<p>LINC01094 Down-Regulates miR-330-3p and Enhances the Expression of MSI1 to Promote the Progression of Glioma</p>

Abstract

Background: This study aims at probing into the expression, function, and mechanism of LINC01094 and miR-330-3p in glioma. Materials and Methods: qRT-PCR was employed to examine LINC01094 and miR-330-3p expressions in gliomas. After gain-of-function and loss-of-function models were constructed, CCK-8 and Transwell assays were used to detect the proliferation, migration and invasion of LN229 and U251 cells, respectively. Additionally, dual luciferase reporter gene assay was utilized to verify the binding site between m4iR-330-3p and LINC01094, miR-330-3p, and the 3ʹUTR of musashi RNA binding protein 1 (MSI1). Then, RNA pull-down, RIP, qRT-PCR and Western blot were employed to detect the regulatory relationships among LINC01094, miR-330-3p, and MSI1. Results: The expression of LINC01094 was elevated in glioma tissues and cell lines, and the high expression of LINC01094 was associated with high grade of glioma. In contrast, miR-330-3p was lowly expressed in glioma tissue. Overexpression of LINC01094 or downregulation of miR-330-3p promoted the proliferation, migration, and invasion of glioma cells, while LINC01094 knockdown or miR-330-3p up-regulation impeded these processes. miR-330-3p was identified as a target miRNA of LINC01094, and it could be negatively regulated by LINC01094. In addition, miR-330-3p antagonized the function of LINC01094 by negatively regulating MSI1. Conclusion: LINC01094 promotes the proliferation, migration, and invasion of glioma cells by adsorbing miR-330-3p and up-regulating the expression of MSI1.

LINC01094 promotes the invasion of ovarian cancer cells and regulates the Wnt/β‑catenin signaling pathway by targeting miR‑532‑3p

“…Moreover, inhibiting LINC01094 attenuated proliferation, migration and invasion of ccRCC cells (17). LINC01094 overexpression promoted the proliferation and motility of glioma cells (45). Consistent with these findings, in the present study, functional assays of LINC01094 were performed in OC cells, revealing that silencing LINC01094 inhibited OC cell viability, migration, invasion and G2/M cycle progression, and promoted OC cell apoptosis.…”

Identification of an Immune-Related LncRNA Signature in Gastric Cancer to Predict Survival and Response to Immune Checkpoint Inhibitors

“…MIR3142HG is a critical regulator of the inflammatory response, and the attenuated expression of MIR3142HG/miR-146a contributes to the reduced inflammatory response in IPF fibroblast ( Hadjicharalambous et al, 2018 ). As for LINC01094, several studies reported that it is a pro-tumorigenic lncRNA, and microRNA-184 ( Xu H. et al, 2020 ), miR-126-5p ( Li and Yu, 2020 ), miR-577 ( Xu J. et al, 2020 ), miR-330-3p ( Zhu et al, 2020 ), and miR-224-5p ( Jiang et al, 2020 ) were identified as its targets. The role of ABALON, AC004009-2, and LINC01711 has not been explored by biological assays, providing directions and clues for future research.…”

A Novel Prognostic Model for Clear Cell Renal Cell Carcinoma with Differentially Expressed Immune-related lncRNA Pairs Based on the Cancer Genome Atlas

“…LINC01094 can promote the development of ccRCC by upregulating SLC2A3 via miR-184 or via miR-224-5p/CHSY1 and triggers radio-resistance in ccRCC via miR-577/CHEK2/FOXM1 axis [28][29][30]. Acting as a ceRNA as well, LINC01094 promotes progression of ovarian cancer and glioma [31][32][33][34].…”