Dataset Information

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

ABSTRACT: Long non-coding RNA (LncRNA) emerges as a regulator in various diseases, including endometriosis (EM). This study aims to uncover the role of long non-coding RNA BRAF-activated non-protein coding RNA (lncRNA BANCR)-mediated competing endogenous RNA mechanism in endometrial stromal cell (ESC) proliferation and invasion in EM by regulating miR-15a-5p/TRIM59. ESCs were isolated from eutopic and ectopic endometrial tissues, followed by the determination of Cytokeratin 19 and Vimentin expressions in cells. Then, expressions of lncRNA BANCR, microRNA (miR)-15a-5p, and tripartite motif-containing 59 (TRIM59) in tissues and cells were determined by real-time quantitative polymerase chain reaction or Western blot assay, and cell proliferation and invasion were evaluated by cell counting kit-8 and transwell assays. After that, the subcellular localization of lncRNA BANCR and binding of miR-15a-5p to lncRNA BANCR or TRIM59 were analyzed. LncRNA BANCR was upregulated in ectopic endometrial tissues and ectopic ESCs (Ect-ESCs). Silencing lncRNA BANCR suppressed Ect-ESC proliferation and invasion. LncRNA BANCR inhibited miR-15a-5p to promote TRIM59 expression. miR-15a-5p downregulation or TRIM59 overexpression both reversed the effects of silencing lncRNA BANCR on Ect-ESC proliferation and invasion. In summary, our findings suggested that lncRNA BANCR facilitated Ect-ESC proliferation and invasion by inhibiting miR-15a-5p and promoting TRIM59.

SUBMITTER: Liu L

PROVIDER: S-EPMC9576446 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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

Liu Lixue L Bai Ru R Li Debang D Dai Bai B Tuo Ya Y Tuo Ya Y

International journal of genomics 20221010

Long non-coding RNA (LncRNA) emerges as a regulator in various diseases, including endometriosis (EM). This study aims to uncover the role of long non-coding RNA BRAF-activated non-protein coding RNA (lncRNA BANCR)-mediated competing endogenous RNA mechanism in endometrial stromal cell (ESC) proliferation and invasion in EM by regulating miR-15a-5p/TRIM59. ESCs were isolated from eutopic and ectopic endometrial tissues, followed by the determination of Cytokeratin 19 and Vim ...[more]

PMID: 36262826

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Project description:BackgroundStudies have considered long non-coding RNA 5 prime to Xist (lncRNA FTX) a key lncRNA for normal uterine development, but it has not been reported whether lncRNA FTX is involved in regulating the development of endometriosis (EMs). The aim of the present study was to explore the effect and mechanism of long non-coding RNA 5 prime to Xist (lncRNA FTX) on the invasion, metastasis, and epithelial-mesenchymal transition (EMT) of endometrial stromal cells (ESCs) caused by EMs.MethodsEctopic or normal endometrial tissues were collected from 38 patients with EMs, who were diagnosed and operated on at Beijing Tongren Hospital from June 2018 to December 2019, and 20 healthy volunteers with normal endometria. The expression of lncRNA FTX in both groups was detected by quantitative reverse transcription polymerase chain reaction. Ectopic endometrial stromal cells (EESC) and ESC from patients with EMs and healthy volunteers were separated and cultured, and the expression of lncRNA FTX in the cells was detected. The expression of lncRNA FTX in EESC was overexpressed or interfered. Proliferation, invasion, and migration was detected by Cell Counting Kit-8, transwell assay, and scratch assay. Apoptosis and cell cycle were detected by flow cytometry. EMT-related protein and PI3K/Akt signaling pathway-related protein expressions were detected by Western blot.ResultsLncRNA FTX was underexpressed in endometrial tissues and EESC from patients with EMs. The overexpression of lncRNA FTX could significantly inhibit the proliferation, invasion, and migration of EESC, but promoted apoptosis and cell cycle arrest in the G0/G1 phase. The overexpression of lncRNA FTX significantly increased the expression of EMT-related protein, E-cadherin, and decreased the protein expression of vimentin, N-cadherin, and zinc finger E-box binding homeobox 1. In addition, the overexpression of lncRNA FTX could decrease the expression of p-PI3K/PI3K and p-Akt/Akt. Interfering with the expression of lncRNA FTX had the opposite result.ConclusionsThe overexpression of lncRNA FTX could decrease the invasion, metastasis, and EMT of ESC caused by EMs by inhibiting the activity of the PI3K/Akt signaling pathway.

Dataset Information

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

Publications

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

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