RETRACTED ARTICLE: Long noncoding RNA LINC00968 inhibits proliferation, migration and invasion of lung adenocarcinoma through targeting miR-22-5p/CDC14A axis

Abstract

BackgroundLung adenocarcinoma (LUAD) is a high aggressive human cancer which usually diagnosed at advanced stages. Accumulating evidences indicate that long noncoding RNAs (lncRNAs) are crucial participants in LUAD progression. MethodsThe mRNA levels of LINC00968, miR-22-5p and cell division cycle 14A (CDC14A) were measured using quantitative real-time PCR. Cell proliferation was evaluated using cell counting kit-8 and ow cytometry. Cell migration and cell invasion were assessed by wound healing and transwell assay, respectively. The interactions between LINC00968 and miR-22-5p were validated by RNA immunoprecipitation, RNA pull down and luciferase reporter assay. ResultsWe found that lncRNA LINC00968 was signi cantly down-regulated in LUAD tissues and cell lines.LINC00968 level was positively correlated to survival rate, and negatively correlated to tumor node metastasis stage, tumor size and lymph node metastasis of LUAD patients. LINC00968 over-expression in LUAD cells inhibited cell proliferation and induced cell cycle arrest at G1 phase. LINC00968 overexpression also suppressed migration, invasion and epithelial mesenchymal transition (EMT) as evidenced by elevated E-cadherin, decreased N-cadherin, TWIST and SNAIL levels. We further validated that LINC00968 localized in cytoplasma and acted as an upstream of microRNA miR-22-5p, which was up-regulated in LUAD tissues and cell lines. Besides, elevated miR-22-5p expression abolished the effect of LINC00968 over-expression on LUAD progression including in vivo tumor growth. In addition, we rst validated that cell division cycle 14A (CDC14A), which was down-regulated in LUAD tissues, was a downstream target of miR-22-5p. We over-expressed CDC14A in LUAD cells and miR-22-5p induced LUAD progression was partially reversed. Conclusionour study demonstrated that LINC00968 inhibited proliferation, migration and invasion of LUAD by sponging miR-22-5p and further restoring CDC14A. This novel regulatory network might provide us with promising diagnostic and therapeutic target in LUAD treatment.

Reverse predictive analysis of Rhizoma Pinelliae and Rhizoma Coptidis on differential miRNA target genes in lung adenocarcinoma

“…The unbalanced expression of miRNAs is a key factor to promote the rapid occurrence and development of tumors, and the expression profiles of miRNAs are generally characterized in tumor tissues, and the expression profiles of these tumor cells are significantly different from the normal cell expression profiles in the same tissue, so the expression of miRNAs is more accurate to distinguish the type of tumor than the mRNA encoded by proteins. [26] The difference between Rhizoma Pinelliae and Rhizoma Coptidis in the treatment of LUAD in this study found a total of 25 miRNAs, and through searching domestic and foreign literature, it was found that these miRNAs were all related to cancer, of which 10 (miR-126-5P, [27] miR-22-5P, [28] miR-183-5P, [29] miR-144-3P, [30] miR-340-5P, [31] miR-142-5P, [3] miR-200A-3P, [32] miR-429, [33] miR-200B-3P, [34] miR-3648 [35] ) are directly associated with LUAD. At the same time, the pathway with the highest significance of “Rhizoma Pinelliae-Rhizoma Coptidis” herb pair in the treatment of LUAD found in this study is the non-small cell lung cancer pathway, and the key target with the highest degree of freedom value is EGFR.…”

Characterization and validation of a ferroptosis-related LncRNA signature as a novel prognostic model for lung adenocarcinoma in tumor microenvironment

“…In addition, another study revealed that IFNG-AS1 could enhance the secretion of IFN-γ in human natural killer cells ( 42 ). A previous study also showed that the down-regulated expression of lncRNA LINC00968 in LUAD was associated with the proliferation, migration and invasion ( 43 ). Emerging evidence has suggested that LANCL1-AS1 plays a key role in regulating NSCLC ( 44 , 45 ).…”

FABP7 inhibits proliferation and invasion abilities of cutaneous squamous cell carcinoma cells via the Notch signaling pathway

“…PCNA, Snail, N-cadherin, Twist, MMP-2 and MMP-7 are crucial proteins associated with cell proliferation and invasion ( 22 ). Following transfection, these proteins were detected by western blotting.…”