Limits...
MiR-26a inhibits proliferation and migration of breast cancer through repression of MCL-1.

Gao J, Li L, Wu M, Liu M, Xie X, Guo J, Tang H, Xie X - PLoS ONE (2013)

Bottom Line: MicroRNAs are a family of small non-coding RNAs 18-25 nucleotides in length that post-transcriptionally modulate gene expression.MCL-1, an anti-apoptotic member of the Bcl-2 family, as novel targets of miR-26a was found to be in reverse correlation with ectopic expression of miR-26a and knockdown of MCL-1 phenocopied the effect of miR-26a in breast cancer cell lines.Thus, miR-26a impacts on cell proliferation and migration of breast cancer by regulating several carcinogenesis-related processes, including a novel mechanism involving the targeting of MCL-1.

View Article: PubMed Central - PubMed

Affiliation: Department of Breast Oncology, Sun Yat-sen University Cancer Center, Guangzhou, PR China.

ABSTRACT
Breast cancer is the most commonly malignancies in women. MicroRNAs are a family of small non-coding RNAs 18-25 nucleotides in length that post-transcriptionally modulate gene expression. MiR-26a has been reported as a tumor suppressor microRNA in breast cancer, which is attributed mainly to targeting of MTDH and EZH2, however, the expression profile and therapeutic potential of miR-26a is still unclear. Here we demonstrate that miR-26a is down-regulated in breast cancer cells and clinical specimens and its modulation in breast cancer cells regulates cell proliferation, colony formation, migration and apoptosis. MCL-1, an anti-apoptotic member of the Bcl-2 family, as novel targets of miR-26a was found to be in reverse correlation with ectopic expression of miR-26a and knockdown of MCL-1 phenocopied the effect of miR-26a in breast cancer cell lines. It was further explored that miR-26a increased sensitivity of breast cancer cells to paclitaxel in which MCL-1 was involved. Thus, miR-26a impacts on cell proliferation and migration of breast cancer by regulating several carcinogenesis-related processes, including a novel mechanism involving the targeting of MCL-1.

Show MeSH

Related in: MedlinePlus

Effect of miR-26a on apoptosis in breast cancer cells.FACS analysis of MDA-MB-231 and MCF-7 cells transfected with miR-26a for 48 hours. The percentage of Annexin V-FITC positive cells to the total cells was shown in the bar graphs. *P<0.05 compared with control.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3672200&req=5

pone-0065138-g004: Effect of miR-26a on apoptosis in breast cancer cells.FACS analysis of MDA-MB-231 and MCF-7 cells transfected with miR-26a for 48 hours. The percentage of Annexin V-FITC positive cells to the total cells was shown in the bar graphs. *P<0.05 compared with control.

Mentions: In order to further investigate the biological effect of miR-26a ectopic restoration on apoptosis in breast cancer cells, we transiently transfected MDA-MB-231 and MCF-7 cells with miR-26a and measured the apoptotic cell death assay using flow cytometric analysis of Annexin V-FITC/PI staining (Fig. 4). The cells in the lower right quadrant of the square chart represent the percentage of early apoptotic cells and in the upper right quadrant represent late apoptotic cells.


MiR-26a inhibits proliferation and migration of breast cancer through repression of MCL-1.

Gao J, Li L, Wu M, Liu M, Xie X, Guo J, Tang H, Xie X - PLoS ONE (2013)

Effect of miR-26a on apoptosis in breast cancer cells.FACS analysis of MDA-MB-231 and MCF-7 cells transfected with miR-26a for 48 hours. The percentage of Annexin V-FITC positive cells to the total cells was shown in the bar graphs. *P<0.05 compared with control.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3672200&req=5

pone-0065138-g004: Effect of miR-26a on apoptosis in breast cancer cells.FACS analysis of MDA-MB-231 and MCF-7 cells transfected with miR-26a for 48 hours. The percentage of Annexin V-FITC positive cells to the total cells was shown in the bar graphs. *P<0.05 compared with control.
Mentions: In order to further investigate the biological effect of miR-26a ectopic restoration on apoptosis in breast cancer cells, we transiently transfected MDA-MB-231 and MCF-7 cells with miR-26a and measured the apoptotic cell death assay using flow cytometric analysis of Annexin V-FITC/PI staining (Fig. 4). The cells in the lower right quadrant of the square chart represent the percentage of early apoptotic cells and in the upper right quadrant represent late apoptotic cells.

Bottom Line: MicroRNAs are a family of small non-coding RNAs 18-25 nucleotides in length that post-transcriptionally modulate gene expression.MCL-1, an anti-apoptotic member of the Bcl-2 family, as novel targets of miR-26a was found to be in reverse correlation with ectopic expression of miR-26a and knockdown of MCL-1 phenocopied the effect of miR-26a in breast cancer cell lines.Thus, miR-26a impacts on cell proliferation and migration of breast cancer by regulating several carcinogenesis-related processes, including a novel mechanism involving the targeting of MCL-1.

View Article: PubMed Central - PubMed

Affiliation: Department of Breast Oncology, Sun Yat-sen University Cancer Center, Guangzhou, PR China.

ABSTRACT
Breast cancer is the most commonly malignancies in women. MicroRNAs are a family of small non-coding RNAs 18-25 nucleotides in length that post-transcriptionally modulate gene expression. MiR-26a has been reported as a tumor suppressor microRNA in breast cancer, which is attributed mainly to targeting of MTDH and EZH2, however, the expression profile and therapeutic potential of miR-26a is still unclear. Here we demonstrate that miR-26a is down-regulated in breast cancer cells and clinical specimens and its modulation in breast cancer cells regulates cell proliferation, colony formation, migration and apoptosis. MCL-1, an anti-apoptotic member of the Bcl-2 family, as novel targets of miR-26a was found to be in reverse correlation with ectopic expression of miR-26a and knockdown of MCL-1 phenocopied the effect of miR-26a in breast cancer cell lines. It was further explored that miR-26a increased sensitivity of breast cancer cells to paclitaxel in which MCL-1 was involved. Thus, miR-26a impacts on cell proliferation and migration of breast cancer by regulating several carcinogenesis-related processes, including a novel mechanism involving the targeting of MCL-1.

Show MeSH
Related in: MedlinePlus