th1/Th2 balance, and the ERK signaling pathway, research on the effects of Xingbi gel on AR may provide new avenues in its prevention and treatment.
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- 2021
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25. ICONE15-10494 900MW PWR CONTAINMENT MECHANICAL BEHAVOIOR CHARACTERISTICS DURING CONTAINMENT TEST
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ShenBin Nie, YueYong Li, and XuYAO Zhang
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Containment (computer programming) ,Materials science ,Strain (chemistry) ,business.industry ,Structural engineering ,Deformation (meteorology) ,business - Published
- 2007
26. Characterizing the DNA Damage Response by Cell Tracking Algorithms and Cell Features Classification Using High-Content Time-Lapse Analysis.
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Walter Georgescu, Alma Osseiran, Maria Rojec, Yueyong Liu, Maxime Bombrun, Jonathan Tang, and Sylvain V Costes
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Medicine ,Science - Abstract
Traditionally, the kinetics of DNA repair have been estimated using immunocytochemistry by labeling proteins involved in the DNA damage response (DDR) with fluorescent markers in a fixed cell assay. However, detailed knowledge of DDR dynamics across multiple cell generations cannot be obtained using a limited number of fixed cell time-points. Here we report on the dynamics of 53BP1 radiation induced foci (RIF) across multiple cell generations using live cell imaging of non-malignant human mammary epithelial cells (MCF10A) expressing histone H2B-GFP and the DNA repair protein 53BP1-mCherry. Using automatic extraction of RIF imaging features and linear programming techniques, we were able to characterize detailed RIF kinetics for 24 hours before and 24 hours after exposure to low and high doses of ionizing radiation. High-content-analysis at the single cell level over hundreds of cells allows us to quantify precisely the dose dependence of 53BP1 protein production, RIF nuclear localization and RIF movement after exposure to X-ray. Using elastic registration techniques based on the nuclear pattern of individual cells, we could describe the motion of individual RIF precisely within the nucleus. We show that DNA repair occurs in a limited number of large domains, within which multiple small RIFs form, merge and/or resolve with random motion following normal diffusion law. Large foci formation is shown to be mainly happening through the merging of smaller RIF rather than through growth of an individual focus. We estimate repair domain sizes of 7.5 to 11 µm2 with a maximum number of ~15 domains per MCF10A cell. This work also highlights DDR which are specific to doses larger than 1 Gy such as rapid 53BP1 protein increase in the nucleus and foci diffusion rates that are significantly faster than for spontaneous foci movement. We hypothesize that RIF merging reflects a "stressed" DNA repair process that has been taken outside physiological conditions when too many DSB occur at once. High doses of ionizing radiation lead to RIF merging into repair domains which in turn increases DSB proximity and misrepair. Such finding may therefore be critical to explain the supralinear dose dependence for chromosomal rearrangement and cell death measured after exposure to ionizing radiation.
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- 2015
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27. Multiple novel alternative splicing forms of FBXW7α have a translational modulatory function and show specific alteration in human cancer.
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Yueyong Liu, Shancheng Ren, Andres Castellanos-Martin, Jesus Perez-Losada, Yong-Won Kwon, Yurong Huang, Zeran Wang, Mar Abad, Juan J Cruz-Hernandez, Cesar A Rodriguez, Yinghao Sun, and Jian-Hua Mao
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Medicine ,Science - Abstract
FBXW7 acts as a tumor suppressor through ubiquitination and degradation of multiple oncoproteins. Loss of FBXW7 expression, which could be partially attributed by the genomic deletion or mutation of FBXW7 locus, is frequently observed in various human cancers. However, the mechanisms regulating FBXW7 expression still remain poorly understood. Here we examined the 5' region of FBXW7 gene to investigate the regulation of FBXW7 expression. We identified seven alternative splicing (AS) 5'-UTR forms of FBXW7α that are composed of multiple novel non-coding exons. A significant difference in translational efficiency among these 5'-UTRs variants was observed by in vivo Luciferase reporter assay and Western blot. Furthermore, we found that the mRNA level of the AS form with high translational efficiency was specifically reduced in more than 80% of breast cancer cell lines and in more than 50% of human primary cancers from various tissues. In addition, we also identified mutations of FBXW7 in prostate cancers (5.6%), kidney cancers (16.7%), and bladder cancers (18.8%). Our results suggest that in addition to mutation, differential expression of FBXW7α AS forms with different translational properties may serve as a novel mechanism for inactivation of FBXW7 in human cancer.
- Published
- 2012
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