Z-R Gu1, W Liu. 1. Department of Obstetrics and Gynecology, the 5th People's Hospital of Ji'nan, Ji'nan, Shandong Province, P.R. China. qianqianliu8009@163.com.
Abstract
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.
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 ECpatients, 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.