Abstract
Increasing evidence confirms that long noncoding RNAs (lncRNAs) exert vital functions in multiple biological process among malignant cancers. In the current study, we uncovered that linc00968 was downregulated in lung adenocarcinoma (LUAD). Furthermore, the low level of linc00968 was correlated with worse prognosis in patients with LUAD. Upregulation of linc00968 restrained the growth and metastatic phenotypes of LUAD cell in vitro and in vivo. Using bioinformation methods and luciferase reporter assay, we identified that linc00968 acted as a competing endogenous RNA (ceRNA) via sponging miR-9-5p to modulate the level of Cytoplasmic Polyadenylation Element Binding Protein 3 (CPEB3) in LUAD. In addition, LUAD cell migration, colony formation and epithelial-mesenchymal transition (EMT) process were suppressed by linc00968 while these aggressive traits were reversed by miR-142-5p or CPEB3 silencing. Altogether, our work disclosed that linc00968 played a critical role in LUAD and linc00968/miR-9-5p/CPEB3 regulatory axis might be a potential treatment target in LUAD.
Highlights
Lung cancer is the major cause of cancer-associated death worldwide
Figure 2. linc00969 inhibits lung adenocarcinoma (LUAD) cell growth. (A) The levels of linc00968 in linc00968 overexpressing A549 and H1975 cell or linc00968 knockdown in HCC827 were detected with qRT-PCR assay, (B) CCK-8 assays showed that overexpression of linc00968 inhibited cell proliferation in A549 and H1975 cell, whereas knockdown of linc00968 increased cell proliferation in HCC827 cell. (C) Colony-forming assays showed that linc00968 reduced A549 and H1975 colony formation, whereas knockdown of linc00968 enhanced the colony formation of HCC827 cell. (D) Representative images and the percentage of migration in wound healing assay. (E) Representative images and the number of invading cells in Transwell invasion assay. (F) The expressions of E-cadherin and N-cadherin were detected using western blotting assay. **P
Among the targets of miR9-5p, we focused on Cytoplasmic Polyadenylation Element Binding Protein 3 (CPEB3), whose mRNA level was significantly decreased by miR-9-5p in LUAD cell
Summary
Lung cancer is the major cause of cancer-associated death worldwide. Nearly 80% of lung cancer diagnoses are non-small-cell lung cancer (NSCLC) and the major subtypes are lung squamous cell carcinoma (LSCC) and lung adenocarcinoma (LUAD) [1]. Accumulating reports have disclosed that lncRNAs are critical regulators that affect the tumorigenesis and progression of cancers through modulating multiple aspects of cancer cell behavior, such as cell growth, apoptosis, autophagy, and metastasis [5,6,7,8]. Linc00968 identified to be downregulated in breast carcinoma and is related to poor prognosis in patients [12]. LncRNA-ROR induces EMT and contributes to breast cancer tumorigenesis and metastasis [16]. We further demonstrated that low level of linc00968 was associated with the metastasis and poor survival of patients with LUAD. The loss-and gain function assays revealed that upregulation of linc00968 distinctly restrained the growth and aggressive traits of LUAD cell through sponging miR-9-5p to inhibit the EMT process of LUAD cell
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