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MicroRNA-20b promotes cell growth of breast cancer cells partly via targeting phosphatase and tensin homologue (PTEN).

Zhou W, Shi G, Zhang Q, Wu Q, Li B, Zhang Z - Cell Biosci (2014)

Bottom Line: MicroRNAs (miRNAs) are endogenous, small non-coding RNAs that play important roles in multiple biological processes.We identified PTEN, a well-known tumor suppressor, as the functional downstream target of miR-20b.Dysregulation of miR-20b plays critical roles in the breast cancer tumorigenesis, at least in part via targeting the tumor suppressor PTEN.

View Article: PubMed Central - PubMed

Affiliation: Center Laboratory, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361003 PR China ; School of Life Sciences, Xiamen University, Xiamen, Fujian 360112 PR China.

ABSTRACT

Background: MicroRNAs (miRNAs) are endogenous, small non-coding RNAs that play important roles in multiple biological processes. MiR-20b has been reported to participate in breast cancer tumorigenic progression, however, the functional roles are still unclear and under debating. The aim of this study is to explicit the molecular mechanism of miR-20b underlying breast cancer tumorigenesis.

Results: In the present study, we showed that miR-20b was overexpressed in human breast cancer tissues and cell lines compared with paired adjacent normal tissues and normal cell lines, respectively. We identified PTEN, a well-known tumor suppressor, as the functional downstream target of miR-20b. Luciferase assays confirmed that miR-20b could directly bind to the 3' untranslated region(UTR) of PTEN and suppress translation. Alteration of miR-20b expression changed PTEN protein level but not mRNA expression in ZR-75-30 and MCF-7 breast cancer cells, suggesting miR-20b regulates PTEN gene expression at the posttranscriptional level. Furthermore, upregulation of miR-20b significantly promoted the proliferation, colony formation and DNA synthesis of ZR-75-30 and MCF-7 breast cancer cells. Conversely, knockdown of miR-20b expression inhibited the growth of breast cancer cells in vitro and in vivo.

Conclusion: Dysregulation of miR-20b plays critical roles in the breast cancer tumorigenesis, at least in part via targeting the tumor suppressor PTEN. This microRNA may serve as a potential diagnostic marker and therapeutic target for breast cancer.

No MeSH data available.


Related in: MedlinePlus

Inhibition of miR-20b suppresses the proliferation of breast cancer cells. ZR-75-30 cells (top-panel) and MCF-7 cells (below-panel) were transfected with miR-20b inhibitor or negative control; 48 hours after transfection, EdU labeling assays were performed. Representative micrographs (200×) and quantification of EdU incorporating-cells after transfection with miR-20b inhibitor or negative control.
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Fig6: Inhibition of miR-20b suppresses the proliferation of breast cancer cells. ZR-75-30 cells (top-panel) and MCF-7 cells (below-panel) were transfected with miR-20b inhibitor or negative control; 48 hours after transfection, EdU labeling assays were performed. Representative micrographs (200×) and quantification of EdU incorporating-cells after transfection with miR-20b inhibitor or negative control.

Mentions: To further investigate the ability of miR-20b to promote cell proliferation, the 5-ethynyl-2′-deoxyuridine (EdU) incorporation assays were performed. The results showed that miR-20b overexpression enhanced DNA synthesis in both ZR-75-30 and MCF-7 breast cancer cells. The percentage of miR-20b mimics transfected ZR-75-30 cells (33.62% ± 2.14%) and of miR-20b mimics transfected MCF-7 cells (29.08% ± 3.61%) showed newly synthesized DNA by the EdU incorporation assays were significantly higher than that of ZR-75-30 control cells (25.61% ± 3.61%) and MCF-7 control cells (19.82% ± 4.41%) (Figure 5; P < 0.05). Meanwhile, miR-20b inhibitor suppressed DNA synthesis in both ZR-75-30 and MCF-7 breast cancer cells. The percentage of EdU positive cells in miR-20b inhibitor transfected ZR-75-30 cells (35.51% ± 2.24%) and MCF-7 cells (25.79% ± 3.95%) were significantly decreased as compared with that of in negative control transfected ZR-75-30 cells (40.47% ± 4.73%) and MCF-7cells (30.88% ± 3.52%) (Figure 6; P < 0.05). Collectively, these results support the role of miR-20b in the promotion of breast cancer cell proliferation, suggesting that miR-20b has an oncogene function.Figure 5


MicroRNA-20b promotes cell growth of breast cancer cells partly via targeting phosphatase and tensin homologue (PTEN).

