LOXL1-AS1 promotes cell proliferation in hepatocellular carcinomathrough miR-1224-5p/ITPRIPL2/AKT axis.

LncRNA has been validated to be related to different cancers, whereas its regulation mechanism in hepatocellular carcinoma (HCC) is poorly known. In this study, LOXL1-AS1 was overexpressed in HCC cell lines, and LOXL1-AS1 knockdown repressed cell proliferation and stimulated apoptosis in HCC. Besides, the activating role of LOXL1-AS1 in the AKT pathway was also confirmed. Further, miR-1224-5p was sponged by LOXL1-AS1, and overexpression exerted inhibitory function in HCC. Moreover, ITPRIPL2 as amiR-1224-5ptarget gene. Meanwhile, ITPRIPL2 deficiency suppressed HCC cell proliferation. Finally, miR-1224-5p inhibitor reversed the hindering role of LOXL1-AS1 depletion in HCC cell proliferation and AKT pathway, and this rescuing effect was offset by ITPRIPL2 silencing. In summary, LOXL1-AS1 induced cell proliferation and suppresses cell apoptosis in primary HCCvia activating AKT pathway, sponging miR-1224-5p and upregulating ITPRIPL2, which may provide some fresh thoughts for researches about the molecular regulation mechanism of lncRNA in HCC.

Mitofusin-2 is a novel anti-angiogenic factor in pancreatic cancer.

BACKGROUND: Aberrant expression of mitofusin-2 (MFN2) has been found to be associated with vascular endothelial growth factor A (VEGFA)-mediated angiogenesis in human umbilical vein endothelial cells (HUVECs). This study aimed to investigate the expression of MFN2 in pancreatic cancer (PC) and the role of MFN2 in vascular endothelial cell growth and angiogenesis. METHODS: Protein and mRNA expression of MFN2 and VEGFA were measured. The CCK-8 assay, tube formation assay, flow cytometry, and transmission electron microscopy were used to examine the effects of MFN2 overexpression on HUVEC growth, angiogenesis, and apoptosis. Western blot and immunocytochemical staining were conducted to measure alterations in cell cycle and apoptosis regulators and vascular endothelial growth factor receptor 2 (VEGFR2), angiopoietin-1 gene (ANGPT1), and tissue inhibitor of metalloproteinase 1 (TIMP1) expression in HUVECs. RESULTS: The results showed that MFN2 levels were significantly decreased in tumor tissues. Contrasting results were observed for VEGFA mRNA levels. MFN2 overexpression inhibited cell growth while promoting the formation of apoptotic bodies in HUVECs. Additionally, MFN2 overexpression enhanced the protein expression of p21 and p27 while attenuating the expression of proliferating cell nuclear antigen, VEGFA, VEGFR2, ANGPT1, and TIPM1 in HUVECs. CONCLUSIONS: In conclusion, MFN2 expression negatively correlates with VEGFA expression in PC and inhibits endothelial cell growth and angiogenesis.