Dataset Information

LncRNA USP2-AS1 promotes colon cancer progression by modulating Hippo/YAP1 signaling.

ABSTRACT: Dysregulation of Hippo signaling by long non-coding RNA (lncRNA) contributes to colon adenocarcinoma (COAD) progression, while the underlying mechanisms remain elusive. Our study shows that lncRNA USP2-AS1 is a Yes-associated protein 1 (YAP1) binding lncRNA, and inactivates Hippo signaling in COAD cells. Moreover, our data indicated that USP2-AS1 lowered the phosph-YAP (S127), elevated the total level of YAP1, and triggered the expression of downstream target genes in COAD cells. The loss- and gain-of function assays demonstrated that USP2-AS1 promotes cellular proliferation and metastasis of COAD cells. Clinically, the USP2-AS1 levels were significantly elevated in COAD tissues and were positively correlated with tumor grade, size, and TNM stage. Collectively, these findings demonstrated that USP2-AS1 modulates and regulates Hippo signaling in COAD and could be a valuable therapeutic target.

SUBMITTER: Li D

PROVIDER: S-EPMC7540120 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

lncRNA USP2-AS1 promotes colon cancer progression by modulating Hippo/YAP1 signaling.

Li Dongying D Bao Jie J Yao Jiayuan J Li Jiansheng J

American journal of translational research 20200915 9

Dysregulation of Hippo signaling by long non-coding RNA (lncRNA) contributes to colon adenocarcinoma (COAD) progression, while the underlying mechanisms remain elusive. Our study shows that lncRNA USP2-AS1 is a Yes-associated protein 1 (YAP1) binding lncRNA, and inactivates Hippo signaling in COAD cells. Moreover, our data indicated that USP2-AS1 lowered the phosph-YAP (S127), elevated the total level of YAP1, and triggered the expression of downstream target genes in COAD cells. The loss- and g ...[more]

PMID: 33042447

Similar Datasets

Project description:IntroductionColon adenocarcinoma (COAD) is the third most common tumor of the digestive tract. Recent studies reported that lncRNA's abnormal expression might play a vital role in the occurrence and development of COAD.MethodsIn the present study, we investigated the expression of ILF3-AS1 in COAD cell lines, human normal colon epithelial cell line, patient tumor tissues and adjacent normal tissues by real-time quantitative PCR (RT-qPCR). Small interfering RNAs (siRNAs) were transfected into COAD cells to inhibit the expression of ILF3-AS1. The effects of ILF3-AS1 on cell proliferation, migration, invasion and apoptosis were measured by CCK-8 assay, transwell migration and invasion assay, and flow cytometry apoptosis assay, respectively. The direct binding of ILF3-AS1 and miR-619-5p/CAMK1D was validated by the luciferase reporter assay. The expression of CAMK1D and epithelial-mesenchymal transformation (EMT)-related proteins was detected by Western Blot analysis. Besides, in vivo experiments were conducted to demonstrate the oncogenic role of ILF3-AS1 in COAD.ResultsThe results showed that the expression of ILF3-AS1 was significantly higher in COAD tissue than in normal adjacent samples, and this conclusion was confirmed in the available public datasets. After ILF3-AS1 knockdown, the proliferation of COAD cell lines SW480 and HT29 was significantly inhibited. At the same time, the apoptosis was increased, and the invasion and migration abilities were decreased. After further exploring the mechanisms, we found that ILF3-AS1 serves as a competitive endogenous RNA of mir-619-5p. It can bind to mir-619-5p and reduce its expression, thus regulating the target gene CAMK1D. In addition, we found that high expression of ILF3-AS1 was significantly associated with tumor grade, tumor size, and distant metastasis in COAD samples. In vivo experiments confirmed that ILF3-AS1 promotes tumor growth in COAD models.ConclusionThe present study demonstrated that ILF3-AS1 plays an oncogenic role in COAD through regulating the miR-619-5p/CAMK1D axis, and inhibition of ILF3-AS1 may pave the way for COAD treatment.

Dataset Information

LncRNA USP2-AS1 promotes colon cancer progression by modulating Hippo/YAP1 signaling.

Publications

lncRNA USP2-AS1 promotes colon cancer progression by modulating Hippo/YAP1 signaling.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets