LINC01783 facilitates cell proliferation, migration and invasion in non-small cell lung cancer by targeting miR-432-5p to activate the notch pathway

Abstract

Background Non-small cell lung cancer (NSCLC) is a common malignancy around the globe. Increasing long non-coding RNAs (lncRNAs) have been confirmed to be associated with the progression of cancers, including NSCLC. Long intergenic non-protein coding RNA 1783 (LINC01783) is a novel lncRNA and its regulatory function as competing endogenous RNA (ceRNA) has not been studied in NSCLC. Methods RT-qPCR measured the expression level of LINC01783 in NSCLC cells. CCK-8, EdU, transwell and wound healing assays were conducted to detect cell proliferation, migration and invasion in NSCLC. The relationship between miR-432-5p and LINC01783 along with delta like 1 (DLL-1) was illustrated by RNA pull down, RIP and luciferase reporter assays. Results LINC01783 was found remarkably increased in NSCLC cell lines, and down-regulation of LINC01783 suppressed cell proliferation, migration and invasion. Then, we discovered Notch pathway was related to the progression of NSCLC, and DLL-1 expression was reduced by LINC01783 knockdown. Furthermore, DLL-1 overexpression could counteract the suppressive effects of LINC01783 down-regulation on the growth of NSCLC cells. MiR-432-5p was observed to be the mutual miRNA that could bind with both LINC01783 and DLL-1. Overexpression of miR-432-5p inhibited DLL-1 expression. In the rescue assays, miR-432-5p depletion offset the impacts of LINC01783 knockdown, and then DLL-1 silence recovered the influence of miR-432-5p down-regulation on NSCLC cell growth. Conclusion LINC01783 aggravates NSCLC cell growth by regulating Notch pathway and sponging miR-432-5p, being a potential target in the treatment for NSCLC.

Circ-TRIO promotes TNBC progression by regulating the miR-432-5p/CCDC58 axis

“…It is acknowledged that the controlled expression of miRNAs is indispensable for normal cells, while the aberrant expression of miRNAs may lead to diseases, including cancers [52,53]. As reported, miR-432-5p could be regarded as a tumor inhibitor in human cancers; for example, DRAIC could promote the growth of breast cancer by sponging miR-432-5p to upregulate SLBP [54], circ-ZNF609 could target miR-432-5p to regulate the expression of LRRC1 to promote cholangiocarcinoma [55], and LINC01783 could facilitate cell proliferation, migration and invasion in non-small cell lung cancer by targeting miR-432-5p [56]. However, the underlying function of miR-432-5p in TNBC has not been reported.…”

Characterization of the microRNA Expression Profiles in the Goat Kid Liver

“…We predicted that miR-15a-5p may silence gene expression, inhibit the apoptosis pathway, and play an important role in promoting cell proliferation. It is reported that LINC01783 may increase in NSCLC cell lines, and down-regulation of LINC01783 suppressed cell proliferation, migration, and invasion by regulating Notch pathway and sponging miR-432-5p ( Deng et al, 2021 ). Guo et al found that Notch2 may negatively regulate cell invasion by inhibiting the PI3K-Akt signaling pathway in gastric cancer ( Guo et al, 2012 ).…”

Epigenetic regulation of stem cells in lung cancer oncogenesis and therapy resistance

“…In the second pathway, SNHG11 directly binds to β -catenin and activates the WNT pathway ( Liu et al, 2020 ). A novel long intergenic non-protein coding RNA (LINC01783) that suppresses miR-432-5p, a route that results in non-small cell carcinogenesis, activates the NOTCH pathway to increase DLL-1 expression and enhances the proliferation of NSCLC cells ( Deng et al, 2021 ) ( Table 1 ).…”