LncRNA GAS6-AS2 promotes non-small-cell lung cancer cell proliferation via regulating miR-144-3p/ MAPK6 axis

ABSTRACT

The function of a new long non-coding RNA GAS6-AS2 in non-small cell lung cancer (NSCLC) is not fully understood. In this study, GAS6-AS2 was identified, and its roles as well as mechanisms in regulating proliferation of NSCLCs cells were investigated. qRT-PCR was used to analyze GAS6-AS2, miR-144-3p, and MAPK6 expression. Protein expression was detected by Western blotting. Cell Counting Kit-8 (CCK8) assay was used to examine the cell proliferation ability. The interaction between GAS6-AS2 and miR-144-3p was confirmed by dual-luciferase reporter assay and RNA pull down assay. A xenograft model was constructed to monitor the mice NSCLC tumor growth in vivo. GAS6-AS2 was up-regulated, while miR-144-3p was suppressed in NSCLC cells compared with normal lung cells. GAS6-AS2 suppression could inhibit the progression of NSCLC cells, and miR-144-3p could attenuate the effect. GAS6-AS2 could function as a competitive endogenous RNA (ceRNA) via direct sponging miR-144-3p-3p, which further regulating the expression of MAPK6. The knockdown of GAS6-AS2 could greatly suppress the tumor growth of NSCLC in vivo. GAS6-AS2 up-regulated MAPK6 by sponging miR-144-3p in NSCLC tissues and cells. Thus, GAS6-AS2 is an effective therapeutic target in NSCLC.

KEYWORDS:

• GAS6-AS2
• miR-144-3p
• MAPK6
• NSCLC
• proliferation

Availability of data and materials

The analyzed data sets generated during the study are available from the corresponding author on reasonable request.

Ethics approval and consent to participate

The present study was approved by the Ethics Committee of Henan Provincial People’s Hospital. The research has been carried out in accordance with the World Medical Association Declaration of Helsinki. All patients and healthy volunteers provided written informed consent prior to their inclusion within the study.

Disclosure statement

The authors declare that they have no competing interests.