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TPM4 promotes cell migration by modulating F-actin formation in lung cancer
Background: Tropomyosin 4 (TPM4) is a member of the tropomyosin family of actin-binding proteins. Abnormal level of TPM4 is found in several cancers, and TPM4 is considered as a potential detecting marker for ovarian cancer, breast cancer, colon cancer, keratoacanthoma and esophageal squamous cell c...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6554522/ https://www.ncbi.nlm.nih.gov/pubmed/31239699 http://dx.doi.org/10.2147/OTT.S198542 |
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author | Zhao, Xiaoting Jiang, Mei Wang, Ziyu |
author_facet | Zhao, Xiaoting Jiang, Mei Wang, Ziyu |
author_sort | Zhao, Xiaoting |
collection | PubMed |
description | Background: Tropomyosin 4 (TPM4) is a member of the tropomyosin family of actin-binding proteins. Abnormal level of TPM4 is found in several cancers, and TPM4 is considered as a potential detecting marker for ovarian cancer, breast cancer, colon cancer, keratoacanthoma and esophageal squamous cell carcinoma. In this paper, the function of TPM4 in lung cancer cell lines was determined. Materials and methods: TPM4 knockout cells were constructed by CRISPR/CAS9 technique. TPM4 overexpression cells were also constructed based on TPM4 knockout cells. Cell growth ability was detected by MTS assay. The potency of cell motility was investigated using transwell assay and wound scratch assay. The protein levels in lung cancer cells were determined by western-blot. Immunofluorescence technique was used to image the structure of F-actin. Results: As a result, TPM4 downregulation and TPM4 upregulation cell models were obtained successfully. Cell motility was inhibited by the suppression of TPM4 while cell migration was enhanced in TPM4 upregulated cells. But TPM4 was not involved in cell proliferation and EMT progression. Microfilaments were depolymerized result from the suppression of TPM4 expression. And F-actin assembly was increased when TPM4 was upregulated. Conclusion: In summary, TPM4 was able to promote cell motility by altering the actin cytoskeleton directly. |
format | Online Article Text |
id | pubmed-6554522 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-65545222019-06-25 TPM4 promotes cell migration by modulating F-actin formation in lung cancer Zhao, Xiaoting Jiang, Mei Wang, Ziyu Onco Targets Ther Original Research Background: Tropomyosin 4 (TPM4) is a member of the tropomyosin family of actin-binding proteins. Abnormal level of TPM4 is found in several cancers, and TPM4 is considered as a potential detecting marker for ovarian cancer, breast cancer, colon cancer, keratoacanthoma and esophageal squamous cell carcinoma. In this paper, the function of TPM4 in lung cancer cell lines was determined. Materials and methods: TPM4 knockout cells were constructed by CRISPR/CAS9 technique. TPM4 overexpression cells were also constructed based on TPM4 knockout cells. Cell growth ability was detected by MTS assay. The potency of cell motility was investigated using transwell assay and wound scratch assay. The protein levels in lung cancer cells were determined by western-blot. Immunofluorescence technique was used to image the structure of F-actin. Results: As a result, TPM4 downregulation and TPM4 upregulation cell models were obtained successfully. Cell motility was inhibited by the suppression of TPM4 while cell migration was enhanced in TPM4 upregulated cells. But TPM4 was not involved in cell proliferation and EMT progression. Microfilaments were depolymerized result from the suppression of TPM4 expression. And F-actin assembly was increased when TPM4 was upregulated. Conclusion: In summary, TPM4 was able to promote cell motility by altering the actin cytoskeleton directly. Dove 2019-05-31 /pmc/articles/PMC6554522/ /pubmed/31239699 http://dx.doi.org/10.2147/OTT.S198542 Text en © 2019 Zhao et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Zhao, Xiaoting Jiang, Mei Wang, Ziyu TPM4 promotes cell migration by modulating F-actin formation in lung cancer |
title | TPM4 promotes cell migration by modulating F-actin formation in lung cancer |
title_full | TPM4 promotes cell migration by modulating F-actin formation in lung cancer |
title_fullStr | TPM4 promotes cell migration by modulating F-actin formation in lung cancer |
title_full_unstemmed | TPM4 promotes cell migration by modulating F-actin formation in lung cancer |
title_short | TPM4 promotes cell migration by modulating F-actin formation in lung cancer |
title_sort | tpm4 promotes cell migration by modulating f-actin formation in lung cancer |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6554522/ https://www.ncbi.nlm.nih.gov/pubmed/31239699 http://dx.doi.org/10.2147/OTT.S198542 |
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