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27. Circular RNA circLMO1 Suppresses Cervical Cancer Growth and Metastasis by Triggering miR-4291/ ACSL4 -Mediated Ferroptosis.

Author

Ou, Rongying, Lu, Shun, Wang, Luhui, Wang, Yebo, Lv, Mingfen, Li, Tian, Xu, Yunsheng, Lu, Jieqiang, and Ge, Ren-shan

Subjects
CIRCULAR RNA, CERVICAL cancer, TUMOR growth, CANCER cell growth, METASTASIS, CANCER cell proliferation
Abstract

Background: A number of studies have demonstrated that circular RNA (circRNA) plays a critical role in tumorigenesis and tumor progression. However, the biological effects of most circRNAs on cervical cancer remain unclear. Hsa_circ_0021087 (thereafter named circLMO1) is a circRNA generated from the circularization of exon 2 and exon 3 of LIM Domain Only 1 (LMO1) and first identified as a tumor suppressor in gastric cancer. We aimed to identify the role of circLMO1 in cervical cancer progression. Methods: CircLMO1 was verified through qPCR and Sanger sequencing. The biological role of circLMO1 in regulating cervical cancer growth and metastasis was investigated both in vitro and in the nude mouse xenograft tumor model. The dual luciferase reporter assay and rescue experiment were conducted to evaluate the interactions among circLMO1, microRNA (miR)-4291, and acyl-CoA synthetase long chain family member 4 (ACSL4). The role of circLMO1 in regulating ferroptosis was assessed by analyzing lipid reactive oxygen species (ROS), and malonyl dialdehyde (MDA), and glutathione (GSH) content. Results: The level of circLMO1 was down-regulated in cervical cancer tissues and was associated with the International Federation of Gynecology and Obstetrics (FIGO) staging. Functionally, circLMO1 overexpression inhibited cervical cancer growth and metastasis both in vitro and in vivo , whereas circLMO1 depletion promoted cervical cancer cell proliferation and invasion. Mechanistically, circLMO1 acted as a competing endogenous RNA (ceRNA) by sponging miR-4192 to repress target gene ACSL4. CircLMO1 promoted cervical cancer cell ferroptosis through up-regulating ACSL4 expression. Overexpression of miR-4291 or knockdown of ACSL4 reversed the effect of circLMO1 on facilitating ferroptosis and repressing cervical cancer cell proliferation and invasion. Conclusion: CircLMO1 acted as a tumor suppressor of cervical cancer by regulating miR-4291/ ACSL4 -mediated ferroptosis, and could be a promising biomarker for the clinical management of cervical cancer. [ABSTRACT FROM AUTHOR]

Published
2022
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28. HPV16 E6 oncoprotein‐induced upregulation of lncRNA GABPB1‐AS1 facilitates cervical cancer progression by regulating miR‐519e‐5p/Notch2 axis

Author

Ou, Rongying, primary, Lv, Mingfen, additional, Liu, Xuan, additional, Lv, Jiangmin, additional, Zhao, Jinduo, additional, Zhao, Ye, additional, Li, Xiangyun, additional, Li, Wenfeng, additional, Zhao, Liang, additional, Li, Jianrong, additional, Ren, Yi, additional, and Xu, Yunsheng, additional

Published
2020
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30. Rescuing Dicer expression in inflamed colon tissues alleviates colitis and prevents colitis-associated tumorigenesis

Author

Wu, Xiaoli, primary, Chen, Xiao, additional, Liu, Hui, additional, He, Zhong-Wei, additional, Wang, Zheng, additional, Wei, Lin-Jie, additional, Wang, Wei-Yun, additional, Zhong, Shouhui, additional, He, Qin, additional, Zhang, Zhechao, additional, Ou, Rongying, additional, Gao, Jian, additional, Lei, Youchun, additional, Yang, Wenjun, additional, Song, Guanbin, additional, Jin, Yi, additional, Zhou, Lingli, additional, Xu, Yunsheng, additional, and Tang, Kai-Fu, additional

Published
2020
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32. MicroRNA-664 suppresses the growth of cervical cancer cells via targeting c-Kit

Author

Lv, Mingfen, Ou, Rongying, Zhang, Qianwen, Lin, Fan, Li, Xiangyun, Wang, Keyu, and Xu, Yunsheng

