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3. Retraction Notice to: Inflammatory-Related P62 Triggers Malignant Transformation of Mesenchymal Stem Cells through the Cascade of CUDR-CTCF-IGFII-RAS Signaling

Author

Xin, Xiaoru, primary, Wang, Chen, additional, Lin, Zhuojia, additional, Xu, Jie, additional, Lu, Yanan, additional, Meng, Qiuyu, additional, Li, Xiaonan, additional, Yang, Yuxin, additional, Zheng, Qidi, additional, Gui, Xin, additional, Li, Tianming, additional, Pu, Hu, additional, Xiong, Wujun, additional, Li, Jiao, additional, Jia, Song, additional, and Lu, Dongdong, additional

Published
2023
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6. miR675 Accelerates Malignant Transformation of Mesenchymal Stem Cells by Blocking DNA Mismatch Repair

Author

Lu, Yanan, primary, Song, Shuting, additional, Jiang, Xiaoxue, additional, Meng, Qiuyu, additional, Wang, Chen, additional, Li, Xiaonan, additional, Yang, Yuxin, additional, Xin, Xiaoru, additional, Zheng, Qidi, additional, Wang, Liyan, additional, Pu, Hu, additional, Gui, Xin, additional, Li, Tianming, additional, and Lu, Dongdong, additional

Published
2019
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8. miR372 Promotes Progression of Liver Cancer Cells by Upregulating erbB-2 through Enhancement of YB-1

Author

Lin, Zhuojia, primary, Lu, Yanan, additional, Meng, Qiuyu, additional, Wang, Chen, additional, Li, Xiaonan, additional, Yang, Yuxin, additional, Xin, Xiaoru, additional, Zheng, Qidi, additional, Xu, Jie, additional, Gui, Xin, additional, Li, Tianming, additional, Pu, Hu, additional, Xiong, Wujun, additional, Li, Jiao, additional, Jia, Song, additional, and Lu, Dongdong, additional

Published
2018
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9. RETRACTED: Inflammatory-Related P62 Triggers Malignant Transformation of Mesenchymal Stem Cells through the Cascade of CUDR-CTCF-IGFII-RAS Signaling

Author

Xin, Xiaoru, primary, Wang, Chen, additional, Lin, Zhuojia, additional, Xu, Jie, additional, Lu, Yanan, additional, Meng, Qiuyu, additional, Li, Xiaonan, additional, Yang, Yuxin, additional, Zheng, Qidi, additional, Gui, Xin, additional, Li, Tianming, additional, Pu, Hu, additional, Xiong, Wujun, additional, Li, Jiao, additional, Jia, Song, additional, and Lu, Dongdong, additional

Published
2018
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12. HistoneH3 demethylase JMJD2A promotes growth of liver cancer cells through up-regulating miR372

Author

An, Jiahui, primary, Xu, Jie, additional, Li, Jiao, additional, Jia, Song, additional, Li, Xiaonan, additional, Lu, Yanan, additional, Yang, Yuxin, additional, Lin, Zhuojia, additional, Xin, Xiaoru, additional, Wu, Mengying, additional, Zheng, Qidi, additional, Pu, Hu, additional, Gui, Xin, additional, Li, Tianming, additional, and Lu, Dongdong, additional

Published
2017
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23. miR675 Accelerates Malignant Transformation of Mesenchymal Stem Cells by Blocking DNA Mismatch Repair.

