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@Article{Cheng2023-06-27,
author={Cheng, Xianyi
and Deng, Xiulan
and Zeng, Huiping
and Zhou, Tao
and Li, Dezhi
and Zheng, Wei V.},
title={Silencing of TMED5 inhibits proliferation, migration and invasion, and enhances apoptosis of hepatocellular carcinoma cells},
title={Silencing of TMED5 inhibits proliferation, migration and invasion, and enhances apoptosis of hepatocellular carcinoma cells},
journal={Advances in Clinical and Experimental Medicine},
year={2023},
volume={32},
number={6},
pages={677--688},
month={06},
day={27},
publisher={Wroclaw Medical University},
abstract={Background. Transmembrane P24 trafficking protein 5 (TMED5) is highly expressed in cervical and bladder cancer cell lines. Moreover, TMED5 promotes nuclear autophagy and the malignant behavior of cervical cancer cells. However, the role of TMED5 in hepatocellular carcinoma (HCC) has not been extensively reported.Objectives. To investigate the role of TMED5 in HCC cells.Material and Methods. Bioinformatics was used to analyze the messenger-ribonucleic acid (mRNA) expression of TMED5 in HCC and its relationship with overall survival and disease-free interval of HCC patients. After TMED5 was decreased in SMMC-7721 and Hep3B cells, they were assayed for proliferation, cell cycle, apoptosis, migration, and invasion.Results. The expression of TMED5 mRNA in HCC tissues was higher than in adjacent normal tissues, and the overall survival of HCC patients with high TMED5 transcription levels was worse. Moreover, the overexpression of TMED5 was associated with HCC progression. The downregulation of TMED5 suppressed cell proliferation, migration and invasion, and enhanced apoptosis. Therefore, TMED5 may be involved in the regulation of the cell cycle, the mammalian target of rapamycin signaling pathway, and the transforming growth factor beta (TGF-β) signaling pathway.Conclusion. The TMED5 has the potential to promote HCC progression. Therefore, lowering TMED5 levels could represent a potential strategy for the treatment of HCC.},
issn={1899-5276},
doi={10.17219/acem/156673},
url={http://dx.doi.org/10.17219/acem/156673},