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MiR-30a upregulates BCL2A1, IER3 and cyclin D2 expression by targeting FOXL2.

Wang T, Li F, Tang S - Oncol Lett (2014)

Bottom Line: FOXL2 is a transcription factor that is essential for ovarian development.In the present study, the expression of FOXL2 was suppressed by microRNAs using the Ago2 knockdown method in COV434 cells.Furthermore, miR-30a overexpression upregulates BCL2A1, IER3 and cyclin D2 expression by inhibiting FOXL2. miR-30a is known to function as a tumor suppressor in breast cancer, small cell lung cancer and colorectal carcinoma; however, the present study revealed an opposing function of miR-30a as an oncogene.

View Article: PubMed Central - PubMed

Affiliation: Institute of Plastic Surgery, Weifang Medical College, Weifang, Shandong 261041, P.R. China.

ABSTRACT

FOXL2 is a transcription factor that is essential for ovarian development. Somatic mutations of FOXL2 are associated with ovarian granulosa cell tumorigenesis. In the present study, the expression of FOXL2 was suppressed by microRNAs using the Ago2 knockdown method in COV434 cells. Online bioinformatics tools were utilized to predict that FOXL2 expression may be repressed by miR-30 family members, and dual luciferase assay and western blotting were performed to demonstrate that FOXL2 is a target gene of miR-30a, which is relatively abundant in COV434 cells. Furthermore, miR-30a overexpression upregulates BCL2A1, IER3 and cyclin D2 expression by inhibiting FOXL2. miR-30a is known to function as a tumor suppressor in breast cancer, small cell lung cancer and colorectal carcinoma; however, the present study revealed an opposing function of miR-30a as an oncogene.

No MeSH data available.


Related in: MedlinePlus

FOXL2 expression was significantly repressed by miRNAs in COV434 cells. (A) FOXL2 expression was upregulated when AGO2 was knocked down; therefore, FOXL2 expression was repressed by endogenous microRNAs. (B) Reverse transcription-quantitative polymerase chain reaction of miR-30a/b/c/d/e expression in COV434 cells revealed that miR-30a is relatively abundant compared with other miR-30 family members. (C) The predicted interactions between miR-30a/b/c/d/e and FOXL2 3′-UTR mRNA. miR/miRNA, microRNA; 3′-UTR; 3′-untranslated region.
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f1-ol-09-02-0967: FOXL2 expression was significantly repressed by miRNAs in COV434 cells. (A) FOXL2 expression was upregulated when AGO2 was knocked down; therefore, FOXL2 expression was repressed by endogenous microRNAs. (B) Reverse transcription-quantitative polymerase chain reaction of miR-30a/b/c/d/e expression in COV434 cells revealed that miR-30a is relatively abundant compared with other miR-30 family members. (C) The predicted interactions between miR-30a/b/c/d/e and FOXL2 3′-UTR mRNA. miR/miRNA, microRNA; 3′-UTR; 3′-untranslated region.

Mentions: To explore whether the expression of FOXL2 is regulated by miRNAs, Ago2, a key component of the RNA-induced silencing complex, was knocked down in COV434 cells. This knockdown demonstrated that inactivation of the miRNA system results in upregulation of FOXL2 expression (Fig. 1A), indicating that miRNAs are involved in the negative control of FOXL2 expression.


MiR-30a upregulates BCL2A1, IER3 and cyclin D2 expression by targeting FOXL2.

Wang T, Li F, Tang S - Oncol Lett (2014)

FOXL2 expression was significantly repressed by miRNAs in COV434 cells. (A) FOXL2 expression was upregulated when AGO2 was knocked down; therefore, FOXL2 expression was repressed by endogenous microRNAs. (B) Reverse transcription-quantitative polymerase chain reaction of miR-30a/b/c/d/e expression in COV434 cells revealed that miR-30a is relatively abundant compared with other miR-30 family members. (C) The predicted interactions between miR-30a/b/c/d/e and FOXL2 3′-UTR mRNA. miR/miRNA, microRNA; 3′-UTR; 3′-untranslated region.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4301489&req=5

f1-ol-09-02-0967: FOXL2 expression was significantly repressed by miRNAs in COV434 cells. (A) FOXL2 expression was upregulated when AGO2 was knocked down; therefore, FOXL2 expression was repressed by endogenous microRNAs. (B) Reverse transcription-quantitative polymerase chain reaction of miR-30a/b/c/d/e expression in COV434 cells revealed that miR-30a is relatively abundant compared with other miR-30 family members. (C) The predicted interactions between miR-30a/b/c/d/e and FOXL2 3′-UTR mRNA. miR/miRNA, microRNA; 3′-UTR; 3′-untranslated region.
Mentions: To explore whether the expression of FOXL2 is regulated by miRNAs, Ago2, a key component of the RNA-induced silencing complex, was knocked down in COV434 cells. This knockdown demonstrated that inactivation of the miRNA system results in upregulation of FOXL2 expression (Fig. 1A), indicating that miRNAs are involved in the negative control of FOXL2 expression.

Bottom Line: FOXL2 is a transcription factor that is essential for ovarian development.In the present study, the expression of FOXL2 was suppressed by microRNAs using the Ago2 knockdown method in COV434 cells.Furthermore, miR-30a overexpression upregulates BCL2A1, IER3 and cyclin D2 expression by inhibiting FOXL2. miR-30a is known to function as a tumor suppressor in breast cancer, small cell lung cancer and colorectal carcinoma; however, the present study revealed an opposing function of miR-30a as an oncogene.

View Article: PubMed Central - PubMed

Affiliation: Institute of Plastic Surgery, Weifang Medical College, Weifang, Shandong 261041, P.R. China.

ABSTRACT

FOXL2 is a transcription factor that is essential for ovarian development. Somatic mutations of FOXL2 are associated with ovarian granulosa cell tumorigenesis. In the present study, the expression of FOXL2 was suppressed by microRNAs using the Ago2 knockdown method in COV434 cells. Online bioinformatics tools were utilized to predict that FOXL2 expression may be repressed by miR-30 family members, and dual luciferase assay and western blotting were performed to demonstrate that FOXL2 is a target gene of miR-30a, which is relatively abundant in COV434 cells. Furthermore, miR-30a overexpression upregulates BCL2A1, IER3 and cyclin D2 expression by inhibiting FOXL2. miR-30a is known to function as a tumor suppressor in breast cancer, small cell lung cancer and colorectal carcinoma; however, the present study revealed an opposing function of miR-30a as an oncogene.

No MeSH data available.


Related in: MedlinePlus