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15. Histones Methyltransferase NSD3 Inhibits Lung Adenocarcinoma Glycolysis Through Interacting with PPP1CB to Decrease STAT3 Signaling Pathway.

Author

Zhou, Yanling, Peng, Xintong, Fang, Cheng, Peng, Xin, Tang, Jianing, Wang, Zuli, Long, Yao, Chen, Jielin, Peng, Yuanhao, Zhang, Zewen, Zhou, Yanmin, Tang, Jun, Liao, Jingzhong, Xiao, Desheng, Tao, Yongguang, Shi, Ying, and Liu, Shuang

Subjects
GENETIC transcription, HISTONES, CELLULAR signal transduction, CARBON dioxide, METHYLTRANSFERASES
Abstract

Histones methyltransferase NSD3 targeting H3K36 is frequently disordered and mutant in various cancers, while the function of NSD3 during cancer initiation and progression remains unclear. In this study, it is proved that downregulated level of NSD3 is linked to clinical features and poor survival in lung adenocarcinoma. In vivo, NSD3 inhibited the proliferation, immigration, and invasion ability of lung adenocarcinoma. Meanwhile, NSD3 suppressed glycolysis by inhibiting HK2 translation, transcription, glucose uptake, and lactate production in lung adenocarcinoma. Mechanistically, as an intermediary, NSD3 binds to PPP1CB and p‐STAT3 in protein levels, thus forming a trimer to dephosphorylate the level of p‐STAT3 by PPP1CB, leading to the suppression of HK2 transcription. Interestingly, the phosphorylation function of PPP1CB is related to the concentration of carbon dioxide and pH value in the culture environment. Together, this study revealed the critical non‐epigenetic role of NSD3 in the regulation of STAT3‐dependent glycolysis, providing a piece of compelling evidence for targeting the NSD3/PPP1CB/p‐STAT3 in lung adenocarcinoma. [ABSTRACT FROM AUTHOR]

Published
2024
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20. mRNA‐Lipid Nanoparticle‐Mediated Restoration of PTPN14 Exhibits Antitumor Effects by Overcoming Anoikis Resistance in Triple‐Negative Breast Cancer.

Author

Li, Wei, Huang, Masha, Wu, Zhaoping, Zhang, Yu, Cai, Ying, Su, Juncheng, Xia, Jia, Yang, Fan, Xiao, Desheng, Yang, Wen, Xu, Yingjie, and Liu, Zhaoqian

Subjects
TRIPLE-negative breast cancer, PROTEIN-tyrosine phosphatase, ANOIKIS, PI3K/AKT pathway, BREAST cancer, GENE expression
Abstract

Triple‐negative breast cancer (TNBC) poses a challenging prognosis due to early metastasis driven by anoikis resistance. Identifying crucial regulators to overcome this resistance is vital for improving patient outcomes. In this study, a genome‐wide CRISPR/Cas9 knockout screen in TNBC cells has identified tyrosine‐protein phosphatase nonreceptor type 14 (PTPN14) as a key regulator of anoikis resistance. PTPN14 expression has shown a progressive decrease from normal breast tissue to metastatic tumors. Overexpressing PTPN14 has induced anoikis and inhibited cell proliferation in TNBC cells, while normal human breast cells are unaffected. Mechanistically, PTPN14 is identified as a key factor in dephosphorylating breast cancer antiestrogen resistance 3, a novel substrate, leading to the subsequent inhibition of PI3K/AKT and ERK signaling pathways. Local delivery of in vitro transcribed PTPN14 mRNA encapsulated by lipid nanoparticles in a TNBC mouse model has effectively inhibited tumor growth and metastasis, prolonging survival. The study underscores PTPN14 as a potential therapeutic target for metastatic TNBC, with the therapeutic strategy based on mRNA expression of PTPN14 demonstrating clinical application prospects in alleviating the burden of both primary tumors and metastatic disease. [ABSTRACT FROM AUTHOR]

Published
2024
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25. Supplement Figures from Chromatin Remodeling Factor LSH Drives Cancer Progression by Suppressing the Activity of Fumarate Hydratase

Author

He, Xiaozhen, primary, Yan, Bin, primary, Liu, Shuang, primary, Jia, Jiantao, primary, Lai, Weiwei, primary, Xin, Xing, primary, Tang, Can-e, primary, Luo, Dixian, primary, Tan, Tan, primary, Jiang, Yiqun, primary, Shi, Ying, primary, Liu, Yating, primary, Xiao, Desheng, primary, Chen, Ling, primary, Liu, Shao, primary, Mao, Chao, primary, Yin, Gang, primary, Cheng, Yan, primary, Fan, Jia, primary, Cao, Ya, primary, Muegge, Kathrin, primary, and Tao, Yongguang, primary

Published
2023
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26. Supplemental Materials and Methods and Tables from Chromatin Remodeling Factor LSH Drives Cancer Progression by Suppressing the Activity of Fumarate Hydratase

Author

He, Xiaozhen, primary, Yan, Bin, primary, Liu, Shuang, primary, Jia, Jiantao, primary, Lai, Weiwei, primary, Xin, Xing, primary, Tang, Can-e, primary, Luo, Dixian, primary, Tan, Tan, primary, Jiang, Yiqun, primary, Shi, Ying, primary, Liu, Yating, primary, Xiao, Desheng, primary, Chen, Ling, primary, Liu, Shao, primary, Mao, Chao, primary, Yin, Gang, primary, Cheng, Yan, primary, Fan, Jia, primary, Cao, Ya, primary, Muegge, Kathrin, primary, and Tao, Yongguang, primary

