Guosen Li1, Xiangyun Guo2. 1. Queen Mary School of Medical College, Jiangxi Medical College, Qianhu Campus, Nanchang University, No. 1299 Xuefu Street, Nanchang, Jiangxi, China. Electronic address: L1315020551@163.com. 2. Department of Internal Medicine, Jining Infectious Disease Hospital, Jiu Mi Gu Dui, Rencheng District, Jining, Shandong, China.
Abstract
BACKGROUND: This research aims to illustrate the effect of lncRNA StAR Related Lipid Transfer Domain Containing 13 antisense RN (STARD13-AS)/miR-1248/C3A on lung squamous carcinoma cells growth and metastasis. METHODS: Bioinformatics analysis was applied to detect the expression of STARD13-AS/miR-1248/C3A in lung cancer samples and establish the ceRNA network. Transfection was performed to construct over-expression or knockdown models. PCR was implemented to examine the transfection efficiency. The biological function including growth, invasion and migration of LUSC cells were estimated by CCK-8 analysis, colony formation assay and transwell assay. Luciferase assay was executed to analyze the relationship between C3A and miR-1248, as well as miR-1248 and STARD13-AS. RESULTS: By consulting the TCGA database and GEPIA website, we found that C3A expression was significantly reduced in LUSC samples. Additionally, we also discovered that miR-1248, which was a downstream target of STARD13-AS, was presented as an upstream regulator of C3A. Moreover, STARD13-AS was under expressed in LUSC cells and has a negative effect on LUSC cells growth ability. C3A expression was co-regulated by miR-1248 and STARD13-AS. Importantly, the inhibitory effect of C3A or the promoting effect of miR-1248 on LUSC cells growth, invasion and migration abilities can be regulated by STARD13-AS. CONCLUSIONS: Our findings revealed that overexpression of STARD13-AS restricted the growth and aggressiveness of LUSC cells via regulating miR-1248/C3A.
BACKGROUND: This research aims to illustrate the effect of lncRNA StAR Related Lipid Transfer Domain Containing 13 antisense RN (STARD13-AS)/miR-1248/C3A on lung squamous carcinoma cells growth and metastasis. METHODS: Bioinformatics analysis was applied to detect the expression of STARD13-AS/miR-1248/C3A in lung cancer samples and establish the ceRNA network. Transfection was performed to construct over-expression or knockdown models. PCR was implemented to examine the transfection efficiency. The biological function including growth, invasion and migration of LUSC cells were estimated by CCK-8 analysis, colony formation assay and transwell assay. Luciferase assay was executed to analyze the relationship between C3A and miR-1248, as well as miR-1248 and STARD13-AS. RESULTS: By consulting the TCGA database and GEPIA website, we found that C3A expression was significantly reduced in LUSC samples. Additionally, we also discovered that miR-1248, which was a downstream target of STARD13-AS, was presented as an upstream regulator of C3A. Moreover, STARD13-AS was under expressed in LUSC cells and has a negative effect on LUSC cells growth ability. C3A expression was co-regulated by miR-1248 and STARD13-AS. Importantly, the inhibitory effect of C3A or the promoting effect of miR-1248 on LUSC cells growth, invasion and migration abilities can be regulated by STARD13-AS. CONCLUSIONS: Our findings revealed that overexpression of STARD13-AS restricted the growth and aggressiveness of LUSC cells via regulating miR-1248/C3A.
Authors: Giuseppina Catanzaro; Zein Mersini Besharat; Andrea Carai; Natalie Jäger; Elena Splendiani; Carole Colin; Agnese Po; Martina Chiacchiarini; Anna Citarella; Francesca Gianno; Antonella Cacchione; Evelina Miele; Francesca Diomedi Camassei; Marco Gessi; Luca Massimi; Franco Locatelli; David T W Jones; Dominique Figarella-Branger; Stefan M Pfister; Angela Mastronuzzi; Felice Giangaspero; Elisabetta Ferretti Journal: Biomark Res Date: 2022-06-17