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SALL4 activates PI3K/AKT signaling pathway through targeting PTEN, thus facilitating migration, invasion and proliferation of hepatocellular carcinoma cells

This study aims to explore the specific mechanisms of SALL4 on the migration, invasion and proliferation of HCC. HepG2 and SMMC-7721 cells were transfected with SALL4 NC, mimics and inhibitors. The proliferation capability and cell cycle progression of HCC cells were detected through CCK8 assay and...

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Autores principales: Tang, Zhipeng, Zhao, Pei, Zhang, Wanxing, Zhang, Qian, Zhao, Ming, Tan, He
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9831741/
https://www.ncbi.nlm.nih.gov/pubmed/36575044
http://dx.doi.org/10.18632/aging.204446
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author Tang, Zhipeng
Zhao, Pei
Zhang, Wanxing
Zhang, Qian
Zhao, Ming
Tan, He
author_facet Tang, Zhipeng
Zhao, Pei
Zhang, Wanxing
Zhang, Qian
Zhao, Ming
Tan, He
author_sort Tang, Zhipeng
collection PubMed
description This study aims to explore the specific mechanisms of SALL4 on the migration, invasion and proliferation of HCC. HepG2 and SMMC-7721 cells were transfected with SALL4 NC, mimics and inhibitors. The proliferation capability and cell cycle progression of HCC cells were detected through CCK8 assay and flow cytometry, and their migration and invasion capabilities were detected by wound healing assay and Transwell assay. In SALL4 inhibitor NC group and SALL4 inhibitor group, the PTEN inhibitor SF1670 was added, and the expression levels of PI3K/AKT, migration, invasion and proliferation-related proteins were detected by Western blotting. Results showed that after up-regulation of SALL4, the migration distance of HCC cells increased, the numbers of migrated cells and the number of colonies formed significantly rosed, and there were fewer cells in G1 phase but significantly more cells in S phase, thereby down-regulation of SALL4, the opposite results. The results of Western blotting revealed that after SF1670, the specific PTEN inhibitor was added in SALL4 inhibitor group and SALL4 inhibitor NC group, the protein expression of PTEN in HCC cells significantly declined, while the protein expressions of p-PI3K, p-AKT, MMP2, MMP9, CyclinD, CyclinA1, PCNA and P62 significantly rose. In conclusion, SALL4 activates the PI3K/AKT signaling pathway through targeting PTEN, thereby facilitating the migration, invasion and proliferation of HCC cells.
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spelling pubmed-98317412023-01-11 SALL4 activates PI3K/AKT signaling pathway through targeting PTEN, thus facilitating migration, invasion and proliferation of hepatocellular carcinoma cells Tang, Zhipeng Zhao, Pei Zhang, Wanxing Zhang, Qian Zhao, Ming Tan, He Aging (Albany NY) Research Paper This study aims to explore the specific mechanisms of SALL4 on the migration, invasion and proliferation of HCC. HepG2 and SMMC-7721 cells were transfected with SALL4 NC, mimics and inhibitors. The proliferation capability and cell cycle progression of HCC cells were detected through CCK8 assay and flow cytometry, and their migration and invasion capabilities were detected by wound healing assay and Transwell assay. In SALL4 inhibitor NC group and SALL4 inhibitor group, the PTEN inhibitor SF1670 was added, and the expression levels of PI3K/AKT, migration, invasion and proliferation-related proteins were detected by Western blotting. Results showed that after up-regulation of SALL4, the migration distance of HCC cells increased, the numbers of migrated cells and the number of colonies formed significantly rosed, and there were fewer cells in G1 phase but significantly more cells in S phase, thereby down-regulation of SALL4, the opposite results. The results of Western blotting revealed that after SF1670, the specific PTEN inhibitor was added in SALL4 inhibitor group and SALL4 inhibitor NC group, the protein expression of PTEN in HCC cells significantly declined, while the protein expressions of p-PI3K, p-AKT, MMP2, MMP9, CyclinD, CyclinA1, PCNA and P62 significantly rose. In conclusion, SALL4 activates the PI3K/AKT signaling pathway through targeting PTEN, thereby facilitating the migration, invasion and proliferation of HCC cells. Impact Journals 2022-12-26 /pmc/articles/PMC9831741/ /pubmed/36575044 http://dx.doi.org/10.18632/aging.204446 Text en Copyright: © 2022 Tang et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Tang, Zhipeng
Zhao, Pei
Zhang, Wanxing
Zhang, Qian
Zhao, Ming
Tan, He
SALL4 activates PI3K/AKT signaling pathway through targeting PTEN, thus facilitating migration, invasion and proliferation of hepatocellular carcinoma cells
title SALL4 activates PI3K/AKT signaling pathway through targeting PTEN, thus facilitating migration, invasion and proliferation of hepatocellular carcinoma cells
title_full SALL4 activates PI3K/AKT signaling pathway through targeting PTEN, thus facilitating migration, invasion and proliferation of hepatocellular carcinoma cells
title_fullStr SALL4 activates PI3K/AKT signaling pathway through targeting PTEN, thus facilitating migration, invasion and proliferation of hepatocellular carcinoma cells
title_full_unstemmed SALL4 activates PI3K/AKT signaling pathway through targeting PTEN, thus facilitating migration, invasion and proliferation of hepatocellular carcinoma cells
title_short SALL4 activates PI3K/AKT signaling pathway through targeting PTEN, thus facilitating migration, invasion and proliferation of hepatocellular carcinoma cells
title_sort sall4 activates pi3k/akt signaling pathway through targeting pten, thus facilitating migration, invasion and proliferation of hepatocellular carcinoma cells
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9831741/
https://www.ncbi.nlm.nih.gov/pubmed/36575044
http://dx.doi.org/10.18632/aging.204446
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