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7. Structural insights into the ubiquitylation strategy of the oligomeric CRL2FEM1B E3 ubiquitin ligase.

Author

Dai, Zonglin, Liang, Ling, Wang, Weize, Zuo, Peng, Yu, Shang, Liu, Yaqi, Zhao, Xuyang, Lu, Yishuo, Jin, Yan, Zhang, Fangting, Ding, Dian, Deng, Weiwei, and Yin, Yuxin

Subjects
UBIQUITIN ligases, UBIQUITINATION, ALZHEIMER'S disease, OLIGOMERIZATION
Abstract

Cullin-RING E3 ubiquitin ligase (CRL) family members play critical roles in numerous biological processes and diseases including cancer and Alzheimer's disease. Oligomerization of CRLs has been reported to be crucial for the regulation of their activities. However, the structural basis for its regulation and mechanism of its oligomerization are not fully known. Here, we present cryo-EM structures of oligomeric CRL2FEM1B in its unneddylated state, neddylated state in complex with BEX2 as well as neddylated state in complex with FNIP1/FLCN. These structures reveal that asymmetric dimerization of N8-CRL2FEM1B is critical for the ubiquitylation of BEX2 while FNIP1/FLCN is ubiquitylated by monomeric CRL2FEM1B. Our data present an example of the asymmetric homo-dimerization of CRL. Taken together, this study sheds light on the ubiquitylation strategy of oligomeric CRL2FEM1B according to substrates with different scales. Synopsis: The structural basis and biological importance of cullin-RING ubiquitin ligase (CRL) oligomerization remain largely unclear. Here, high-resolution cryo-EM and biochemical data reveal that oligomerization of CRL2FEM1B serves as a structural foundation for accommodating substrates of varying sizes. Cryo-EM structures show oligomeric CRL2FEM1B in its unneddylated state and as neddylated form in complex with different substrates. RBX1 and CUL2 participate in the assembly of CRL2FEM1B oligomers. Asymmetric homo-dimerization allows CRL2FEM1B to ubiquitinate substrates with small scales, such as BEX2. Large substrates such as FNIP1/FLCN complexes are ubiquitinated by monomeric CRL2FEM1B. Asymmetric homo-dimerization allows ubiquitination of substrates with small scales, while large substrates are targeted by monomeric CRL2-FEM1B E3. [ABSTRACT FROM AUTHOR]

Published
2024
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15. Acetate Promotes SNAI1 Expression by ACSS2-Mediated Histone Acetylation Under Glucose Limitation in Renal Cell Carcinoma Cell

Author

Yao, Lv, Jiang, Linying, Zhang, Fuxing, Li, Minghua, Yang, Bo, Zhang, Fangting, Guo, Xiaoqiang, Yao, Lv, Jiang, Linying, Zhang, Fuxing, Li, Minghua, Yang, Bo, Zhang, Fangting, and Guo, Xiaoqiang

Abstract

Metastasis is the main cause of cancer-associated deaths, yet this complex process is still not well understood. Many studies have shown that acetate is involved in cancer metastasis, but the molecular mechanisms remain to be elucidated. In the present study, we first measured the effect of acetate on zinc finger transcriptional repressor SNAI1 and acetyl-CoA synthetase 2 (ACSS2) under glucose limitation in renal cell carcinoma cell lines, 786-O and ACHN. Then, RNA interference and overexpression of ACSS2 were used to detect the role of acetate on SNAI1 expression and cell migration. Finally, chromatin immunoprecipitation assay (ChIP) was used to investigate the regulatory mechanism of acetate on SNAI1 expression. The results showed that acetate increased the expressions of SNAI1 and ACSS2 under glucose limitation. ACSS2 knockdown significantly decreased acetate-induced SNAI1 expression and cell migration, whereas overexpression of ACSS2 increased SNAI1 level and histone H3K27 acetylation (H3K27ac). ChIP results revealed that acetate increased H3K27ac levels in regulatory region of SNAI1, but did not increase ACSS2-binding ability. Our study identified a novel inducer, acetate, which can promote SNAI1 expression by ACSS2-mediated histone acetylation in partly. This finding has important implication in treatment of metastatic cancers.

Published
2020

20. TBC1D20 deficiency induces Sertoli cell apoptosis by triggering irreversible endoplasmic reticulum stress in mice

Author

Chang, Wen-Lin, Cui, Lina, Gu, Yanli, Li, Minghua, Ma, Qian, Zhang, Zeng, Ye, Jing, Zhang, Fangting, Yu, Jing, Gui, Yaoting, Chang, Wen-Lin, Cui, Lina, Gu, Yanli, Li, Minghua, Ma, Qian, Zhang, Zeng, Ye, Jing, Zhang, Fangting, Yu, Jing, and Gui, Yaoting

