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MiR-142-3p May Be Involved in the Development of Solitary and Multiple Uterine Leiomyomasby Interacting with CTNNB1 and AXIN-2 Through Wnt Signaling Pathway

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Abstract Background The pathogenesis and clinical behaviors between solitary uterine leiomyoma (SUL) and multiple uterine leiomyomas (MUL) vary, which lead to the difference in management for childbearing-aged patients. Herein, we aim to find the potential miRNAs involved in the development of SUL and MUL. Results The top 5 differentially expressed miRNAs, Wnt signalling pathway and its two central molecules APC and CTNNB1 were screened out according to microarray analysis and bioinformatics. MiR-142-3p was selected for further exploration. In validation of qRT-PCR, MiR-142-3p was significantly upregulated in SUL, while downregulated in MUL, CTNNB1 and sequencing target AXIN-2 were expressed at higher level in MUL than SUL. Overexpression of MiR-142-3p resulted in lower transcription level of CTNNB1 and AXIN-2, and lower cell proliferation level. Conclusions MiR-142-3p may be involved in the development of SUL and MUL by interacting with CTNNB1 and AXIN-2 through Wnt signaling pathway. MiR-142-3p could serve as a potential biomarker for individualized treatment between SUL and MUL in the future.
Title: MiR-142-3p May Be Involved in the Development of Solitary and Multiple Uterine Leiomyomasby Interacting with CTNNB1 and AXIN-2 Through Wnt Signaling Pathway
Description:
Abstract Background The pathogenesis and clinical behaviors between solitary uterine leiomyoma (SUL) and multiple uterine leiomyomas (MUL) vary, which lead to the difference in management for childbearing-aged patients.
Herein, we aim to find the potential miRNAs involved in the development of SUL and MUL.
Results The top 5 differentially expressed miRNAs, Wnt signalling pathway and its two central molecules APC and CTNNB1 were screened out according to microarray analysis and bioinformatics.
MiR-142-3p was selected for further exploration.
In validation of qRT-PCR, MiR-142-3p was significantly upregulated in SUL, while downregulated in MUL, CTNNB1 and sequencing target AXIN-2 were expressed at higher level in MUL than SUL.
Overexpression of MiR-142-3p resulted in lower transcription level of CTNNB1 and AXIN-2, and lower cell proliferation level.
Conclusions MiR-142-3p may be involved in the development of SUL and MUL by interacting with CTNNB1 and AXIN-2 through Wnt signaling pathway.
MiR-142-3p could serve as a potential biomarker for individualized treatment between SUL and MUL in the future.

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