Author

Lu Y, Song S, Jiang X, Meng Q, Wang C, Li X, Yang Y, Xin X, Zheng Q, Wang L, Pu H, Gui X, Li T, and Lu D

Abstract

miR675 is highly expressed in several human tumor tissues and positively regulates cell progression. Herein, we demonstrate that miR675 promotes malignant transformation of human mesenchymal stem cells. Mechanistically, we reveal that miR675 enhances the expression of the polyubiquitin-binding protein p62. Intriguingly, P62 competes with SETD2 to bind histone H3 and then significantly reduces SETD2-binding capacity to substrate histone H3, triggering drastically the reduction of three methylation on histone H3 36th lysine (H3K36me3). Thereby, the H3K36me3-hMSH6-SKP2 triplex complex is significantly decreased. Notably, the ternary complex's occupancy capacity on chromosome is absolutely reduced, preventing it from DNA damage repair. By virtue of the reductive degradation ability of SKP2 for aging histone H3.3 bound to mismatch DNA, the aging histone H3.3 repair is delayed. Therefore, the mismatch DNA escapes from repair, triggering the abnormal expression of several cell cycle-related genes and causing the malignant transformation of mesenchymal stem cells. These observations strongly suggest understanding the novel functions of miR675 will help in the development of novel therapeutic approaches in a broad range of cancer types., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)

Published
2019
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24. Inflammatory-Related P62 Triggers Malignant Transformation of Mesenchymal Stem Cells through the Cascade of CUDR-CTCF-IGFII-RAS Signaling.

Author

Xin X, Wang C, Lin Z, Xu J, Lu Y, Meng Q, Li X, Yang Y, Zheng Q, Gui X, Li T, Pu H, Xiong W, Li J, Jia S, and Lu D

Abstract

Inflammatory and autophagy-related gene P62 is highly expressed in most human tumor tissues. Herein, we demonstrate that P62 promotes human mesenchymal stem cells' malignant transformation via the cascade of P62-tumor necrosis factor alpha (TNF-α)-CUDR-CTCF-insulin growth factor II (IGFII)-H-Ras signaling. Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells., (Copyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved.)

Published
2018
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25. miR372 Promotes Progression of Liver Cancer Cells by Upregulating erbB-2 through Enhancement of YB-1.

Author

Lin Z, Lu Y, Meng Q, Wang C, Li X, Yang Y, Xin X, Zheng Q, Xu J, Gui X, Li T, Pu H, Xiong W, Li J, Jia S, and Lu D

Abstract

MicroRNAs are known to be involved in carcinogenesis. Recently, microRNA-372 (miR372) has been proven to play a substantial role in several human cancers, but its functions in liver cancer remain unclear. Herein, our results demonstrate that miR372 accelerates growth of liver cancer cells in vitro and in vivo. Mechanistically, miR372 enhances expression of Y-box-binding protein 1 (YB-1) by targeting for phosphatase and tensin homolog (PTEN) directly and consequently promotes phosphorylation of YB-1 via HULC looping dependent on ERK1/2 and PTEN. In particular, HULC knockdown or PTEN overexpression abrogated this miR372 action. Moreover, miR372 inhibits the degradation of β-catenin dependent on phosphorylation of YB-1 and then enhances the expression and activity of pyruvate kinase M2 isoform (PKM2) by β-catenin-LEF/TCF4 pathway. Furthermore, the loading of LEF/TCF4 on PKM2 promoter region was significantly increased in miR372 overexpressing Hep3B, and thus, glycolytic proton efflux rate (glycoPER) was significantly increased in rLV-miR372 group compared to the rLV group. Moreover, β-catenin knockdown abrogates this function of miR372. Ultimately, miR372 promotes the expression of erbB-2 through PKM2-pH3T11-acetylation on histone H3 lysine 9 (H3K9Ac) pathway. Of significance, both YB-1 knockdown and erbB-2 knockdown abrogate oncogenic action of miR372. Our observations suggest that miR372 promotes liver cancer cell cycle progress by activating cyclin-dependent kinase 2 (CDK2)-cyclin E-P21/Cip1 complex through miR372-YB-1-β-catenin-LEF/TCF4-PKM2-erbB-2 axis. This study elucidates a novel mechanism for miR372 in liver cancer cells and suggests that miR372 can be used as a novel therapeutic target of liver cancer., (Copyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved.)

Published
2018
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