Abstract

Male 'blind sterile' mice with the causative TBC1 domain family member 20 (TBC1D20) deficiency are infertile with excessive germ cell apoptosis and spermatogenesis arrest at the spermatid stage. Sertoli cells are characterised as 'nurse cells' essential for normal spermatogenesis, but the role and corresponding molecular mechanisms of TBC1D20 deficiency in Sertoli cells of mice are not clear to date. In the present study, the histopathology of the testis and Sertoli cell proliferation and apoptosis were determined, and the corresponding molecular mechanisms were investigated by western blotting. Our data showed that TBC1D20 exhibits a testis-abundant expression pattern, and its expression level is positively associated with spermatogenesis. TBC1D20 is assembled in the Golgi and endoplasmic reticulum and is widely expressed by various germ cell subtypes and Sertoli cells. TBC1D20 deficiency in Sertoli cells led to an excessive apoptosis ratio and G1/S arrest. The increased apoptosis of TBC1D20-deficient Sertoli cells resulted from caspase-12 activation. TBC1D20-deficient Sertoli cells had an abnormal Golgi-endoplasmic reticulum structure, which led to endoplasmic reticulum stress, resulting in cell cycle arrest and excessive apoptosis. It suggested that TBC1D20 deficiency triggers irreversible endoplasmic reticulum stress resulting in G1/S arrest and excessive apoptosis in TBC1D20-deficient Sertoli cells, and TBC1D20 deficiency in Sertoli cells may also contribute to the infertility phenotype in 'blind sterile' male mice.

Published
2019

24. Corrigendum to “MiR-23a-3p acts as an oncogene and potential prognostic biomarker by targeting PNRC2 in RCC” [Biomed. Pharmacother. 110 (2019) 656–666]

Author

Quan, Jing, primary, Pan, Xiang, additional, Li, Yawen, additional, Hu, Yimin, additional, Tao, Lingzhi, additional, Li, Zuwei, additional, Zhao, Liwen, additional, Wang, Jingyao, additional, Li, Hang, additional, Lai, Yulin, additional, Zhou, Liang, additional, Lin, Canbin, additional, Gui, Yaoting, additional, Ye, Jing, additional, Zhang, Fangting, additional, and Lai, Yongqing, additional

Published
2019
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25. MiR-23a-3p acts as an oncogene and potential prognostic biomarker by targeting PNRC2 in RCC

Author

Quan, Jing, primary, Pan, Xiang, additional, Li, Yawen, additional, Hu, Yimin, additional, Tao, Lingzhi, additional, Li, Zuwei, additional, Zhao, Liwen, additional, Wang, Jingyao, additional, Li, Hang, additional, Lai, Yulin, additional, Zhou, Liang, additional, Lin, Canbin, additional, Gui, Yaoting, additional, Ye, Jing, additional, Zhang, Fangting, additional, and Lai, Yongqing, additional

Published
2019
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28. Oncogenic miR-425-5p is Associated with Cellular Migration, Proliferation and Apoptosis in Renal Cell Carcinoma

Author

Quan, Jing, Li, Yawen, Pan, Xiang, Lai, Yulin, He, Tao, Lin, Canbin, Zhou, Liang, Zhao, Liwen, Sun, Shuolei, Ding, Yu, Tao, Lingzhi, Hu, Yimin, Wu, Xionghui, Chen, Zebo, Zhang, Fangting, Ye, Jing, Ni, Liangchao, Lai, Yongqing, Quan, Jing, Li, Yawen, Pan, Xiang, Lai, Yulin, He, Tao, Lin, Canbin, Zhou, Liang, Zhao, Liwen, Sun, Shuolei, Ding, Yu, Tao, Lingzhi, Hu, Yimin, Wu, Xionghui, Chen, Zebo, Zhang, Fangting, Ye, Jing, Ni, Liangchao, and Lai, Yongqing

Abstract

An increasing number of studies have demonstrated the function of microRNAs (miRNAs) in the initiation and development of various types of cancer. Among them, miR-425-5p is proven to serve an important function in several types of cancer, including gastric, cervical cancer, and hepatocellular carcinoma. However, the function of miR-425-5p in renal cell carcinoma (RCC) remains unclear. In the present study, it was demonstrated that the expression level of miR-425-5p was upregulated in RCC tissues and cell lines compared with normal tissues and cell lines (P<0.05). Additionally, Cell Counting kit-8 and MTT assays were employed to assess cell viability and proliferation, whereas wound healing and Transwell assays were employed to examine migration and invasion. The results demonstrated that upregulation of miR-425-5p promoted cell viability and the invasion and migration of ACHN and 786O cells (P<0.05). Flow cytometric analysis confirmed that upregulation of miR-425-5p inhibited apoptosis of ACHN and 786O cells (P<0.05). Downregulation of miR-425-5p inhibited the viability and invasion and migration of ACHN and 786O cells (P<0.05). In the present study, upregulation of miR-425-5p inhibited apoptosis of ACHN and 786O cells whereas no differences in early apoptotic rate were observed between the inhibitor and inhibitor NC groups for 786O and ACHN cells. These results indicate that miR-425-5p may act as an oncogene in RCC.

