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Yingli Wu on Muck Rack

Yingli Wu

As seen in: Nature, MDPI, ACS Publications, Dove Medical Press
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Articles

Identification of YL064 as a novel inhibitor of ATXN3 to suppress tumor growth and metastasis by promoting degradation of oncogenic substrates

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By Wenhui Bai, Guanyi Li, Youping Zhang, Wenxuan Wu, Chujiao Zhu, Xingyu Liu, Manyu Zhang, Hu Lei, Hanzhang Xu, Ligen Liu, Yaxue Zhao, Zhujun Yao, Qi Zhu, Yingying Wang, Yingli Wu, Zhenge Zhang, Yayue Tan
| Nature Verified
Abstract ATXN3 has recently emerged as a pro-oncogenic deubiquitinating enzyme (DUB) involved in the progression of multiple cancers, including breast and prostate cancer. However, the therapeutic potential of targeting ATXN3 remains largely unexplored due to the lack of effective inhibitors.
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TRMT1-mediated tRNA m 2 2 G modification drives Osimertinib resistance via the ATXN3/USP25 axis in lung adenocarcinoma

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By Jiaqi Li, Bo Jing, Yingying Wang, Wenhui Bai, Qiuyu Wei, Meng Liu, Kuofang Huang, Shifei Pan, Haijiao Lu, Jialin Qian, Yanjie Ji, Wanting Liu, Hua Zhong, Youping Zhang, Wenxuan Wu, Luo Hao, Hu Lei, Hanzhang Xu, Yingli Wu, Tianqing Chu, Chujiao Zhu, Xuxinyi Ling, Huishu Dong, Yuanhui Zhai
| Nature Verified
Abstract Acquired resistance to Osimertinib, a third-generation EGFR tyrosine kinase inhibitor (TKI), remains a critical challenge in lung adenocarcinoma. Here, we identify ATXN3, a deubiquitinating enzyme, as a driver of Osimertinib resistance and a predictor of poor patient survival. Osimertinib treatment dynamically upregulates ATXN3 transcription, which stabilizes USP25 through deubiquitination, activating an ATXN3-USP25-TRMT1 signaling cascade.
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Coinhibition of the MEK/RTK pathway has high therapeutic efficacy in KRAS-mutant non-small cell lung cancer - Signal Transduction and Targeted Therapy

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By Xinlei Cai, Liang Hu, Yingli Wu, Hongbin Ji
| Nature Verified
Abstract Oncogenic KRAS mutations are frequently detected in NSCLC. It remains a major challenge to target all KRAS mutants. MEK inhibitors are considered candidates for treating KRAS-mutant NSCLC; however, their easy adaptive resistance precludes further application.
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