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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.

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Related in: MedlinePlus

Overexpression of miR-26a lead to reduced cell viability and decreased clonogenicity.A. Dose effect. Cells were transfected with miR-26a at the indicated concentrations for 48 hours. B. Time effect. Cells were transfected with 50 µM of miR-26a for indicated periods. C. Morphologic changes of MDA-MB-231 and MCF-7 cells in response to miR-26a inhibition. D. Influence of miR-26a on colony formation of MDA-MB-231 and MCF-7 cells. Representative dishes are presented (left). The number of colony was counted for each well of six-well plates and the evaluation of colony numbers was shown in the y-axis of the right panel. *P<0.05 compared with control.
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pone-0065138-g002: Overexpression of miR-26a lead to reduced cell viability and decreased clonogenicity.A. Dose effect. Cells were transfected with miR-26a at the indicated concentrations for 48 hours. B. Time effect. Cells were transfected with 50 µM of miR-26a for indicated periods. C. Morphologic changes of MDA-MB-231 and MCF-7 cells in response to miR-26a inhibition. D. Influence of miR-26a on colony formation of MDA-MB-231 and MCF-7 cells. Representative dishes are presented (left). The number of colony was counted for each well of six-well plates and the evaluation of colony numbers was shown in the y-axis of the right panel. *P<0.05 compared with control.

Mentions: To explore the effect of miR-26a on cell growth, MDA-MB-231, MCF-7, MDA-MB-435 and MDA-MB-468 cells were transfected with miR-26a mimic. The impact of different doses of miR-26a was evaluated firstly. Cells were transfected with 0–200 µM miR-26a or miR-Ctrl for 48 hours and the relative viability was determined by MTT assay. As shown in Fig. 2A, miR-26a inhibited cell growth in a dose-dependent manner, compared with miR-Ctrl at any of the corresponding concentrations. Next, cells were transfected with 50 µM of miR-26a or miR-Ctrl for varying periods. The result of MTT assay indicated that miR-26a led to growth inhibition in all 4 breast cancer cell lines as early as 48 hours posttransfection, persisting for 72 hours (Fig. 2B).


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)

Overexpression of miR-26a lead to reduced cell viability and decreased clonogenicity.A. Dose effect. Cells were transfected with miR-26a at the indicated concentrations for 48 hours. B. Time effect. Cells were transfected with 50 µM of miR-26a for indicated periods. C. Morphologic changes of MDA-MB-231 and MCF-7 cells in response to miR-26a inhibition. D. Influence of miR-26a on colony formation of MDA-MB-231 and MCF-7 cells. Representative dishes are presented (left). The number of colony was counted for each well of six-well plates and the evaluation of colony numbers was shown in the y-axis of the right panel. *P<0.05 compared with control.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0065138-g002: Overexpression of miR-26a lead to reduced cell viability and decreased clonogenicity.A. Dose effect. Cells were transfected with miR-26a at the indicated concentrations for 48 hours. B. Time effect. Cells were transfected with 50 µM of miR-26a for indicated periods. C. Morphologic changes of MDA-MB-231 and MCF-7 cells in response to miR-26a inhibition. D. Influence of miR-26a on colony formation of MDA-MB-231 and MCF-7 cells. Representative dishes are presented (left). The number of colony was counted for each well of six-well plates and the evaluation of colony numbers was shown in the y-axis of the right panel. *P<0.05 compared with control.
Mentions: To explore the effect of miR-26a on cell growth, MDA-MB-231, MCF-7, MDA-MB-435 and MDA-MB-468 cells were transfected with miR-26a mimic. The impact of different doses of miR-26a was evaluated firstly. Cells were transfected with 0–200 µM miR-26a or miR-Ctrl for 48 hours and the relative viability was determined by MTT assay. As shown in Fig. 2A, miR-26a inhibited cell growth in a dose-dependent manner, compared with miR-Ctrl at any of the corresponding concentrations. Next, cells were transfected with 50 µM of miR-26a or miR-Ctrl for varying periods. The result of MTT assay indicated that miR-26a led to growth inhibition in all 4 breast cancer cell lines as early as 48 hours posttransfection, persisting for 72 hours (Fig. 2B).

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