Gastric cancer is one of the most common types of malignant tumor of the gastrointestinal tract worldwide. Cisplatin (DDP) is a commonly used chemotherapeutic drug in the clinic; however, the resistance of gastric cancer cells to DDP limits its efficacy. In the present study, drug-resistant gastric cancer cell lines were constructed using the stepwise continuous selection method, and the relative expression levels of long non-coding RNA (lncRNA) CDKN2B antisense RNA 1 (ANRIL) and microRNA (miR)-181a-5p were detected using reverse transcription-quantitative PCR. The knockdown of lncRNA ANRIL and miR-181a-5p expression was performed by transfection with shRNA-ANRIL and an miR-181a-5p inhibitor, respectively. Cellular proliferation and sensitivity to DDP were assessed using Cell Counting Kit-8 analysis. Cell apoptosis and cell cycle distribution were assessed using flow cytometry and western blotting. The binding relationships between ANRIL, miR-181a-5p and cyclin G1 (CCNG1) were verified using a dual luciferase reporter assay. The results revealed that the expression levels of miR-181a-5p were downregulated in all drug-resistant cell lines. ANRIL-knockdown inhibited cellular proliferation, and promoted apoptosis and cell cycle arrest; however, following the knockdown of miR-181a-5p, the inhibition of cell cycle arrest was alleviated. Notably, miR-181a-5p, ANRIL and CCNG1 were found to have targeting relationships. In conclusion, the findings of the present study suggested that knocking down the expression of ANRIL inhibited cellular proliferation, and promoted apoptosis and cell cycle arrest. Furthermore, its downstream target, miR-181a-5p, inhibited the proliferation of drug-resistant cells and enhanced their sensitivity to DDP.

Non-small cell lung cancer (NSCLC) accounts for approximately 80% of all lung cancers. Identifying key molecular targets related to the initiation, development, and metastasis of lung cancer is important for its diagnosis and target therapy. The ADAMTS families of multidomain extracellular protease enzymes have been reported to be involved in many physiological processes. In this study, we found that ADAMTS1 was highly expressed in NSCLC tissues, which promoted cell proliferation, migration, invasion, and epithelial to mesenchymal transition (EMT) of NSCLC cells. In the NSCLC tumor metastasis model involving nude mice, overexpression of ADAMTS1 promoted EMT and lung metastasis of tumor cells. Moreover, ADAMTS1 positively regulated TGF-β expression, and TGF-β was highly expressed in NSCLC tumor tissues. si-TGF-β or inhibition of TGF-β expression through the short peptide KTFR on ADAMTS1 protein could reverse the oncogenic effects of ADAMTS1 on lung cancer cells. Taken together, ADAMTS1 functioned as an oncogene in NSCLC cells by promoting TGF-β expression, indicating that ADAMTS1 has important regulatory roles in the progression of NSCLC.