Long non‐coding RNA CASC19 facilitates non‐small cell lung cancer cell proliferation and metastasis by targeting the miR‐301b‐3p/LDLR axis

Abstract

Background: Non-small cell lung cancer (NSCLC) is a lethal tumor resulting in a large number of cancer-related deaths globally. Long noncoding RNAs (lncRNAs) may modulate tumor initiation and metastasis. Although dysregulation of lncRNA cancer susceptibility 19 (CASC19) is validated in NSCLC, further exploration of the CASC19-regulated mechanism in NSCLC is still needed. Methods: CASC19 expression was examined in NSCLC cells by a quantitative reverse transcriptase-polymerase chain reaction. The specific role of CASC19 in NSCLC was analyzed by cell counting kit-8, EdU, Transwell and western blot assays. The interaction between miR-301b-3p and CASC19 or low-density lipoprotein receptor (LDLR) was confirmed by luciferase reporter and RNA immunoprecipitation assays. Results: CASC19 is markedly overexpressed in NSCLC. Its deficiency impairs cell proliferation, as well as metastasis in NSCLC. Molecular mechanism experiments indicated that CASC19 negatively modulates the expression of miR-301b-3p and miR-301b-3p can bind with CASC19 in NSCLC. In addition, miR-301b-3p binds to LDLR to impair its expression in NSCLC. Finally, rescue experiments showed that miR-301b-3p inhibition or LDLR overexpression counteracted the CASC19 knockdown-mediated function on cell proliferation and metastasis in NSCLC. Conclusions: CASC19 facilitates NSCLC cell proliferation and metastasis by targeting the miR-301b-3p/LDLR axis, offering a possible strategy for lncRNA-targeted treatment in NSCLC.

A Radioresponse-Related lncRNA Biomarker Signature for Risk Classification and Prognosis Prediction in Non-Small-Cell Lung Cancer

“…In addition, CASC19 also has an oncogenic effect on NSCLC. Wang et al found that CASC19 could bind with miR-301b-3p to regulate the expression of low-density lipoprotein receptor (LDLR), which promotes NSCLC cell proliferation and metastasis [ 47 ]. The LINC01977 is a novel carcinogenic promoter reported in breast cancer (BC).…”

LncRNA CASC19 accelerates chondrocytes apoptosis and proinflammatory cytokine production to exacerbate osteoarthritis development through regulating the miR-152-3p/DDX6 axis

“…P < 0.05 was supposed as statistically significant. [14][15][16], but its role in OA keeps unknown. To probe whether CASC19 is altered in OA, RT-qPCR assay was conducted to test CASC19 expression in OA tissues, and the results indicated that CASC19 exhibited higher expression in OA samples (Fig.…”

“…With the fast development of science and technology, an increasing number of lncRNAs have been identified as crucial regulators in various diseases [27,28]. CASC19 has been uncovered to be implicated in various cancers [14][15][16], but its function in OA remains indistinct. In this work, CASC19 exhibited higher expression in OA tissues and cell model.…”

“…CASC19, one of the recently identified lncRNA, has been demonstrated to participate in various cancers. For example, lncRNA CASC19 absorbs miR-301b-3p to modulate LDLR and accelerates non-small cell lung cancer tumorigenesis [ 14 ]. LncRNA CASC19/miR-454-3p/RAB5A axis to facilitate glioma progression [ 15 ].…”

Identification of an Epithelial-Mesenchymal Transition-Related Long Non-coding RNA Prognostic Signature for Hepatocellular Carcinoma

“…A study revealed that LINC00942 acts as an oncogene that promotes cell proliferation and colony formation and inhibits cell apoptosis, subsequently elevating METTL14-mediated m6A methylation levels in breast cancer initiation and progression by LNC942-METTL14-CXCR4/CYP1B1 signaling axis [31]. The lncRNA CASC19 was widely reported and markedly upregulated in multiple tumor tissues and cells, higher CASC19 expression is associated with tumor progression and poorer prognoses, including colorectal cancer, advanced gastric cancer, non-small lung cancer cells, and pancreatic cancer [32][33][34][35]. Two other studies revealed that a high expression level of CASC19 was positively correlated with radio resistance in cervical cancer and nasopharyngeal carcinoma [36,37].…”