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6 results on '"Chen, Fenrong"'

1. Hypermethylation of DHRS3 as a Novel Tumor Suppressor Involved in Tumor Growth and Prognosis in Gastric Cancer

Author

Sha Sumei, Kong Xiangyun, Chen Fenrong, Sun Xueguang, Hu Sijun, Bai Bin, Shi Xiaolei, Tu Yongjiu, Wu Kaichun, Zhao Qingchuan, Nie Yongzhan, and Xu Bin

Subjects
gastric cancer, DNA methylation, DHRS3, Mass-Array, carcinogenesis, Biology (General), QH301-705.5
Abstract

Background/AimsThe role of DHRS3 in human cancer remains unclear. Our study explored the role of DHRS3 in gastric cancer (GC) and its clinicopathological significance and associated mechanisms.MaterialsBisulfite-assisted genomic sequencing PCR and a Mass-Array system were used to evaluate and quantify the methylation levels of the promoter. The expression levels and biological function of DHRS3 was examined by both in vitro and in vivo assays. A two-way hierarchical cluster analysis was used to classify the methylation profiles, and the correlation between the methylation status of the DHRS3 promoter and the clinicopathological characteristics of GC were then assessed.ResultsThe DHRS3 promoter was hypermethylated in GC samples, while the mRNA and protein levels of DHRS3 were significantly downregulated. Ectopic expression of DHRS3 in GC cells inhibited cell proliferation and migration in vitro, decreased tumor growth in vivo. DHRS3 methylation was correlated with histological type and poor differentiation of tumors. GC patients with high degrees of CpG 9.10 methylation had shorter survival times than those with lower methylation.ConclusionDHRS3 was hypermethylated and downregulated in GC patients. Reduced expression of DHRS3 is implicated in gastric carcinogenesis, which suggests DHRS3 is a tumor suppressor.

Published
2021
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5. Cover Image, Volume 43, Issue 11.

Author

Nie, Yongzhan, Gao, Xianchun, Cai, Xiqiang, Wu, Zhen, Liang, Qiaoyi, Xu, Guobing, Liu, Na, Gao, Peng, Deng, Jingyu, Xu, Hongzhi, Shen, Zhanlong, Cao, Changqi, Chen, Fenrong, Zhang, Nannan, Song, Yongxi, Sun, Mingjun, Liu, Chengyin, Zhou, Guangpeng, Han, Weili, and Dou, Jianhua

Published
2023
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6. Periostin down-regulation attenuates the pro-fibrogenic response of hepatic stellate cells induced by TGF-β1

Author

Zhao Gang, Dai She-jiao, Dong Lei, Chen Fenrong, and Li Hong

Subjects
Liver Cirrhosis, Pathology, medicine.medical_specialty, Down-Regulation, SMAD, Periostin, Biology, Collagen Type I, Extracellular matrix, Transforming Growth Factor beta1, Fibrosis, TGF-β1, medicine, Hepatic Stellate Cells, Humans, RNA, Small Interfering, Cell Proliferation, periostin, Cell growth, Cell adhesion molecule, Cell Cycle, fibrosis, Cell Biology, Original Articles, medicine.disease, Actins, Cell biology, Up-Regulation, Hepatic stellate cell, Molecular Medicine, Hepatic fibrosis, Cell Adhesion Molecules, Signal Transduction
Abstract

Liver fibrosis is characterized by an exacerbated accumulation of deposition of the extracellular matrix (ECM), and the activation of hepatic stellate cells (HSC) plays a pivotal role in the development of liver fibrosis. Periostin has been shown to regulate cell adhesion, proliferation, migration and apoptosis; however, the involvement of periostin and its role in transforming growth factor (TGF)-β1-induced HSC activation remains unclear. We used RT-PCR and Western blot to evaluate the expression level of periostin in hepatic fibrosis tissues and HSCs, respectively. Cell proliferation was determined using the Cell Proliferation ELISA BrdU kit, cell cycle was analysed by flow cytometry. The expression of α-smooth muscle actin (α-SMA), collagen I, TGF-β1, p-Smad2 and p-Smad3 were determined by western blot. Our study found that periostin was up-regulated in liver fibrotic tissues and activated HSCs. In addition, siRNA-periostin suppressed TGF-β1-induced HSC proliferation. The HSC transfected with siRNA-periostin significantly inhibited TGF-β1-induced expression levels of α-SMA and collagen I. Furthermore, TGF-β1 stimulated the expression of periostin, and siRNA-periostin attenuated TGF-β1-induced Smad2/3 activation in HSCs. These results suggest that periostin may function as a novel regulator to modulate HSC activation, potentially by promoting the TGF-β1/Smad signalling pathway, and propose a strategy to target periostin for the treatment of liver fibrosis.

Published
2015

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