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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

Ectopic restoration of miR-26a inhibited cell migration.In the wound healing assay, uniform scratches were made in MDA-MB-231 and MCF-7 cells, then serial photographs were obtained at indicated time posttransfection.
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pone-0065138-g003: Ectopic restoration of miR-26a inhibited cell migration.In the wound healing assay, uniform scratches were made in MDA-MB-231 and MCF-7 cells, then serial photographs were obtained at indicated time posttransfection.

Mentions: Given that cell migration is among the common functions required by tumor cells for metastatic progression [24], as well as the strong association between tumor cell migration and tumor cell invasion and metastasis [25], we asked whether miR-26a could affect breast cancer cell migration in vitro. In wound healing assay, ectopic restoration of miR-26a did obviously delay the closure rate of both MDA-MB-231 and MCF-7 cells forward the wound area, compared with cells transfected with miR-Ctrl (Fig. 3), which suggested that miR-26a has the ability to inhibit migration for breast cancer 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)

Ectopic restoration of miR-26a inhibited cell migration.In the wound healing assay, uniform scratches were made in MDA-MB-231 and MCF-7 cells, then serial photographs were obtained at indicated time posttransfection.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0065138-g003: Ectopic restoration of miR-26a inhibited cell migration.In the wound healing assay, uniform scratches were made in MDA-MB-231 and MCF-7 cells, then serial photographs were obtained at indicated time posttransfection.
Mentions: Given that cell migration is among the common functions required by tumor cells for metastatic progression [24], as well as the strong association between tumor cell migration and tumor cell invasion and metastasis [25], we asked whether miR-26a could affect breast cancer cell migration in vitro. In wound healing assay, ectopic restoration of miR-26a did obviously delay the closure rate of both MDA-MB-231 and MCF-7 cells forward the wound area, compared with cells transfected with miR-Ctrl (Fig. 3), which suggested that miR-26a has the ability to inhibit migration for breast cancer 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