RNAi-mediated knockdown of FANCF suppresses cell proliferation, migration, invasion, and drug resistance potential of breast cancer cells
Fanconi anemia complementation group F protein (FANCF) is a key factor, which maintains the function of FA/BRCA, a DNA damage response pathway. However, the functional role of FANCF in breast cancer has not been elucidated. We performed a specific FANCF-shRNA knockdown of endogenous FANCF in vitro....
| Main Authors: | , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Associação Brasileira de Divulgação Científica
2014-01-01
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| Series: | Brazilian Journal of Medical and Biological Research |
| Subjects: | |
| Online Access: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2014000100024&lng=en&tlng=en |
| _version_ | 1819176955191230464 |
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| author | L. Zhao N. Li J.K. Yu H.T. Tang Y.L. Li M. He Z.J. Yu X.F. Bai Z.H. Zheng E.H. Wang M.J. Wei |
| author_facet | L. Zhao N. Li J.K. Yu H.T. Tang Y.L. Li M. He Z.J. Yu X.F. Bai Z.H. Zheng E.H. Wang M.J. Wei |
| author_sort | L. Zhao |
| collection | DOAJ |
| description | Fanconi anemia complementation group F protein (FANCF) is a key factor, which maintains the function of FA/BRCA, a DNA damage response pathway. However, the functional role of FANCF in breast cancer has not been elucidated. We performed a specific FANCF-shRNA knockdown of endogenous FANCF in vitro. Cell viability was measured with a CCK-8 assay. DNA damage was assessed with an alkaline comet assay. Apoptosis, cell cycle, and drug accumulation were measured by flow cytometry. The expression levels of protein were determined by Western blot using specific antibodies. Based on these results, we used cell migration and invasion assays to demonstrate a crucial role for FANCF in those processes. FANCF shRNA effectively inhibited expression of FANCF. We found that proliferation of FANCF knockdown breast cancer cells (MCF-7 and MDA-MB-435S) was significantly inhibited, with cell cycle arrest in the S phase, induction of apoptosis, and DNA fragmentation. Inhibition of FANCF also resulted in decreased cell migration and invasion. In addition, FANCF knockdown enhanced sensitivity to doxorubicin in breast cancer cells. These results suggest that FANCF may be a potential target for molecular, therapeutic intervention in breast cancer. |
| first_indexed | 2024-12-22T21:18:59Z |
| format | Article |
| id | doaj.art-31cac723498d498595279486c87964d9 |
| institution | Directory Open Access Journal |
| issn | 1414-431X |
| language | English |
| last_indexed | 2024-12-22T21:18:59Z |
| publishDate | 2014-01-01 |
| publisher | Associação Brasileira de Divulgação Científica |
| record_format | Article |
| series | Brazilian Journal of Medical and Biological Research |
| spelling | doaj.art-31cac723498d498595279486c87964d92022-12-21T18:12:14ZengAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research1414-431X2014-01-01471243410.1590/1414-431X20132938S0100-879X2014000100024RNAi-mediated knockdown of FANCF suppresses cell proliferation, migration, invasion, and drug resistance potential of breast cancer cellsL. ZhaoN. LiJ.K. YuH.T. TangY.L. LiM. HeZ.J. YuX.F. BaiZ.H. ZhengE.H. WangM.J. WeiFanconi anemia complementation group F protein (FANCF) is a key factor, which maintains the function of FA/BRCA, a DNA damage response pathway. However, the functional role of FANCF in breast cancer has not been elucidated. We performed a specific FANCF-shRNA knockdown of endogenous FANCF in vitro. Cell viability was measured with a CCK-8 assay. DNA damage was assessed with an alkaline comet assay. Apoptosis, cell cycle, and drug accumulation were measured by flow cytometry. The expression levels of protein were determined by Western blot using specific antibodies. Based on these results, we used cell migration and invasion assays to demonstrate a crucial role for FANCF in those processes. FANCF shRNA effectively inhibited expression of FANCF. We found that proliferation of FANCF knockdown breast cancer cells (MCF-7 and MDA-MB-435S) was significantly inhibited, with cell cycle arrest in the S phase, induction of apoptosis, and DNA fragmentation. Inhibition of FANCF also resulted in decreased cell migration and invasion. In addition, FANCF knockdown enhanced sensitivity to doxorubicin in breast cancer cells. These results suggest that FANCF may be a potential target for molecular, therapeutic intervention in breast cancer.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2014000100024&lng=en&tlng=enFanconi anemia complementation group F proteinBreast neoplasmsTumor cell line |
| spellingShingle | L. Zhao N. Li J.K. Yu H.T. Tang Y.L. Li M. He Z.J. Yu X.F. Bai Z.H. Zheng E.H. Wang M.J. Wei RNAi-mediated knockdown of FANCF suppresses cell proliferation, migration, invasion, and drug resistance potential of breast cancer cells Brazilian Journal of Medical and Biological Research Fanconi anemia complementation group F protein Breast neoplasms Tumor cell line |
| title | RNAi-mediated knockdown of FANCF suppresses cell proliferation, migration, invasion, and drug resistance potential of breast cancer cells |
| title_full | RNAi-mediated knockdown of FANCF suppresses cell proliferation, migration, invasion, and drug resistance potential of breast cancer cells |
| title_fullStr | RNAi-mediated knockdown of FANCF suppresses cell proliferation, migration, invasion, and drug resistance potential of breast cancer cells |
| title_full_unstemmed | RNAi-mediated knockdown of FANCF suppresses cell proliferation, migration, invasion, and drug resistance potential of breast cancer cells |
| title_short | RNAi-mediated knockdown of FANCF suppresses cell proliferation, migration, invasion, and drug resistance potential of breast cancer cells |
| title_sort | rnai mediated knockdown of fancf suppresses cell proliferation migration invasion and drug resistance potential of breast cancer cells |
| topic | Fanconi anemia complementation group F protein Breast neoplasms Tumor cell line |
| url | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2014000100024&lng=en&tlng=en |
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