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Chengqian Yin on Muck Rack

Chengqian Yin

As seen in: Nature, Frontiers, Cell Press, The Journal of Clinical Investigation
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Articles

A targetable ALDH3A2-NRF2 axis mediates KEAP1-mutant tumour development via ferroptosis inhibition

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By Xiao Vincent Zhuang, Jing Han, Weiwei Cui, Yudan Zhang, Ziqi Wang, Dandan Song, Chao Zhou, Shaohui Huang, Kai Cui, Chenchen Lin, Min Xu, Xingru Zhao, Shuai Wang, Bin Huang, Hui Wang, Shuang Shi, Lutao Du, Qiankun Luo, Quncheng Zhang, Chengqian Yin, Bo Chu, Xiaoju Zhang, Zeheng Ma
| Nature Verified
Abstract The transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) is a master regulator of the cellular antioxidant response that defends against ferroptosis and facilitates tumour development. Here, by performing an aldehyde dehydrogenase (ALDH) family shRNA screen, our study identifies aldehyde dehydrogenase 3 family member A2 (ALDH3A2) as a potent NRF2 activator that inhibits ferroptosis.
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S-acyl transferase ZDHHC13 modulates tumor microenvironment interactions to suppress metastasis in melanoma models

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By Hongjin Li, Yu Sun, Chengqian Yin, Jianke Lyu
| The Journal of Clinical Investigation
ResearchImmunologyOncology Open Access | 10.1172/JCI188249 J Clin Invest. https://doi.org/10.1172/JCI188249. Copyright © 2025, Li et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. View PDF Abstract The intratumor microenvironment shapes the metastatic potential of cancer cells and their susceptibility to any immune response.
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Pharmacological targeting of casein kinase 1δ suppresses oncogenic NRAS-driven melanoma - Nature Communications

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By Zhengqiu Li, Chengqian Yin, Xiangchun Shen
| Nature Verified
Abstract Activating mutations in NRAS account for 15–20% of melanoma, yet effective anti-NRAS therapies are still lacking. In this study, we unveil the casein kinase 1δ (CK1δ) as an uncharacterized regulator of oncogenic NRAS mutations, specifically Q61R and Q61K, which are the most prevalent NRAS mutations in melanoma. The genetic ablation or pharmacological inhibition of CK1δ markedly destabilizes NRAS mutants and suppresses their oncogenic functions.
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