Subjects
Drug Design, Development and Therapy, cervical cancer, Gene Expression Profiling, apoptosis, Uterine Cervical Neoplasms, MicroRNAs, Proto-Oncogene Proteins c-kit, c-Kit, Tumor Cells, Cultured, Humans, microRNA-664, Female, Original Research, Cell Proliferation
Abstract

Mingfen Lv,1,2Rongying Ou,3 Qianwen Zhang,1 Fan Lin,1 Xiangyun Li,4 Keyu Wang,2 Yunsheng Xu1,41Department of Dermatology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, People’s Republic of China; 2Department of Dermatology, Qilu Hospital, Shandong University, Jinan, Shandong 250012, People’s Republic of China; 3Department of Gynaecology and Obstetrics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, People’s Republic of China; 4Department of Dermatology, The Seventh Affiliated Hospital of Sun Yat-sen university, Shenzhen, Guangdong 518107, People’s Republic of ChinaBackground: Cervical cancer is the second most common malignant cancer in women worldwide. Evidence indicated that miR-664 was significantly downregulated in cervical cancer. However, the mechanisms by which miR-664 regulates the tumorigenesis of cervical cancer remain unclear. Thus, this study aimed to investigate the role of miR-664 in cervical cancer.Methods: Quantitative reverse transcription polymerase chain reaction was used to detect the level of miR-664 in tumor tissues and cell line. The dual luciferase reporter system assay and Western blotting were used to explore the interaction of miR-664 and c-Kit in cervical cancer.Results: The expression of miR-664 in patients with cervical cancer was dramatically decreased compared with that in adjacent tissues. MiR-664 mimics significantly inhibited proliferation in SiHa cells via inducing apoptosis. In addition, miR-664 mimics induced apoptosis in SiHa cells via increasing the expressions of Bax and active caspase 3 and decreasing the level of Bcl-2. Moreover, dual-luciferase assay showed that c-Kit was the directly binding target of miR-664 in SiHa cells; overexpression of miR-664 downregulated the expression of c-Kit. Meanwhile, upregulation of miR-664 significantly decreased the levels of c-Myc and Cyclin D in cells. Furthermore, miR-664 markedly inhibited tumor growth of cervical cancer in xenograft.Conclusion: Our data indicated that miR-664 exerted antitumor effects on SiHa cells by directly targeting c-Kit in vitro and in vivo. Therefore, miR-664 might be a potential therapeutic target for the treatment of patients with cervical cancer.Keywords: microRNA-664, c-Kit, cervical cancer, apoptosis &nbsp

Published
2019

37. MicroRNA-34a promotes MICB expression in hepatocytes

Author

Zhou, Meng-Tao, primary, Zhao, Chunming, additional, Chen, Xiao, additional, Zhang, Heng-Chao, additional, Li, Guiling, additional, Lou, Hongyan, additional, Huang, Wen-Jie, additional, Wei, Lin-Jie, additional, Li, De-Wei, additional, Wu, Xiaoli, additional, Zhang, Zhe-Chao, additional, Liu, Hui, additional, Ou, Rongying, additional, Yang, Wen-Jun, additional, Hu, Shanshan, additional, Xu, Yunsheng, additional, and Tang, Kai-Fu, additional

Published
2018
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40. UCH-LI acts as a novel prognostic biomarker in gastric cardiac adenocarcinoma

Author

Yang, Honghong, Zhang, Chunhong, Fang, Shan, Ou, Rongying, Li, Wenfeng, and Xu, Yunsheng

Subjects
Male, Time Factors, Kaplan-Meier Estimate, Adenocarcinoma, Transfection, Cell Movement, Risk Factors, Stomach Neoplasms, Cell Line, Tumor, Biomarkers, Tumor, Humans, Neoplasm Invasiveness, Cell Proliferation, Neoplasm Staging, Proportional Hazards Models, Chi-Square Distribution, Middle Aged, Immunohistochemistry, Tumor Burden, Treatment Outcome, Tissue Array Analysis, Multivariate Analysis, Original Article, Female, RNA Interference, Ubiquitin Thiolesterase
Abstract