Zhou W, Shi G, Zhang Q, Wu Q, Li B, Zhang Z - Cell Biosci (2014)

Inhibition of miR-20b suppresses the proliferation of breast cancer cells. ZR-75-30 cells (top-panel) and MCF-7 cells (below-panel) were transfected with miR-20b inhibitor or negative control; 48 hours after transfection, EdU labeling assays were performed. Representative micrographs (200×) and quantification of EdU incorporating-cells after transfection with miR-20b inhibitor or negative control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4216355&req=5

Fig6: Inhibition of miR-20b suppresses the proliferation of breast cancer cells. ZR-75-30 cells (top-panel) and MCF-7 cells (below-panel) were transfected with miR-20b inhibitor or negative control; 48 hours after transfection, EdU labeling assays were performed. Representative micrographs (200×) and quantification of EdU incorporating-cells after transfection with miR-20b inhibitor or negative control.
Mentions: To further investigate the ability of miR-20b to promote cell proliferation, the 5-ethynyl-2′-deoxyuridine (EdU) incorporation assays were performed. The results showed that miR-20b overexpression enhanced DNA synthesis in both ZR-75-30 and MCF-7 breast cancer cells. The percentage of miR-20b mimics transfected ZR-75-30 cells (33.62% ± 2.14%) and of miR-20b mimics transfected MCF-7 cells (29.08% ± 3.61%) showed newly synthesized DNA by the EdU incorporation assays were significantly higher than that of ZR-75-30 control cells (25.61% ± 3.61%) and MCF-7 control cells (19.82% ± 4.41%) (Figure 5; P < 0.05). Meanwhile, miR-20b inhibitor suppressed DNA synthesis in both ZR-75-30 and MCF-7 breast cancer cells. The percentage of EdU positive cells in miR-20b inhibitor transfected ZR-75-30 cells (35.51% ± 2.24%) and MCF-7 cells (25.79% ± 3.95%) were significantly decreased as compared with that of in negative control transfected ZR-75-30 cells (40.47% ± 4.73%) and MCF-7cells (30.88% ± 3.52%) (Figure 6; P < 0.05). Collectively, these results support the role of miR-20b in the promotion of breast cancer cell proliferation, suggesting that miR-20b has an oncogene function.Figure 5

Bottom Line: MicroRNAs (miRNAs) are endogenous, small non-coding RNAs that play important roles in multiple biological processes.We identified PTEN, a well-known tumor suppressor, as the functional downstream target of miR-20b.Dysregulation of miR-20b plays critical roles in the breast cancer tumorigenesis, at least in part via targeting the tumor suppressor PTEN.

View Article: PubMed Central - PubMed

Affiliation: Center Laboratory, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361003 PR China ; School of Life Sciences, Xiamen University, Xiamen, Fujian 360112 PR China.

ABSTRACT

Background: MicroRNAs (miRNAs) are endogenous, small non-coding RNAs that play important roles in multiple biological processes. MiR-20b has been reported to participate in breast cancer tumorigenic progression, however, the functional roles are still unclear and under debating. The aim of this study is to explicit the molecular mechanism of miR-20b underlying breast cancer tumorigenesis.

Results: In the present study, we showed that miR-20b was overexpressed in human breast cancer tissues and cell lines compared with paired adjacent normal tissues and normal cell lines, respectively. We identified PTEN, a well-known tumor suppressor, as the functional downstream target of miR-20b. Luciferase assays confirmed that miR-20b could directly bind to the 3' untranslated region(UTR) of PTEN and suppress translation. Alteration of miR-20b expression changed PTEN protein level but not mRNA expression in ZR-75-30 and MCF-7 breast cancer cells, suggesting miR-20b regulates PTEN gene expression at the posttranscriptional level. Furthermore, upregulation of miR-20b significantly promoted the proliferation, colony formation and DNA synthesis of ZR-75-30 and MCF-7 breast cancer cells. Conversely, knockdown of miR-20b expression inhibited the growth of breast cancer cells in vitro and in vivo.

Conclusion: Dysregulation of miR-20b plays critical roles in the breast cancer tumorigenesis, at least in part via targeting the tumor suppressor PTEN. This microRNA may serve as a potential diagnostic marker and therapeutic target for breast cancer.

No MeSH data available.


Related in: MedlinePlus