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Overexpression of TROP2 promotes proliferation and invasion of ovarian cancer cells
Human trophoblastic cell-surface marker, tumor-associated calcium signal transducer 2 (TROP2), is a newly identified marker that has a vital role in the proliferation and invasion of various tumors. However, its specific function in ovarian cancer has not been researched. The purpose of the present...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5609167/ https://www.ncbi.nlm.nih.gov/pubmed/28962108 http://dx.doi.org/10.3892/etm.2017.4788 |
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author | Wu, Bin Yu, Chunli Zhou, Bin Huang, Tingting Gao, Lei Liu, Tao Yang, Xingsheng |
author_facet | Wu, Bin Yu, Chunli Zhou, Bin Huang, Tingting Gao, Lei Liu, Tao Yang, Xingsheng |
author_sort | Wu, Bin |
collection | PubMed |
description | Human trophoblastic cell-surface marker, tumor-associated calcium signal transducer 2 (TROP2), is a newly identified marker that has a vital role in the proliferation and invasion of various tumors. However, its specific function in ovarian cancer has not been researched. The purpose of the present study was to investigate the role of TROP2 in the formation of ovarian cancer and its possible mechanism. TROP2 was knocked down by small interfering (si)RNA in ovarian cancer cell line, A2780. The expression of TROP2 protein following transfection was detected by western blot analysis. Cell viability was determined using a Cell Counting kit-8. Cancer cell migration and invasion were examined by wound healing and cell invasion assays, respectively. Apoptosis-related proteins, such as B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax), were measured by western blotting. Results demonstrated that the expression levels of TROP2 were markedly downregulated by siRNA in A2780 cells compared with the control groups, which led to strong inhibition of proliferation and invasion. Furthermore, TROP2 downregulation also reduced cell migratory ability. Additionally, in the TROP2-knockout group, Bcl-2 was downregulated and Bax was upregulated compared with the control. The present study suggested that the expression of TROP2 was related to cellular proliferation, migration and invasion. TROP2 may disrupt the balance in the Bax family to participate in apoptosis regulation in A2780 cells. Therefore, the overexpression of TROP2 may have a crucial role in tumorigenesis and tumor progression by disturbing the Bax/Bcl-2 balance in ovarian cancer. |
format | Online Article Text |
id | pubmed-5609167 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-56091672017-09-28 Overexpression of TROP2 promotes proliferation and invasion of ovarian cancer cells Wu, Bin Yu, Chunli Zhou, Bin Huang, Tingting Gao, Lei Liu, Tao Yang, Xingsheng Exp Ther Med Articles Human trophoblastic cell-surface marker, tumor-associated calcium signal transducer 2 (TROP2), is a newly identified marker that has a vital role in the proliferation and invasion of various tumors. However, its specific function in ovarian cancer has not been researched. The purpose of the present study was to investigate the role of TROP2 in the formation of ovarian cancer and its possible mechanism. TROP2 was knocked down by small interfering (si)RNA in ovarian cancer cell line, A2780. The expression of TROP2 protein following transfection was detected by western blot analysis. Cell viability was determined using a Cell Counting kit-8. Cancer cell migration and invasion were examined by wound healing and cell invasion assays, respectively. Apoptosis-related proteins, such as B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax), were measured by western blotting. Results demonstrated that the expression levels of TROP2 were markedly downregulated by siRNA in A2780 cells compared with the control groups, which led to strong inhibition of proliferation and invasion. Furthermore, TROP2 downregulation also reduced cell migratory ability. Additionally, in the TROP2-knockout group, Bcl-2 was downregulated and Bax was upregulated compared with the control. The present study suggested that the expression of TROP2 was related to cellular proliferation, migration and invasion. TROP2 may disrupt the balance in the Bax family to participate in apoptosis regulation in A2780 cells. Therefore, the overexpression of TROP2 may have a crucial role in tumorigenesis and tumor progression by disturbing the Bax/Bcl-2 balance in ovarian cancer. D.A. Spandidos 2017-09 2017-07-12 /pmc/articles/PMC5609167/ /pubmed/28962108 http://dx.doi.org/10.3892/etm.2017.4788 Text en Copyright: © Wu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Wu, Bin Yu, Chunli Zhou, Bin Huang, Tingting Gao, Lei Liu, Tao Yang, Xingsheng Overexpression of TROP2 promotes proliferation and invasion of ovarian cancer cells |
title | Overexpression of TROP2 promotes proliferation and invasion of ovarian cancer cells |
title_full | Overexpression of TROP2 promotes proliferation and invasion of ovarian cancer cells |
title_fullStr | Overexpression of TROP2 promotes proliferation and invasion of ovarian cancer cells |
title_full_unstemmed | Overexpression of TROP2 promotes proliferation and invasion of ovarian cancer cells |
title_short | Overexpression of TROP2 promotes proliferation and invasion of ovarian cancer cells |
title_sort | overexpression of trop2 promotes proliferation and invasion of ovarian cancer cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5609167/ https://www.ncbi.nlm.nih.gov/pubmed/28962108 http://dx.doi.org/10.3892/etm.2017.4788 |
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