Carbonic anhydrase 12 gene silencing reverses the sensitivity of paclitaxel in drug-resistant breast cancer cells

This study aimed to investigate the effects of carbonic anhydrase 12 (CA12)-siRNA on the paclitaxel sensitivity of breast cancer cells. Normal mammary glandular cell (MCF-10), breast cancer cell (MCF-7), and paclitaxel-resistant breast cancer cells (MCF-7 TaxR) were cultured in experimental control...

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Autores principales: Ting Huang, Lijuan Tang, Huan Wang, Lu Lin, Jing Fu
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Lenguaje:EN
Publicado: Taylor & Francis Group 2021
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spelling oai:doaj.org-article:49a2e28d480b4f0d82da9a6f56e0ce7a2021-11-04T15:51:54ZCarbonic anhydrase 12 gene silencing reverses the sensitivity of paclitaxel in drug-resistant breast cancer cells2165-59792165-598710.1080/21655979.2021.1995575https://doaj.org/article/49a2e28d480b4f0d82da9a6f56e0ce7a2021-10-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1995575https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987This study aimed to investigate the effects of carbonic anhydrase 12 (CA12)-siRNA on the paclitaxel sensitivity of breast cancer cells. Normal mammary glandular cell (MCF-10), breast cancer cell (MCF-7), and paclitaxel-resistant breast cancer cells (MCF-7 TaxR) were cultured in experimental control group. Western blot was adopted to detect the expressions of CA12 protein and apoptosis-related proteins in mitochondrial pathway of MCF-10, MCF-7, and MCF-7 TaxR cells. The methylthialazole tetrazolium (MTT) method was used to measure cell proliferation. The apoptosis of MCF-7 and MCF-7 TaxR cells was observed in phase contrast microscope, fluorescence inverted phase contrastmicroscope, and flow cytometry (FACS). The results showed that CA12 protein expression in MCF-7 and MCF-7 TaxR cells was significant higher than that in MCF-10 cell. The growth rate of CA12-siRNA treated MCF-7 TaxR cells with paclitaxel (PTX) co-culture was markedly declined at 48 hours. Phase contrast microscope, fluorescence inverted phase contrastmicroscope, and FACS showed that apoptotic cells in the CA12-siRNA treated MCF-7 TaxR groups were significantly higher than that in CA12-siRNA treated MCF-7 cells. The expressions of pro-apoptotic proteins, Bax and Bid, were dramatically increased in CA12 siRNA treated MCF-7 TaxR cells. The expression quantity of the downstream effective molecules caspase-9, caspase-7, and the activated proteins of poly (ADP-ribose) polymerase (PARP), also were significantly increased. Our results indicated that the application of PTX combined silencing CA12 was able to activate the mitochondrial apoptosis pathway and promote MCF-7 TaxR apoptosis. CA12 silencing in the PTX-resistant breast cancer cell can reverse the sensitivity of PTX.Ting HuangLijuan TangHuan WangLu LinJing FuTaylor & Francis Grouparticlecarbonic anhydrase 12sirnabreast cancerpaclitaxel resistantapoptosisBiotechnologyTP248.13-248.65ENBioengineered, Vol 0, Iss 0 (2021)
institution DOAJ
collection DOAJ
language EN
topic carbonic anhydrase 12
sirna
breast cancer
paclitaxel resistant
apoptosis
Biotechnology
TP248.13-248.65
spellingShingle carbonic anhydrase 12
sirna
breast cancer
paclitaxel resistant
apoptosis
Biotechnology
TP248.13-248.65
Ting Huang
Lijuan Tang
Huan Wang
Lu Lin
Jing Fu
Carbonic anhydrase 12 gene silencing reverses the sensitivity of paclitaxel in drug-resistant breast cancer cells
description This study aimed to investigate the effects of carbonic anhydrase 12 (CA12)-siRNA on the paclitaxel sensitivity of breast cancer cells. Normal mammary glandular cell (MCF-10), breast cancer cell (MCF-7), and paclitaxel-resistant breast cancer cells (MCF-7 TaxR) were cultured in experimental control group. Western blot was adopted to detect the expressions of CA12 protein and apoptosis-related proteins in mitochondrial pathway of MCF-10, MCF-7, and MCF-7 TaxR cells. The methylthialazole tetrazolium (MTT) method was used to measure cell proliferation. The apoptosis of MCF-7 and MCF-7 TaxR cells was observed in phase contrast microscope, fluorescence inverted phase contrastmicroscope, and flow cytometry (FACS). The results showed that CA12 protein expression in MCF-7 and MCF-7 TaxR cells was significant higher than that in MCF-10 cell. The growth rate of CA12-siRNA treated MCF-7 TaxR cells with paclitaxel (PTX) co-culture was markedly declined at 48 hours. Phase contrast microscope, fluorescence inverted phase contrastmicroscope, and FACS showed that apoptotic cells in the CA12-siRNA treated MCF-7 TaxR groups were significantly higher than that in CA12-siRNA treated MCF-7 cells. The expressions of pro-apoptotic proteins, Bax and Bid, were dramatically increased in CA12 siRNA treated MCF-7 TaxR cells. The expression quantity of the downstream effective molecules caspase-9, caspase-7, and the activated proteins of poly (ADP-ribose) polymerase (PARP), also were significantly increased. Our results indicated that the application of PTX combined silencing CA12 was able to activate the mitochondrial apoptosis pathway and promote MCF-7 TaxR apoptosis. CA12 silencing in the PTX-resistant breast cancer cell can reverse the sensitivity of PTX.
format article
author Ting Huang
Lijuan Tang
Huan Wang
Lu Lin
Jing Fu
author_facet Ting Huang
Lijuan Tang
Huan Wang
Lu Lin
Jing Fu
author_sort Ting Huang
title Carbonic anhydrase 12 gene silencing reverses the sensitivity of paclitaxel in drug-resistant breast cancer cells
title_short Carbonic anhydrase 12 gene silencing reverses the sensitivity of paclitaxel in drug-resistant breast cancer cells
title_full Carbonic anhydrase 12 gene silencing reverses the sensitivity of paclitaxel in drug-resistant breast cancer cells
title_fullStr Carbonic anhydrase 12 gene silencing reverses the sensitivity of paclitaxel in drug-resistant breast cancer cells
title_full_unstemmed Carbonic anhydrase 12 gene silencing reverses the sensitivity of paclitaxel in drug-resistant breast cancer cells
title_sort carbonic anhydrase 12 gene silencing reverses the sensitivity of paclitaxel in drug-resistant breast cancer cells
publisher Taylor & Francis Group
publishDate 2021
url https://doaj.org/article/49a2e28d480b4f0d82da9a6f56e0ce7a
work_keys_str_mv AT tinghuang carbonicanhydrase12genesilencingreversesthesensitivityofpaclitaxelindrugresistantbreastcancercells
AT lijuantang carbonicanhydrase12genesilencingreversesthesensitivityofpaclitaxelindrugresistantbreastcancercells
AT huanwang carbonicanhydrase12genesilencingreversesthesensitivityofpaclitaxelindrugresistantbreastcancercells
AT lulin carbonicanhydrase12genesilencingreversesthesensitivityofpaclitaxelindrugresistantbreastcancercells
AT jingfu carbonicanhydrase12genesilencingreversesthesensitivityofpaclitaxelindrugresistantbreastcancercells
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