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The LncRNA AL161431.1 targets miR-1252-5p and facilitates cellular proliferation and migration via MAPK signaling in endometrial carcinoma.

OBJECTIVE
The aim of this study was to determine the expression profile and the underlying mechanism of the long intergenic non-protein coding RNA AL161431.1 in EC (endometrial carcinoma).


MATERIALS AND METHODS
In this study, the expression data for the lncRNA AL161431.1 in EC was downloaded from The Cancer Genome Atlas (TCGA) database and used to examine its expression profile. quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot analysis were used to detect gene and protein expression, respectively. A subcellular fractionation assay was used to determine the location of AL161431.1. Cell Counting Kit-8 (CCK-8) and colony formation assays were used to evaluate cellular proliferation. Cell migration and wound healing assays were used to detect the effects on cell migration. RNA pull-down and Luciferase reporter assays were used to confirm the interaction between AL161431.1 and miR-1252-5p.


RESULTS
High expression levels of AL161431.1 were observed in EC patients, tissues, and cells. Loss-of-function experiments validated the carcinogenic role of AL161431.1. Based on the determined cytoplasmic location of AL161431.1, we investigated the ceRNA network and its relation to AL161431.1, miR-1252-5p, and MAPK (mitogen-activated protein kinase) signaling in EC. The molecular mechanism of the interaction between AL161431.1 and miR-1252-5p, and its effects on the MAPK signaling pathway was validated using rescue experiments in Ishikawa cells.


CONCLUSIONS
Our novel results indicate that AL161431.1 targets and binds to miR-1252-5p, resulting in the de-repression of MAPK signaling in EC cells. This highlights the potential for AL161431.1 to be targeted as a potent therapeutic strategy in the treatment of EC.