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Your search keyword '"Xu, Zhengshui"' showing total 15 results
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15 results on '"Xu, Zhengshui"'

8. DFNA5 inhibits colorectal cancer proliferation by suppressing the mTORC1/2 signaling pathways via upregulation of DEPTOR

Author

Guo, Jing, Yu, Junhui, Mu, Mingchao, Chen, Zilu, Xu, Zhengshui, Zhao, Chenye, Yang, Kui, Zheng, Jianbao, Qin, Xiao, Zhao, Wei, and Sun, Xuejun

Subjects
Pore Forming Cytotoxic Proteins, Hearing Loss, Sensorineural, Intracellular Signaling Peptides and Proteins, Cell Biology, Mechanistic Target of Rapamycin Complex 1, Up-Regulation, Gene Expression Regulation, Neoplastic, Cell Line, Tumor, Colonic Neoplasms, Cyclin E, Humans, Cyclin D1, Colorectal Neoplasms, Molecular Biology, Cell Proliferation, Signal Transduction, Developmental Biology
Abstract

The human deafness, autosomal dominant 5 gene (DFNA5), a newly discovered executor of pyroptosis, has been strongly implicated in the tumorigenesis of several human cancers. However, an understanding of the functional role of DFNA5 in the development and progression of colorectal cancer (CRC) is limited. In this study, we demonstrated that DFNA5 was downregulated in CRC tissues. Ectopic expression of DFNA5 inhibited tumor cell growth in vitro, retarded tumor formation in vivo, and blocked a cell-cycle transition from the G0/G1 to the S phase, whereas a DFNA5 knockdown promoted cell proliferation. Western blotting showed that the levels of cell cycle-related proteins, including cyclin D1, cyclin E, CDK2, and p21, were accordingly altered upon DFNA5 overexpression or DFNA5 knockdown. Mechanistic studies indicated that DFNA5 exerted its tumor suppressor functions by antagonizing mTORC1/2 signaling via upregulation of DEPTOR. In addition, blockage of mTORC1/2 signaling by Torin-1 abolished the accelerative proliferation by DFNA5 knockdown. In conclusion, these results indicated that DFNA5 inhibits the proliferation and tumor formation of colon cancer cells by suppressing mTORC1/2 signaling.

Published
2022

15. Design, synthesis and antiproliferative evaluation of tetrahydro-β-carboline histone deacetylase inhibitors bearing an aliphatic chain linker.

Author

Shi J, Wang J, Wang X, Qu C, Ye C, Li X, Chen X, and Xu Z

Abstract

The use of histone deacetylase inhibitors (HDACis) is an effective approach for cancer treatment. In this work, a series of hydroxamic acid-based HDACis with a tetrahydro-β-carboline core and aliphatic linker have been designed and synthesized. The optimal compound 13d potently inhibited HDAC1 and showed good antiproliferative activity against different tumor cell lines in vitro . Molecular docking of 13d was conducted to rationalize the high binding affinity for HDAC1. Therefore, this work provides a new structure design for HDAC inhibitors and also offers a promising treatment for solid tumors., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (This journal is © The Royal Society of Chemistry.)

Published
2024
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