Long non-coding RNA CACNA1G-AS1 promotes cell migration, invasion and epithelial-mesenchymal transition by HNRNPA2B1 in non-small cell lung cancer.

Abstract

In recent years, long non-coding RNAs (lncRNAs) have been identified to participate in tumor progression. The purpose of this study was to investigate the role of CACNA1G-AS1 in non-small cell lung cancer (NSCLC). Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was used to detect the CACNA1G-AS1 expression level in 122 pairs of NSCLC and para-carcinoma normal tissue samples as well as in NSCLC cell lines. Moreover, the relationship of clinical pathological features with CACNA1G-AS1 was analyzed. Functional experiment cell lines were established using lentivirus and siRNA to study the effects of CACNA1G-AS1 on cell invasion and migration abilities. Several epithelial-mesenchymal transition (EMT) markers were measured using Western blotting. The expression level of HNRNPA2B1 was analyzed to further investigate the mechanism. The expression level of CACNA1G-AS1 in NSCLC tissues was significantly higher than that in para-carcinoma normal tissues, and the expression of CACNA1G-AS1 was higher in NSCLC cell lines than that in normal BEAS-2B cells. The higher CACNA1G-AS1 level was relative to more lymph node metastasis and distant metastasis. Function experiments revealed that CACNA1G-AS1 promoted cell invasion and migration. Also, CACNA1G-AS1 over-expression increased EMT in NSCLC cells. Besides, HNRNPA2B1 was regulated by CACNA1G-AS1 in NSCLC cells. CACNA1G-AS1 was identified as an oncogene in NSCLC for the first time, and could promote cell invasion, migration and EMT via increasing HNRNPA2B1 expression, providing a novel target for the biological therapy and prevention.