TRPV4 induces apoptosis via p38 MAPK in human lung cancer cells
Lung cancer is one of the most common cancers worldwide. TRPV4 belongs to the ‘transient receptor potential' (TRP) superfamily. It has been identified to profoundly affect a variety of physiological processes, including nociception, heat sensation, and inflammation. Unlike other TRP superfamily...
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Format: | Article |
Language: | English |
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Associação Brasileira de Divulgação Científica
2021-10-01
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Series: | Brazilian Journal of Medical and Biological Research |
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Online Access: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2021001200606&tlng=en |
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author | Yanyan Zhao Jiaying Wang Xuehui Liu |
author_facet | Yanyan Zhao Jiaying Wang Xuehui Liu |
author_sort | Yanyan Zhao |
collection | DOAJ |
description | Lung cancer is one of the most common cancers worldwide. TRPV4 belongs to the ‘transient receptor potential' (TRP) superfamily. It has been identified to profoundly affect a variety of physiological processes, including nociception, heat sensation, and inflammation. Unlike other TRP superfamily channels, its roles in cancers are unknown. Here, we elucidated the effects of TRPV4 and molecular mechanisms in human lung cancer cells. The levels of TRPV4 were detected in human lung cancer tissues and the paired paracarcinoma tissues by real-time PCR and western blotting analysis. The proliferation of human lung cancer cells was determined by MTT assay. Cell apoptosis was determined by FACS assay. The results demonstrated that low levels of TRPV4 were detected in clinical lung carcinoma specimens. Over-expression of TRPV4 induced cell death and inhibited cell proliferation and migration in A549 cells and H460 cells. Moreover, over-expression of TRPV4 enhanced the activation of p38 MAPK signal pathway. Inhibition of p38 MAPK abolished the effects of TRPV4 on cell proliferation, apoptosis, and migration in A549 cells. Collectively, our findings indicated that TRPV4 induced apoptosis via p38 MAPK in human lung cancer cells and suggested that TRPV4 was a potential target for therapy of human lung cancers. |
first_indexed | 2024-04-11T16:50:08Z |
format | Article |
id | doaj.art-8cad7be921ba4cb78ec88f136ddf3a00 |
institution | Directory Open Access Journal |
issn | 1414-431X |
language | English |
last_indexed | 2024-04-11T16:50:08Z |
publishDate | 2021-10-01 |
publisher | Associação Brasileira de Divulgação Científica |
record_format | Article |
series | Brazilian Journal of Medical and Biological Research |
spelling | doaj.art-8cad7be921ba4cb78ec88f136ddf3a002022-12-22T04:13:28ZengAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research1414-431X2021-10-01541210.1590/1414-431x2021e10867TRPV4 induces apoptosis via p38 MAPK in human lung cancer cellsYanyan Zhaohttps://orcid.org/0000-0002-8522-4622Jiaying Wanghttps://orcid.org/0000-0002-9864-7632Xuehui Liuhttps://orcid.org/0000-0003-1270-8455Lung cancer is one of the most common cancers worldwide. TRPV4 belongs to the ‘transient receptor potential' (TRP) superfamily. It has been identified to profoundly affect a variety of physiological processes, including nociception, heat sensation, and inflammation. Unlike other TRP superfamily channels, its roles in cancers are unknown. Here, we elucidated the effects of TRPV4 and molecular mechanisms in human lung cancer cells. The levels of TRPV4 were detected in human lung cancer tissues and the paired paracarcinoma tissues by real-time PCR and western blotting analysis. The proliferation of human lung cancer cells was determined by MTT assay. Cell apoptosis was determined by FACS assay. The results demonstrated that low levels of TRPV4 were detected in clinical lung carcinoma specimens. Over-expression of TRPV4 induced cell death and inhibited cell proliferation and migration in A549 cells and H460 cells. Moreover, over-expression of TRPV4 enhanced the activation of p38 MAPK signal pathway. Inhibition of p38 MAPK abolished the effects of TRPV4 on cell proliferation, apoptosis, and migration in A549 cells. Collectively, our findings indicated that TRPV4 induced apoptosis via p38 MAPK in human lung cancer cells and suggested that TRPV4 was a potential target for therapy of human lung cancers.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2021001200606&tlng=enLung cancerTRPV4ApoptosisP38 MAPKProliferation |
spellingShingle | Yanyan Zhao Jiaying Wang Xuehui Liu TRPV4 induces apoptosis via p38 MAPK in human lung cancer cells Brazilian Journal of Medical and Biological Research Lung cancer TRPV4 Apoptosis P38 MAPK Proliferation |
title | TRPV4 induces apoptosis via p38 MAPK in human lung cancer cells |
title_full | TRPV4 induces apoptosis via p38 MAPK in human lung cancer cells |
title_fullStr | TRPV4 induces apoptosis via p38 MAPK in human lung cancer cells |
title_full_unstemmed | TRPV4 induces apoptosis via p38 MAPK in human lung cancer cells |
title_short | TRPV4 induces apoptosis via p38 MAPK in human lung cancer cells |
title_sort | trpv4 induces apoptosis via p38 mapk in human lung cancer cells |
topic | Lung cancer TRPV4 Apoptosis P38 MAPK Proliferation |
url | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2021001200606&tlng=en |
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