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Overexpression of PIK3R1 promotes hepatocellular carcinoma progression
BACKGROUND: Phosphoinositide-3-kinase, regulatory subunit 1 (PIK3R1) could regulate cancer cell proliferation important for cancer cell proliferation; however, its role in Hepatocellular carcinoma (HCC) remains largely unknown. Here, we investigated the role of PIK3R1 in HCC and examined the underly...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6264640/ https://www.ncbi.nlm.nih.gov/pubmed/30497511 http://dx.doi.org/10.1186/s40659-018-0202-7 |
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author | Ai, Xuejun Xiang, Lei Huang, Zhi Zhou, Shi Zhang, Shuai Zhang, Tao Jiang, Tianpeng |
author_facet | Ai, Xuejun Xiang, Lei Huang, Zhi Zhou, Shi Zhang, Shuai Zhang, Tao Jiang, Tianpeng |
author_sort | Ai, Xuejun |
collection | PubMed |
description | BACKGROUND: Phosphoinositide-3-kinase, regulatory subunit 1 (PIK3R1) could regulate cancer cell proliferation important for cancer cell proliferation; however, its role in Hepatocellular carcinoma (HCC) remains largely unknown. Here, we investigated the role of PIK3R1 in HCC and examined the underlying molecular mechanisms. METHODS: The expression of PIK3R1 was evaluated by immunohistochemistry and qRT-PCR in a series of HCC tissues. The mRNA and protein expression of PIK3R1 was used by qRT-PCR and western blot assays in a series of human HCC cell lines, and then we choose MHCC97H and HCCLM3 cells as a model to investigate the effect of PIK3R1 on HCC progression. The effects of PIK3R1 knowdown on cell proliferation, migration, apoptosis of HCC were assessed by the MTT assay, clonogenic assays, wound healing assay and flow cytometry in vitro. Western blot assay was performed to assess the expression changes of PI3K/AKT/mTOR signaling pathway. RESULTS: Our results found that PIK3R1 was highly expressed in HCC tissues compared with adjacent normal tissues. Knockdown of PIK3R1 inhibited the proliferation, migration and promoted apoptosis of HCC cell lines. In addition, we proved that knockdown of PIK3R1 downregulated p-PI3K, p-AKT, and p-mTOR expressions in MHCC97H and HCCLM3 cells. CONCLUSIONS: In conclusion, PIK3R1 providing potential novel targets for the treatment of HCC. |
format | Online Article Text |
id | pubmed-6264640 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-62646402018-12-05 Overexpression of PIK3R1 promotes hepatocellular carcinoma progression Ai, Xuejun Xiang, Lei Huang, Zhi Zhou, Shi Zhang, Shuai Zhang, Tao Jiang, Tianpeng Biol Res Research Article BACKGROUND: Phosphoinositide-3-kinase, regulatory subunit 1 (PIK3R1) could regulate cancer cell proliferation important for cancer cell proliferation; however, its role in Hepatocellular carcinoma (HCC) remains largely unknown. Here, we investigated the role of PIK3R1 in HCC and examined the underlying molecular mechanisms. METHODS: The expression of PIK3R1 was evaluated by immunohistochemistry and qRT-PCR in a series of HCC tissues. The mRNA and protein expression of PIK3R1 was used by qRT-PCR and western blot assays in a series of human HCC cell lines, and then we choose MHCC97H and HCCLM3 cells as a model to investigate the effect of PIK3R1 on HCC progression. The effects of PIK3R1 knowdown on cell proliferation, migration, apoptosis of HCC were assessed by the MTT assay, clonogenic assays, wound healing assay and flow cytometry in vitro. Western blot assay was performed to assess the expression changes of PI3K/AKT/mTOR signaling pathway. RESULTS: Our results found that PIK3R1 was highly expressed in HCC tissues compared with adjacent normal tissues. Knockdown of PIK3R1 inhibited the proliferation, migration and promoted apoptosis of HCC cell lines. In addition, we proved that knockdown of PIK3R1 downregulated p-PI3K, p-AKT, and p-mTOR expressions in MHCC97H and HCCLM3 cells. CONCLUSIONS: In conclusion, PIK3R1 providing potential novel targets for the treatment of HCC. BioMed Central 2018-11-29 /pmc/articles/PMC6264640/ /pubmed/30497511 http://dx.doi.org/10.1186/s40659-018-0202-7 Text en © The Author(s) 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Ai, Xuejun Xiang, Lei Huang, Zhi Zhou, Shi Zhang, Shuai Zhang, Tao Jiang, Tianpeng Overexpression of PIK3R1 promotes hepatocellular carcinoma progression |
title | Overexpression of PIK3R1 promotes hepatocellular carcinoma progression |
title_full | Overexpression of PIK3R1 promotes hepatocellular carcinoma progression |
title_fullStr | Overexpression of PIK3R1 promotes hepatocellular carcinoma progression |
title_full_unstemmed | Overexpression of PIK3R1 promotes hepatocellular carcinoma progression |
title_short | Overexpression of PIK3R1 promotes hepatocellular carcinoma progression |
title_sort | overexpression of pik3r1 promotes hepatocellular carcinoma progression |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6264640/ https://www.ncbi.nlm.nih.gov/pubmed/30497511 http://dx.doi.org/10.1186/s40659-018-0202-7 |
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