Published
2018

29. Oncogenic miR‑425‑5p is associated with cellular migration, proliferation and apoptosis in renal cell carcinoma

Author

Quan, Jing, primary, Li, Yawen, additional, Pan, Xiang, additional, Lai, Yulin, additional, He, Tao, additional, Lin, Canbin, additional, Zhou, Liang, additional, Zhao, Liwen, additional, Sun, Shuolei, additional, Ding, Yu, additional, Tao, Lingzhi, additional, Hu, Yimin, additional, Wu, Xionghui, additional, Chen, Zebo, additional, Zhang, Fangting, additional, Ye, Jing, additional, Ni, Liangchao, additional, and Lai, Yongqing, additional

Published
2018
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31. Review of the research on soil animals in degraded ecosystem

Author

Zhang FangTing, Fan YunLong, Chen Hu, and Su XiaoLiang

Subjects
Soil health, Ecology, Soil biodiversity, Soil biology, Soil Science, Plant Science, Environmental soil science, Soil retrogression and degradation, Soil ecology, Environmental science, Ecosystem, Agronomy and Crop Science, Restoration ecology, Ecology, Evolution, Behavior and Systematics
Published
2010

32. Overexpression of long non-coding RNA differentiation antagonizing non-protein coding RNA inhibits the proliferation, migration and invasion and promotes apoptosis of renal cell carcinoma

Author

Jin, Lu, primary, Fu, Huifang, additional, Quan, Jing, additional, Pan, Xiang, additional, He, Tao, additional, Hu, Jia, additional, Li, Yifan, additional, Li, Hang, additional, Yang, Yu, additional, Ye, Jing, additional, Zhang, Fangting, additional, Ni, Liangchao, additional, Yang, Shangqi, additional, and Lai, Yongqing, additional

Published
2017
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38. miR-638 acts as an oncogene and predicts poor prognosis in renal cell carcinoma.

Author

Pan X, He T, Peng X, Li H, Zhang F, and Lai Y

Abstract

Objective: The aim of this study was to investigate the function and prognostic value of miR-638 in renal cell carcinoma (RCC)., Methods: Expression of miR-638 in RCC tissues and corresponding noncancerous tissues were examined by reverse transcription quantitative polymerase chain reaction (RT-qPCR). To explore the effects of miR-638 on cell migration, invasion, viability, and apoptosis of RCC cells, wound scratch, transwell, MTT, CCK-8, and flow cytometry assays were performed. Kaplan-Meier and Cox regression analyses were used to evaluate the relationship between miR-638 expression and prognosis of RCC patients. Potential target genes of miR-638 were predicted and validated via multiple bioinformatics analyses., Results: miR-638 was upregulated in RCC tissues when compared with corresponding noncancerous tissues ( P < 0.05). Upregulation of miR-638 expression by transfection with a synthetic miR-638 mimic promoted cell migration, invasion, and viability and suppressed cell apoptosis. Moreover, Kaplan-Meier analysis revealed that upregulation of miR-638 associated with shorter overall survival (OS; P = 0.001). Cox univariate and multivariate regression analysis suggested that miR-638 expression is an independent predictive factor for the prognosis of RCC patients ( P = 0.004). KCNQ1, DNAJC6, and PNP were identified as potential target genes of miR-638., Conclusions: The results of this study demonstrated that miR-638 functions as an oncogene in RCC and has the potential to be a prognostic biomarker for RCC., Competing Interests: None., (AJTR Copyright © 2020.)

Published
2020

39. [Preliminary study on the development of germ cells from human fetal testicular tissues xenografted into the mouse].

Author

Yu J, Ye J, Zhang F, Wan H, Fang J, Wang Y, Zong S, and Cai Z

Subjects
Animals, Humans, Male, Mice, Mice, Inbred BALB C, Mice, Nude, Testis cytology, Transplantation, Heterologous, Fetal Tissue Transplantation, Spermatids growth & development, Testis transplantation
Abstract

Objective: To investigate the development of xenografted primitive human germ cells by using fetal testicular tissues as donor tissues and an immunodeficient mouse as the recipient., Methods: Testicular tissue fragments of a 26-week fetus were grafted under the back skin of a castrated immunodeficient mouse. Grafts were taken out after 135 days and processed for morphological and histological analyses., Results: The mass of grafts grew from about 1 mm in diameter and 5 mg in wet weight to about 3 mm and more than 20 mg 135 days after grafting. Histological observations showed a significant expansion of seminiferous tubules after grafting (80 +/- 25 microm in diameter) in comparison with seminiferous cords at the time of grafting (60 +/- 15 microm in diameter). The seminiferous cords developed into seminiferous tubules with the epithelial border and lumen. After 135 days of grafting, most of the dispersedly distributed primitive Sertoli cells and germ cells migrated to the basal part of seminiferous epithelium, located on the basement membrane and few of germ cells differentiated into spermatogonia., Conclusion: Human fetal testicular tissues could survive and continuously develop after being xenograft into castrated immunodeficient mice.

Published
2004

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