LncRNA IRAIN inhibits mantle cell lymphoma progression by inducing cell cycle arrest and apoptosis: an in vitro study

Long non-coding RNA (lncRNA) insulin-like growth factor 1 receptor antisense imprinted non-protein coding RNA (IRAIN) and lysine-specific demethylase 1 (LSD1) are aberrantly expressed in various malignancies. However, their roles in the progression of mantle cell lymphoma (MCL) remain unclear. This study aimed to investigate the expression pattern and biological role of IRAIN in MCL progression and to further explore the relationship between IRAIN and LSD1. In this study, the expression levels of IRAIN and LSD1 in MCL cells were detected by RT-qPCR. An IRAIN-overexpressing lentiviral vector (LV-IRAIN-up) was constructed and transduced into MCL cells, and the transduction efficiency was verified by flow cytometry (FACS) and RT-qPCR. The effects of IRAIN overexpression on cell viability, apoptosis, and cell cycle progression were evaluated using CCK-8 assays and FACS analysis. In addition, RT-qPCR and Western blot analyses were performed to determine the regulatory effects of IRAIN overexpression on LSD1 expression, apoptosis-related proteins (including Bax, Bcl-2, pro-caspase-3, and cleaved-caspase-3), and cell cycle-related proteins (Cyclin D1, CDK2, and p21). Furthermore, LSD1 was overexpressed in IRAIN-overexpressing MCL cells to investigate its effects on cell proliferation, apoptosis, and cell cycle progression. The results demonstrated that IRAIN expression was significantly downregulated, whereas LSD1 expression was markedly upregulated in MCL cells. IRAIN overexpression significantly inhibited cell viability, promoted apoptosis, and induced G1-phase cell cycle arrest. Meanwhile, IRAIN overexpression markedly downregulated the expression of LSD1, Bcl-2, pro-caspase-3/cleaved-caspase-3, Cyclin D1, and CDK2, while upregulating the expression of Bax and p21. Further experiments showed that LSD1 overexpression partially reversed the inhibitory effects of IRAIN overexpression on MCL cell proliferation, apoptosis induction, and G1-phase arrest. Collectively, these findings suggest that IRAIN may participate in the regulation of proliferation, apoptosis, and cell cycle progression in MCL cells, potentially through modulation of LSD1. These results provide preliminary experimental evidence for further understanding the potential biological function of IRAIN in MCL.