Fig. 4: miR-192-SET8 axis inhibits p53/p21 to regulate GC cell proliferation and metastasis. | Cell Death & Disease

Fig. 4: miR-192-SET8 axis inhibits p53/p21 to regulate GC cell proliferation and metastasis.

From: Histone methyltransferase SET8 is regulated by miR-192/215 and induces oncogene-induced senescence via p53-dependent DNA damage in human gastric carcinoma cells

Fig. 4

A Up: detection of mRNA and protein levels of SET8 regulated by miR-192/215. Transfection of miR-192/215 inhibitors, SET8 was significantly increased in SGC7901 and HFE145. Conversely, SET8 was significantly downregulated in cells treated with miR-192/215 mimics. Down: results of the luciferase reporter assays. Transfection of miR-192/215 mimics significantly downregulated the firefly luciferase activity of SET8-3′-UTR-wt vector, whereas the SET8-3′-UTR-mut vector was upregulated. NC, negative control in all experiments. B Subcutaneous tumor xenograft assays. The growth of subcutaneous tumors was suppressed by inhibition of miR-192. Co-miR-192inh and SET8si significantly reversed this growth suppression. C Assays of lung metastasis of nude mice. The results suggest that the number of metastatic lesions decreased significantly after transfection of miR-192 inhibitors, whereas co-transfection of miR-192 inhibitors and SET8si led to an increase in the metastatic lesions. D Examination of mRNA levels of SET8, p53, and p21. In mice tissues, knockdown of SET8 was effective. Meanwhile, p53 and p21 were clearly regulated by SET8. 192, miR-192; inh, inhibitor; si, siRNA. GAPDH as a loading control; mut, mutation; S, SET8-3′-UTR-wt vector. S-mut, SET8-3′-UTR-mutant vector. *P < 0.05. Error bars represent ±SD.

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