Cargando…
Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts
Stromal interaction molecule 1 (STIM1) is a calcium-sensing protein localized in the membrane of the endoplasmic reticulum. The expression of STIM1 has been shown to be closely associated with cell proliferation. The aim of the present study was to investigate the role of STIM1 in the regulation of...
Autores principales: | , , , , , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2019
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6779409/ https://www.ncbi.nlm.nih.gov/pubmed/31564210 http://dx.doi.org/10.1080/21655979.2019.1669518 |
_version_ | 1783456918111518720 |
---|---|
author | Ge, Chunlei Zeng, Baozhen Li, Ruilei Li, Zhen Fu, Qiaofen Wang, Weiwei Wang, Zhenyu Dong, Suwei Lai, Zhangchao Wang, Ying Xue, Yuanbo Guo, Jiyin Di, Tiannan Song, Xin |
author_facet | Ge, Chunlei Zeng, Baozhen Li, Ruilei Li, Zhen Fu, Qiaofen Wang, Weiwei Wang, Zhenyu Dong, Suwei Lai, Zhangchao Wang, Ying Xue, Yuanbo Guo, Jiyin Di, Tiannan Song, Xin |
author_sort | Ge, Chunlei |
collection | PubMed |
description | Stromal interaction molecule 1 (STIM1) is a calcium-sensing protein localized in the membrane of the endoplasmic reticulum. The expression of STIM1 has been shown to be closely associated with cell proliferation. The aim of the present study was to investigate the role of STIM1 in the regulation of cancer progression and its clinical relevance. The data demonstrated that the expression of the STIM1 was significantly higher in non-small-cell lung cancer (NSCLC) tissues than in benign lesions and was associated with advanced NSCLC T stage. Knockdown of STIM1 expression in NSCLC cell lines A549 and SK-MES-1 significantly inhibited cell proliferation and induces A549 and SK-MES-1 cell arrest at the G2/M and S phases of the cell cycle. Western blotting showed that the expression of cyclin-dependent kinase (CDK) 1 and CDK2 were reduced while knockdown of STIM1 expression. Furthermore, knockdown of STIM1 in NSCLC cells significantly reduced the levels of xenograft tumor growth in nude mice. These data indicate that aberrant expression of the STIM1 protein may contribute to NSCLC progression. Future studies should focus on targeting STIM1 as a novel strategy for NSCLC therapy. |
format | Online Article Text |
id | pubmed-6779409 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-67794092020-09-28 Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts Ge, Chunlei Zeng, Baozhen Li, Ruilei Li, Zhen Fu, Qiaofen Wang, Weiwei Wang, Zhenyu Dong, Suwei Lai, Zhangchao Wang, Ying Xue, Yuanbo Guo, Jiyin Di, Tiannan Song, Xin Bioengineered Research Paper Stromal interaction molecule 1 (STIM1) is a calcium-sensing protein localized in the membrane of the endoplasmic reticulum. The expression of STIM1 has been shown to be closely associated with cell proliferation. The aim of the present study was to investigate the role of STIM1 in the regulation of cancer progression and its clinical relevance. The data demonstrated that the expression of the STIM1 was significantly higher in non-small-cell lung cancer (NSCLC) tissues than in benign lesions and was associated with advanced NSCLC T stage. Knockdown of STIM1 expression in NSCLC cell lines A549 and SK-MES-1 significantly inhibited cell proliferation and induces A549 and SK-MES-1 cell arrest at the G2/M and S phases of the cell cycle. Western blotting showed that the expression of cyclin-dependent kinase (CDK) 1 and CDK2 were reduced while knockdown of STIM1 expression. Furthermore, knockdown of STIM1 in NSCLC cells significantly reduced the levels of xenograft tumor growth in nude mice. These data indicate that aberrant expression of the STIM1 protein may contribute to NSCLC progression. Future studies should focus on targeting STIM1 as a novel strategy for NSCLC therapy. Taylor & Francis 2019-09-28 /pmc/articles/PMC6779409/ /pubmed/31564210 http://dx.doi.org/10.1080/21655979.2019.1669518 Text en © 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Paper Ge, Chunlei Zeng, Baozhen Li, Ruilei Li, Zhen Fu, Qiaofen Wang, Weiwei Wang, Zhenyu Dong, Suwei Lai, Zhangchao Wang, Ying Xue, Yuanbo Guo, Jiyin Di, Tiannan Song, Xin Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts |
title | Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts |
title_full | Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts |
title_fullStr | Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts |
title_full_unstemmed | Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts |
title_short | Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts |
title_sort | knockdown of stim1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6779409/ https://www.ncbi.nlm.nih.gov/pubmed/31564210 http://dx.doi.org/10.1080/21655979.2019.1669518 |
work_keys_str_mv | AT gechunlei knockdownofstim1expressioninhibitsnonsmallcelllungcancercellproliferationinvitroandinnudemousexenografts AT zengbaozhen knockdownofstim1expressioninhibitsnonsmallcelllungcancercellproliferationinvitroandinnudemousexenografts AT liruilei knockdownofstim1expressioninhibitsnonsmallcelllungcancercellproliferationinvitroandinnudemousexenografts AT lizhen knockdownofstim1expressioninhibitsnonsmallcelllungcancercellproliferationinvitroandinnudemousexenografts AT fuqiaofen knockdownofstim1expressioninhibitsnonsmallcelllungcancercellproliferationinvitroandinnudemousexenografts AT wangweiwei knockdownofstim1expressioninhibitsnonsmallcelllungcancercellproliferationinvitroandinnudemousexenografts AT wangzhenyu knockdownofstim1expressioninhibitsnonsmallcelllungcancercellproliferationinvitroandinnudemousexenografts AT dongsuwei knockdownofstim1expressioninhibitsnonsmallcelllungcancercellproliferationinvitroandinnudemousexenografts AT laizhangchao knockdownofstim1expressioninhibitsnonsmallcelllungcancercellproliferationinvitroandinnudemousexenografts AT wangying knockdownofstim1expressioninhibitsnonsmallcelllungcancercellproliferationinvitroandinnudemousexenografts AT xueyuanbo knockdownofstim1expressioninhibitsnonsmallcelllungcancercellproliferationinvitroandinnudemousexenografts AT guojiyin knockdownofstim1expressioninhibitsnonsmallcelllungcancercellproliferationinvitroandinnudemousexenografts AT ditiannan knockdownofstim1expressioninhibitsnonsmallcelllungcancercellproliferationinvitroandinnudemousexenografts AT songxin knockdownofstim1expressioninhibitsnonsmallcelllungcancercellproliferationinvitroandinnudemousexenografts |