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Miao Yin

As seen in: Nature, Wiley Online Library, Cell Press, The Journal of Biological Chemistry, Pakistan Journal of Zoology
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Articles

The splicing factor hnRNPA1 promotes osimertinib resistance in lung adenocarcinoma by regulating NEDD4L alternative splicing

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By Yanfeng Liang, Yudong Guo, Qu Wang, YanXia Wu, Haiyin Ye, Ming Pang, Xiao Lei, Miao Yin, Yongyang Chen, Yuexin Zheng, Xiaoqing Xu, Jinghua Yang, Jialing Chen, Jinhui Chen, Haiwen Li, Wenmei Su, Xiaobi Huang, Qihe Long, Yuetong Jiang, Yuliu Xie
| Nature Verified
Abstracts Resistance to osimertinib in lung adenocarcinoma presents a significant hurdle in contemporary lung cancer therapy, with splicing dysregulation being instrumental in tumorigenesis and progression. The mechanism via which alternate splicing facilitates osimertinib resistance in lung cancer is still ambiguous. We aimed to examine the pivotal function of the splicing factor hnRNPA1 in osimertinib resistance in lung cancer.
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Diversity of fecal viromes and zoonotic risk assessment in captive wild felids using viral metagenomics

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By Miao Yin, Xiwen Chen, Rui Lu, Yanan Dong, Wentao Luo, Zhihao Tang, Yuanhao Xu, Yi Qing, Chen Xi, Xiaoshan Feng, Hailin Guo, Shiheng Mo, Jing Luo, Mingxia Zeng
| Nature Verified
Abstract Emerging viral diseases-particularly zoonotic pathogens-affect the health and conservation of endangered felids, including Panthera tigris altaica (Amur tiger) and Panthera pardus (leopard). To address this challenge, we employed a viromics approach to investigate the diversity of the fecal virome in wild felids and assess its zoonotic potential.
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Tumor-derived branched-chain α-keto acids activate Notch signaling in tumor-associated macrophages to limit immunity

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By Qi-Xiang Ma, Ru Zhao, Xiao-yan Zhang, Guo-Quan Yan, Wen-Yu Wen, Min Luo, Miao Yin, Jin-Tao Li, Qun-Ying Lei, Jiang-Xue Han, Wen-Ying Zhu, Mi-Die Xu, Guang-Chun Han
| Nature Verified
Abstract Tumor cells are highly dependent on branched-chain amino acids, which can activate mechanistic target of rapamycin complex 1, but the downstream catabolite branched-chain α-keto acids (BCKAs) are not well studied in this context. Here, using clinical samples and genetically engineered mouse tumor models, we showed that tumor-derived BCKAs are secreted actively into the tumor microenvironment (TME) where they reprogram tumor-associated macrophages (TAMs) to promote tumor progression.
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