Berberine inhibits the proliferation, invasion and migration of endometrial stromal cells by downregulating miR‑429

Abstract

Endometriosis (EM) is a common gynecological disease, and its pathological process is accompanied by the migration and proliferation of uterine cells. Berberine (BBR) has been shown to exhibit antitumor activity; however, the effects of BBR on EM have seldom been reported to date. The expression of microRNA (miR)-429 is upregulated in EM and miR-429 can be used as a target for drug regulation of cancer cells. Whether BBR plays a regulatory role in EM by targeting miR-429 has not been reported. Thus, the aim of the present study was to determine the effects of BBR on EM cells. The survival rate of immortalized human endometrial stromal cells (HESCs) was determined using a Cell Counting Kit-8 assay. A colony formation assay was used to detect the rate of cell proliferation. The expression levels of proliferation-related proteins, including proliferation marker protein Ki-67 (Ki-67) and proliferating cell nuclear antigen (PCNA), were detected by reverse transcription-quantitative PCR (RT-qPCR) and western blotting. Wound healing and Transwell assays were performed to detect cell migration and invasion, and western blotting was used to detect the expression of the migration-and invasion-related proteins, including matrix metalloproteinase (MMP)2, MMP4 and MMP9. The expression of miR-429 was detected by RT-qPCR following its overexpression via cell transfection. The results revealed that treatment with 80 µM BBR significantly inhibited cell proliferation and colony formation, and inhibited the expression of Ki-67 and PCNA proteins in HESCs. BBR inhibited cell invasion and migration, as well as the expression of MMP2, MMP4 and MMP9. In this process, it was found that the expression of miR-429 decreased following treatment of the cells with BBR, whereas the inhibitory effects of BBR on cell proliferation, invasion and migration were suppressed following the overexpression of miR-429. Overall, the findings of the present study indicated that BBR inhibited the proliferation, invasion and migration of HESCs by downregulating the expression of miR-429.

Current Advances in Coptidis Rhizoma for Gastrointestinal and Other Cancers

“…Given that botanical drugs are characterized by multiple components with multiple effects from a holistic point of view, modulation of the gut microbiota foresees a much larger role for the effects of C. Rhizoma on carcinogenesis. miRNA miRNAs are small non-coding RNA molecules of around 20 nucleotides in length (Ambros, 2004;Bartel, 2004;Gu and Zhou, 2021). miRNAs are capable of suppressing target gene expression via binding to its target mRNA, causing mRNA cleavage or translation inhibition (Wightman et al, 1993;O'carroll and Schaefer, 2013).…”

“…miRNAs are small non-coding RNA molecules of around 20 nucleotides in length ( Ambros, 2004 ; Bartel, 2004 ; Gu and Zhou, 2021 ). miRNAs are capable of suppressing target gene expression via binding to its target mRNA, causing mRNA cleavage or translation inhibition ( Wightman et al, 1993 ; O’carroll and Schaefer, 2013 ).…”

LncRNA BANCR Promotes Endometrial Stromal Cell Proliferation and Invasion in Endometriosis via the miR-15a-5p/TRIM59 Axis

“…To further evaluate the functionality of lncRNA BANCR in Ect-ESC proliferation and invasion, lncRNA BANCR was silenced in Ect-ESCs using si-BANCR, upon which the proliferation and invasion potentials of Ect-ESCs were declined. It might be correlated with the effects of lncRNA BANCR on promoting the expression levels of ESCs mobility-related proteins, such as matrix metalloproteinase 1 and 2 [42][43][44]. Therefore, it is plausible to suggest that silencing lncRNA BANCR suppresses Ect-ESC proliferation and invasion.…”

Research Progress of PCNA in Reproductive System Diseases

“…Berberine (BBR), which is a typical component of Coptis chinensis Franch, is a potential treatment for endometrial cancer (EC) that inhibits the growth and metastasis of EC cells through the miRNA/miR-101/cyclooxygenase-2/prostaglandin E2 signaling pathway [ 18 ]. Gu and Zhou [ 19 ] demonstrated that 80 μ M BBR significantly suppressed the proliferation and colony formation of human endometrial stromal cells by downregulating the expression of miR-429 and inhibiting the expression of the PCNA protein, which provided a theoretical basis for using BBR to treat EM. Furthermore, some data suggest that RNA crosstalk is a crucial factor in the development of EM.…”