Published
2023
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27. Figure Legends from Chromatin Remodeling Factor LSH Drives Cancer Progression by Suppressing the Activity of Fumarate Hydratase

Author

He, Xiaozhen, primary, Yan, Bin, primary, Liu, Shuang, primary, Jia, Jiantao, primary, Lai, Weiwei, primary, Xin, Xing, primary, Tang, Can-e, primary, Luo, Dixian, primary, Tan, Tan, primary, Jiang, Yiqun, primary, Shi, Ying, primary, Liu, Yating, primary, Xiao, Desheng, primary, Chen, Ling, primary, Liu, Shao, primary, Mao, Chao, primary, Yin, Gang, primary, Cheng, Yan, primary, Fan, Jia, primary, Cao, Ya, primary, Muegge, Kathrin, primary, and Tao, Yongguang, primary

Published
2023
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28. Data from Chromatin Remodeling Factor LSH Drives Cancer Progression by Suppressing the Activity of Fumarate Hydratase

Author

He, Xiaozhen, primary, Yan, Bin, primary, Liu, Shuang, primary, Jia, Jiantao, primary, Lai, Weiwei, primary, Xin, Xing, primary, Tang, Can-e, primary, Luo, Dixian, primary, Tan, Tan, primary, Jiang, Yiqun, primary, Shi, Ying, primary, Liu, Yating, primary, Xiao, Desheng, primary, Chen, Ling, primary, Liu, Shao, primary, Mao, Chao, primary, Yin, Gang, primary, Cheng, Yan, primary, Fan, Jia, primary, Cao, Ya, primary, Muegge, Kathrin, primary, and Tao, Yongguang, primary

Published
2023
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31. Exosomal miR-17-5p derived from epithelial cells is involved in aberrant epithelium-fibroblast cross-talk and induces the development of oral submucosal fibrosis

Author

Tao, Yongguang, primary, Xie, Changqing, additional, Zhong, Liang, additional, Feng, Hui, additional, Wang, Rifu, additional, Shi, Yuxin, additional, Lv, Yonglin, additional, Hu, Yanjia, additional, Li, Jing, additional, Xiao, Desheng, additional, Liu, Shuang, additional, and Chen, Qianming, additional

Published
2023
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38. The ubiquitin‐specific protease 5 mediated deubiquitination of LSH links metabolic regulation of ferroptosis to hepatocellular carcinoma progression

Author

Yan, Bokang, primary, Guo, Jiaxing, additional, Wang, Zuli, additional, Ning, Jieling, additional, Wang, Haiyan, additional, Shu, Long, additional, Hu, Kuan, additional, Chen, Ling, additional, Shi, Ying, additional, Zhang, Lingqiang, additional, Liu, Shuang, additional, Tao, Yongguang, additional, and Xiao, Desheng, additional

Published
2023
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39. The NLRP11 Protein Bridges the Histone Lysine Acetyltransferase KAT7 to Acetylate Vimentin in the Early Stage of Lung Adenocarcinoma

Author

Yang, Rui, primary, Peng, Weilin, additional, Shi, Shuai, additional, Peng, Xiong, additional, Cai, Qidong, additional, Zhao, Zhenyu, additional, He, Boxue, additional, Tu, Guangxu, additional, Yin, Wei, additional, Chen, Yichuan, additional, Zhang, Yuqian, additional, Liu, Fang, additional, Wang, Xiang, additional, Xiao, Desheng, additional, and Tao, Yongguang, additional

Published
2023
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47. GINS4 suppresses ferroptosis by antagonizing p53 acetylation with Snail

Author

Chen, Ling, primary, Cai, Qidong, additional, Yang, Rui, additional, Wang, Haiyan, additional, Ling, Huli, additional, Li, Tiansheng, additional, Liu, Na, additional, Wang, Zuli, additional, Sun, Jingyue, additional, Tao, Tania, additional, Shi, Ying, additional, Cao, Ya, additional, Wang, Xiang, additional, Xiao, Desheng, additional, Liu, Shuang, additional, and Tao, Yongguang, additional

Published
2023
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48. Data from A G3BP1-Interacting lncRNA Promotes Ferroptosis and Apoptosis in Cancer via Nuclear Sequestration of p53

Author

Mao, Chao, primary, Wang, Xiang, primary, Liu, Yating, primary, Wang, Min, primary, Yan, Bin, primary, Jiang, Yiqun, primary, Shi, Ying, primary, Shen, Yi, primary, Liu, Xiaoli, primary, Lai, Weiwei, primary, Yang, Rui, primary, Xiao, Desheng, primary, Cheng, Yan, primary, Liu, Shuang, primary, Zhou, Hu, primary, Cao, Ya, primary, Yu, Weishi, primary, Muegge, Kathrin, primary, Yu, Herbert, primary, and Tao, Yongguang, primary

Published
2023
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49. Supplementary Material and Methods; Supplementary Tables 1-6; and Supplementary Figure S1-15 from A G3BP1-Interacting lncRNA Promotes Ferroptosis and Apoptosis in Cancer via Nuclear Sequestration of p53

Author

Mao, Chao, primary, Wang, Xiang, primary, Liu, Yating, primary, Wang, Min, primary, Yan, Bin, primary, Jiang, Yiqun, primary, Shi, Ying, primary, Shen, Yi, primary, Liu, Xiaoli, primary, Lai, Weiwei, primary, Yang, Rui, primary, Xiao, Desheng, primary, Cheng, Yan, primary, Liu, Shuang, primary, Zhou, Hu, primary, Cao, Ya, primary, Yu, Weishi, primary, Muegge, Kathrin, primary, Yu, Herbert, primary, and Tao, Yongguang, primary

Published
2023
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