Gastric cardiac adenocarcinoma (GCA) accounts for a majority of gastric cancer population and harbors unfavorable outcome. Ubiquitin C-terminal hydrolase L1 (UCH-L1) belongs to the deubiquitinating enzyme family, which could regulate cell growth in human cancers. In the present study, expression of UCH-L1 was evaluated in 196 GCAs by immunohistochemistry using tissue microarray and its function on gastric cancer cells was measured. UCH-L1 expression was increased in GCA specimens, compared with their normal tissues and UCH-L1 overexpression is tightly correlated with tumor size and overall TNM stage. Log-rank analysis showed that UCH-L1 positive is reversely associated with cumulative survival (P

Published
2015

45. HPV16 E7‐induced upregulation of KDM2A promotes cervical cancer progression by regulating miR‐132–radixin pathway.

Author

Ou, Rongying, Zhu, Linyu, Zhao, Liang, Li, Wenfeng, Tao, Fengxing, Lu, Yiyi, He, Qin, Li, Jianrong, Ren, Yi, and Xu, Yunsheng

Subjects
*HUMAN papillomavirus vaccines, *CANCER invasiveness, *MICRORNA, *VIRAL proteins, *CARCINOGENESIS, *DEMETHYLASE
Abstract

Background: Human papillomavirus (HPV) infection and viral proteins expression cause a number of epigenetic alterations leading to cervical carcinogenesis. The recent discovery of a large amount of histone methylation modifiers reveals important roles of these enzymes in regulating tumor progression. Methods: The changes in expression of 48 histone methylation modifiers were assessed following knockdown of HPV16 E7 in CaSki cells. Lysine‐specific demethylase 2A (KDM2A)‐regulated microRNAs (miRNAs) in cervical cancer pathogenesis were disclosed using quantitative real‐time polymerase chain reaction. The function of KDM2A–miRNAs on cervical cancer was investigated in vitro and in vivo. Results: Upregulation of KDM2A induced by HPV16 E7 promotes cervical cancer cell proliferation and invasion and is correlated with poor prognosis in patients with cervical cancer. KDM2A physically interacts with the promoter of miR‐132 and suppresses its expression by removing the mono or dimethyl group from H3K36 at the miR‐132 locus. Functionally, miR‐132 represses cancer cell proliferation and invasion by inhibiting radixin (RDX). Upregulated KDM2A promotes cervical cancer progression by repressing miR‐132, which results in a derepression of RDX. Therefore, KDM2A functions as a tumor activator in cervical cancer pathogenesis by binding miR‐132 promoter and abrogating its tumor suppressive function. Conclusion: Our results suggest a function for KDM2A in cervical cancer progression and suggest its candidacy as a new prognostic biomarker and target for clinical management of cervical cancer. KDM2A–miR‐132–RDX promotes cervical cancer. [ABSTRACT FROM AUTHOR]

Published
2019
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50. Downregulation of pyrroline-5-carboxylate reductase-2 induces the autophagy of melanoma cells via AMPK/mTOR pathway.

Author

Ou, Rongying, Zhang, Xueqi, Cai, Jianfeng, Shao, Xiaohong, Lv, Mingfen, Qiu, Wei, Xuan, Xuan, Liu, Jingjing, Li, Zhiming, and Xu, Yunsheng

Abstract

Melanoma is the most aggressive form of skin cancer and causes 50,000 deaths annually worldwide. The roles of proline-dependent process and autophagy have both been reported in studies on melanoma. In the present study, we focused on the effect of pyrroline-5-carboxylate reductase-2 (PYCR2) on inducing autophagy process in melanoma. The expression of PYCR2 was regulated by an RNAi technique, and the cell proliferation of A375 cell line was determined by methyl thiazolyl tetrazolium test; the effect of PYCR2 on the apoptosis process and AMPK/mTOR pathway was evaluated by flow cytometry assay and Western blot. It was found that silence of PYCR2 resulted in the decrease of proliferative ability and activation of AMPK/mTOR-induced autophagy of A375 cells. PYCR2 silencing also activated AMPK/mTOR pathway in another melanoma cell line, CHL-1. However, the overexpression of PYCR2 seemed to make no difference to the cell viability and targeted pathway. Our results offered a preliminary illustration on the mechanism of the PYCR2-dependent autophagy and showed that PYCR2 was a potential therapeutic target of melanoma. [ABSTRACT FROM AUTHOR]

Published
2016
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