Knockdown of the long non‑coding RNA CACNA1G‑AS1 enhances cytotoxicity and apoptosis of human diffuse large B cell lymphoma by regulating miR‑3160‑5p

Long non‑coding RNAs (lncRNAs) have been confirmed to be connected with tumor proliferation, apoptosis, metastasis and recurrence. Previous studies have indicated that lncRNA calcium voltage‑gated channel subunit α1 G (CACNA1G)‑antisense 1 (AS1) can function as a pro-oncogene in several types of cancer. However, the specific role and mechanism of CACNA1G‑AS1 have not been fully elucidated in human diffuse large B cell lymphoma (DLBCL). In the present study, CACNA1G‑AS1 expression was verified in DLBCL tissues and cells by reverse transcription‑quantitative PCR, and the relationship between CACNA1G‑AS1 and microRNA (miR)‑3160‑5p was confirmed using luciferase reporter assays. After CACNA1G‑AS1‑knockdown and miR‑3160‑5p‑overexpression, MTT, colony formation and flow cytometry assays were conducted to assess the changes in the cytotoxicity and apoptosis of OCI‑Ly10 and SUDHL‑4 cells. In addition, in vivo experiments were performed to determine the impact of CACNA1G‑AS1‑knockdown on tumor growth and apoptosis. It was revealed that CACNA1G‑AS1 was highly expressed in DLBCL tissues and cells and that expression of CACNA1G‑AS1 was associated with the clinical stage of DLBCL. Functionally, CACNA1G‑AS1‑knockdown was demonstrated to increase cytotoxicity and expedite apoptosis in DLBCL cells in vitro and in vivo. In addition, CACNA1G‑AS1 could downregulate miR‑3160‑5p by targeting binding in DLBCL cells. Overexpression of miR‑3160‑5p had the same effects on the cytotoxicity and apoptosis of DLBCL cells as CACNA1G‑AS1‑knockdown. Overall, the present study revealed that CACNA1G‑AS1‑knockdown and miR‑3160‑5p‑overexpression could prevent DLBCL carcinogenesis, which might provide novel therapeutic targets for DLBCL.