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Your search keyword '"Xiang, Jin"' showing total 16 results
Start Over Author "Xiang, Jin" Journal acta pharmacologica sinica
16 results on '"Xiang, Jin"'

11. ADH1C inhibits progression of colorectal cancer through the ADH1C/PHGDH /PSAT1/serine metabolic pathway

Author

Sha Li, Hong Yang, Wan Li, Jin-yi Liu, Li-wen Ren, Yi-hui Yang, Bin-bin Ge, Yi-zhi Zhang, Wei-qi Fu, Xiang-jin Zheng, Guan-hua Du, and Jin-Hua Wang

Subjects
Pharmacology, Alcohol Dehydrogenase, Mice, Nude, General Medicine, Gene Expression Regulation, Neoplastic, Mice, Cell Movement, Cell Line, Tumor, Serine, Animals, Humans, Pharmacology (medical), Female, RNA, Messenger, Colorectal Neoplasms, Metabolic Networks and Pathways, Cell Proliferation
Abstract

Colorectal cancer (CRC) is the third most common cancer in men and the second most common cancer in women worldwide. CRC is the second leading cause of cancer-related deaths. Although some progress in the treatment of CRC has been achieved, the molecular mechanism of CRC is still unclear. In this study, alcohol dehydrogenase 1C(ADH1C) was first identified as a target gene closely associated with the development of CRC by the comprehensive application of transcriptomics, proteomics, metabonomics and in silico analysis. The ADH1C mRNA and protein expression in CRC cell lines and tumor tissues was lower than that in normal intestinal epithelial cell lines and healthy tissues. Overexpression of ADH1C inhibited the growth, migration, invasion and colony formation of CRC cell lines and prevented the growth of xenograft tumors in nude mice. The inhibitory effects of ADH1C on CRC cells in vitro were exerted by reducing the expression of PHGDH/PSAT1 and the serine level. This inhibition could be partially reversed by adding serine to the culture medium. These results showed that ADH1C is a potential drug target in CRC.

Published
2021

15. EZH2 regulates expression of FOXC1 by mediating H3K27me3 in breast cancers

Author

Zheng, Xiang-jin, Li, Wan, Yi, Jie, Liu, Jin-yi, Ren, Li-wen, Zhu, Xiao-ming, Liu, Shi-wei, Wang, Jin-hua, and Du, Guan-hua

Abstract

Triple-negative breast cancer (TNBC) is characterized by low expression of human epidermal growth factor receptor-2 (HER2), estrogen receptor (ER), and progesterone receptor (PR), which is the most aggressive subtype with poor outcome among breast cancers. The underlying mechanisms of TNBC remain unclear and there is a lack of biomarkers. In this study we conducted an in silico assay and found that FOXC1 was highly expressed in ER−/PR−/HER2−breast cancers, which was confirmed by qRT-PCR, immunohistochemistry, and Western blot analysis. FOXC1 was more highly expressed in TNBCs than the other breast cancers. Kaplan–Meier plotter revealed that expression of FOXC1 was associated with overall survival (OS) of patients with breast cancers. Expression of FOXC1 was reversely associated with level of H3K27me3, which was methylated by EZH2. In MCF-7 and T47D cells, inhibition of EZH2 by DZNeP or GSK343 concentration- and time-dependently increased expression of FOXC1. Finally, we demonstrated that the expression of FOXC1 was associated with resistance of doxorubicin treatment of breast cancer cells. In conclusion, these results suggest that FOXC1 may be a potential biomarker or drug target for TNBCs, and that downregulation of FOXC1 could have therapeutic value in treatment of TNBCs.

Published
2021
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