Clinical significance, functional role and correlation with SEMA3B of long non-coding RNA SEMA3B-AS1 in gastric adenocarcinoma

Background Gastric adenocarcinoma (GA) is a prevalent malignant tumor with poor prognosis owing to late diagnosis and high metastatic potential. Long non-coding RNAs (lncRNAs) are key regulators in GA initiation and progression, representing promising diagnostic and therapeutic targets. This study aimed to investigate the clinical significance, in vitro biological functions of lncRNA SEMA3B-AS1 in GA, and its expression correlation with the tumor suppressor gene SEMA3B. Methods Based on our previous lncRNA expression microarray data, lncRNA SEMA3B-AS1, which was downregulated in GA, was selected for further investigation. Tissue samples were collected from 120 patients with GA who had undergone surgical treatment. The expression level of SEMA3B-AS1 in GA tissues was verified by quantitative reverse-transcription PCR (qRT-PCR); its clinical significance in GA was statistically analyzed. A SEMA3B-AS1 overexpression plasmid vector was constructed and transfected into the GA cell lines BGC-823 and SGC-7901; G418 screening was used to establish cells stably overexpressing SEMA3B-AS1. In vitro functional assays (cell proliferation, colony formation, migration, invasion and apoptosis) were performed to systematically evaluate the effects of SEMA3B-AS1 overexpression on GA cells. Additionally, the correlation between SEMA3B-AS1 and SEMA3B expression in GA tissues was analyzed by qRT-PCR. Results SEMA3B-AS1 expression in GA tissues was significantly downregulated by 7.141-fold ( P < 0.01) compared with that in corresponding paracancerous tissues, with a downregulation rate of 76.67% (92/120). Abnormal SEMA3B-AS1 expression was closely correlated with lymph node metastasis (unadjusted P = 0.004) in GA. SEMA3B-AS1 overexpression significantly inhibited GA cell proliferation, colony formation, migration and invasion ( P < 0.05), and promoted cell apoptosis ( P < 0.05). Moreover, SEMA3B-AS1 expression in GA tissues was positively correlated with SEMA3B expression ( r = 0.483, P < 0.01), a known tumor suppressor gene. Conclusion SEMA3B-AS1 is downregulated in GA tissues and exhibits tumor-suppressive properties by regulating multiple biological behaviors of GA cells (proliferation, colony formation, migration, invasion and apoptosis). Its expression is significantly positively correlated with that of tumor suppressor SEMA3B. Collectively, SEMA3B-AS1 may participate in the progression of GA and serve as a potential molecular marker for GA.