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TGF-β1 induced deficiency of linc00261 promotes epithelial–mesenchymal-transition and stemness of hepatocellular carcinoma via modulating SMAD3

Emerging evidence suggests that long non-coding RNAs (lncRNAs) play important roles in the metastasis and recurrence of hepatocellular carcinoma (HCC). A kinds of lncRNAs were found to be involved in regulating epithelial–mesenchymal transition (EMT) or stem-like traits in human cancers, however, th...

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Autores principales: Chen, Zhanjun, Xiang, Leyang, Li, Longhai, Ou, Huohui, Fang, Yinghao, Xu, Yuyan, Liu, Qin, Hu, Zhigang, Huang, Yu, Li, Xianghong, Yang, Dinghua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8818189/
https://www.ncbi.nlm.nih.gov/pubmed/35123494
http://dx.doi.org/10.1186/s12967-022-03276-z
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author Chen, Zhanjun
Xiang, Leyang
Li, Longhai
Ou, Huohui
Fang, Yinghao
Xu, Yuyan
Liu, Qin
Hu, Zhigang
Huang, Yu
Li, Xianghong
Yang, Dinghua
author_facet Chen, Zhanjun
Xiang, Leyang
Li, Longhai
Ou, Huohui
Fang, Yinghao
Xu, Yuyan
Liu, Qin
Hu, Zhigang
Huang, Yu
Li, Xianghong
Yang, Dinghua
author_sort Chen, Zhanjun
collection PubMed
description Emerging evidence suggests that long non-coding RNAs (lncRNAs) play important roles in the metastasis and recurrence of hepatocellular carcinoma (HCC). A kinds of lncRNAs were found to be involved in regulating epithelial–mesenchymal transition (EMT) or stem-like traits in human cancers, however, the molecular mechanism and signaling pathways targeting EMT and stemness remains largely unknown. Previously, we found that linc00261 was down-regulated in HCC and associated with multiple worse clinical pathological parameters and poor prognosis. Here, we show that linc00261 was down-regulated in TGF-β1 stimulated cells, and forced expression of linc00261 attenuated EMT and stem-like traits in HCC. Linc00261 also inhibited the tumor sphere forming in vitro and decreased the tumorigenicity in vivo. Furthermore, we revealed that linc00261 suppressed the expression and phosphorylation of SMAD3 (p-SMAD3), which could be core transcriptional modulator in TGF-β1 signaling mediated EMT and the acquisition of stemness traits. A negative correlation between linc00261 and p-SMAD3 was determined in HCC samples. Conclusion: Our study revealed that linc00261 suppressed EMT and stem-like traits in HCC cells by inhibiting TGF-β1/SMAD3 signaling. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12967-022-03276-z.
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spelling pubmed-88181892022-02-07 TGF-β1 induced deficiency of linc00261 promotes epithelial–mesenchymal-transition and stemness of hepatocellular carcinoma via modulating SMAD3 Chen, Zhanjun Xiang, Leyang Li, Longhai Ou, Huohui Fang, Yinghao Xu, Yuyan Liu, Qin Hu, Zhigang Huang, Yu Li, Xianghong Yang, Dinghua J Transl Med Research Emerging evidence suggests that long non-coding RNAs (lncRNAs) play important roles in the metastasis and recurrence of hepatocellular carcinoma (HCC). A kinds of lncRNAs were found to be involved in regulating epithelial–mesenchymal transition (EMT) or stem-like traits in human cancers, however, the molecular mechanism and signaling pathways targeting EMT and stemness remains largely unknown. Previously, we found that linc00261 was down-regulated in HCC and associated with multiple worse clinical pathological parameters and poor prognosis. Here, we show that linc00261 was down-regulated in TGF-β1 stimulated cells, and forced expression of linc00261 attenuated EMT and stem-like traits in HCC. Linc00261 also inhibited the tumor sphere forming in vitro and decreased the tumorigenicity in vivo. Furthermore, we revealed that linc00261 suppressed the expression and phosphorylation of SMAD3 (p-SMAD3), which could be core transcriptional modulator in TGF-β1 signaling mediated EMT and the acquisition of stemness traits. A negative correlation between linc00261 and p-SMAD3 was determined in HCC samples. Conclusion: Our study revealed that linc00261 suppressed EMT and stem-like traits in HCC cells by inhibiting TGF-β1/SMAD3 signaling. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12967-022-03276-z. BioMed Central 2022-02-05 /pmc/articles/PMC8818189/ /pubmed/35123494 http://dx.doi.org/10.1186/s12967-022-03276-z Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Chen, Zhanjun
Xiang, Leyang
Li, Longhai
Ou, Huohui
Fang, Yinghao
Xu, Yuyan
Liu, Qin
Hu, Zhigang
Huang, Yu
Li, Xianghong
Yang, Dinghua
TGF-β1 induced deficiency of linc00261 promotes epithelial–mesenchymal-transition and stemness of hepatocellular carcinoma via modulating SMAD3
title TGF-β1 induced deficiency of linc00261 promotes epithelial–mesenchymal-transition and stemness of hepatocellular carcinoma via modulating SMAD3
title_full TGF-β1 induced deficiency of linc00261 promotes epithelial–mesenchymal-transition and stemness of hepatocellular carcinoma via modulating SMAD3
title_fullStr TGF-β1 induced deficiency of linc00261 promotes epithelial–mesenchymal-transition and stemness of hepatocellular carcinoma via modulating SMAD3
title_full_unstemmed TGF-β1 induced deficiency of linc00261 promotes epithelial–mesenchymal-transition and stemness of hepatocellular carcinoma via modulating SMAD3
title_short TGF-β1 induced deficiency of linc00261 promotes epithelial–mesenchymal-transition and stemness of hepatocellular carcinoma via modulating SMAD3
title_sort tgf-β1 induced deficiency of linc00261 promotes epithelial–mesenchymal-transition and stemness of hepatocellular carcinoma via modulating smad3
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8818189/
https://www.ncbi.nlm.nih.gov/pubmed/35123494
http://dx.doi.org/10.1186/s12967-022-03276-z
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