HO-1 protects liver against I/R injury by inhibiting TLR2/TLR4-triggered MyD88- and TRIF-dependent signaling pathways and increasing expression of negative regulators of TLR signaling in rats.
miR-210 is closely related to the occurrence of pancreatic cancer. In addition, Runx3 is a tumor suppressor gene and inhibits tumorigenesis. However, miR-210?s effect on Runx3 level is unclear. Therefore, Our study explored miR-210?s effect on the proliferation and migration of pancreatic
cancer cells. PANC-1 cell line was transfected with miR-210 Mimics or miR-210 Mimic+pFBD-Runx3 plasmids followed by analysis of miR-210 and Runx3 level by qRT-PCR, targeting relationship by the dual fluorescein reporter assay, Runx3 and Tubulin protein expression by Western blot, cell proliferation
by MTT assay and cell migration by Transwell assay. Compared with normal tissue, miR-210 was significantly upregulated in pancreatic cancer tissue (P < 0.01), while Runx3 mRNA was significantly downregulated (P < 0.01). Runx3 was a target protein of miR-210. miR-210 Mimics
transfection significantly reduced Runx3 level and increased cell proliferation, which was significantly reduced in the miR-210 Mimic+pFBD-Runx3 group. miR-210 Mimics significantly promote cell migration and the addition of Runx3 prevented miR-210 Mimics-induced cell migration. miR-210 binds
to the 3′-UTR region of Runx3 mRNA, reduces Runx3 expression, and promotes cell proliferation and migration. Increased Runx3 can inhibit miR-210?s effect on pancreatic cancer cells.
Irigenin has been reported to exhibit remarkable anticancer effects against several human cancers. Nonetheless, the anticancer effects of irigenin against the human liver cancer cells are still largely unexplored. Consistently, this study was designed to evaluate the anticancer effects of irigenin against human liver cancer cells and to unveil the underlying molecular mechanisms. The results showed that irigenin significantly (p < 0.05) inhibited the growth of the human HepG2 and SNU-182 liver cancer cells with an IC50 value of 14 µM. Nonetheless, the cytotoxic effects of irigenin against the normal THLE-2 cells were comparatively lower as evident from the IC50 of 120 μM. The AO/EB and DAPI staining showed that irigenin induces apoptosis in the human liver cancer cells. Annexin V/PI staining assay revealed a significant (p < 0.05) increase in the percentage of apoptotic HepG2 and SNU-182 liver cancer cells upon treatment with irigenin. It was found that the number of apoptotic HepG2 and SNU-182 cells enhanced from 2.3 to 41.75% and 1.16 to 51.9% at IC50, respectively. Western blot showed a considerable increase in Bax and decrease in the Bcl-2 expression upon irigenin treatment further confirming the induction of apoptosis. Flow cytometric analysis revealed that irigenin also induces G2/M cell cycle arrest of HepG2 and SNU-182 cells. The percentage of G2/M phase HepG2 and SNU-182 cells increased from 17.92 to 34.35% and 23.97 to 38.23% at IC50, respectively This was also accompanied by decrease in the expression of CDK1 and Cyclin-B in HepG2 and SNU-182 cells. Taken together, the results of the present study suggest that irigenin inhibits the growth of the human liver cancer cells via induction of apoptosis and cell cycle arrest. These results point towards the potential of irigenin as a lead for the development of chemotherapy for liver cancer.
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