ZFPM2-AS1 promotes the proliferation, migration, and invasion of human non-small cell lung cancer cells involving the JAK-STAT and AKT pathways

• Published in: PeerJ (San Francisco, CA) Vol. 8; p. e10225
• Main Authors: Wang, Xiwen, Tang, Jun, Zhao, Jungang, Lou, Bin, Li, Li
• Format: Journal Article
• Language: English
• Published: United States PeerJ. Ltd 26-10-2020; PeerJ Inc
• Subjects: Analysis; Antisense RNA; Biochemistry; Biological response modifiers; Cell Biology; DNA binding proteins; Immune infiltration; LncRNA; Molecular Biology; Non-small cell lung cancer; NSCLC; Oncology; PD-L1; Respiratory Medicine; ZFPM2-AS1; LncRNA; PD-L1; ZFPM2-AS1; NSCLC; Immune infiltration
• ISSN: 2167-8359; 2167-8359
• DOI: 10.7717/peerj.10225

Recent studies have determined that long non-coding RNAs (lncRNAs) are potential prognostic biomarkers for non-small cell lung cancers (NSCLCs). The purpose of this study was to analyze the function and associated pathways of zinc finger protein multitype 2 antisense RNA 1 (ZFPM2-AS1) in NSCLC cells.
We used qRT-PCR to analyze ZFPM2-AS1's transcription level. Its proliferation, migration, and invasion capacities were determined using MTT, colony forming, wound healing, and transwell assays. We additionally analyzed the correlation between ZFPM2 and immune infiltration using the Tumor Immune Estimation Resource (TIMER) database, and the protein expression levels using Western blots.
We found that ZFPM2-AS1 expression in NSCLC specimens and cell lines was elevated compared to the control group. ZFPM2-AS1 is an oncogene and independent prognostic predictor of poor survival in NSCLCs, and its expression had a positive correlation with tumor size and lymph node metastasis in our clinical data. MTT, colony forming, wound healing, and transwell assays showed a positive correlation between ZFPM2-AS1 expression and the proliferation, migration, and invasion of NSCLC cells in the presence and absence of interferon- (IFN-
). Using the TIMER database, we hypothesized that ZFPM2 was negatively correlated with ZFPM2-AS1 expression, as well as the immune infiltration levels in lung adenocarcinoma (LUAD). Finally, we found that ZFPM2-AS1 negatively regulated ZFPM2 expression, and had a positive correlation with PD-L1 expression through the JAK-STAT and AKT pathways.
Our study confirmed that ZFPM2-AS1 promotes the proliferation, migration, and invasion of NSCLC cells via the JAK-STAT and AKT pathways. Further research on the ZFPM2-AS1 pathway regulation mechanism is needed.