Fig. 6: MiR-22 promotes the expression of tumor suppressor genes by inhibiting SAM synthesis and methylation. | Oncogenesis

Fig. 6: MiR-22 promotes the expression of tumor suppressor genes by inhibiting SAM synthesis and methylation.

From: MiR-22, regulated by MeCP2, suppresses gastric cancer cell proliferation by inducing a deficiency in endogenous S-adenosylmethionine

Fig. 6: MiR-22 promotes the expression of tumor suppressor genes by inhibiting SAM synthesis and methylation.The alternative text for this image may have been generated using AI.

a The metabolic flux of SAM. b 5-MTHF and SAM levels were measured by LC-MS after MKN45 cells transfection with LV-miR-22. c SAM levels were examined by ELISA after MKN45 cells transfection with LV-miR-22. d Relative expression of P16, PTEN, P21, and RASSF1A in Aza-treated, miR-22 overexpression and MeCP2 knockdown GC cells compared with that in the respective controls. e The methylation levels of P16, RASSF1A, and PTEN promoter regions were analyzed by BSP in MKN45 cells. The results are shown from the Fisher’s exact test, n = 10. f Small animal imaging of tumor-bearing mice and gross morphology of xenograft 34 days after injection (left); tumors weight at 34 day after initial injection (middle); growth curve of tumors (right). g qRT-PCR of MiR-22, P16, PTEN, P21, and RASSF1A expressions in miR-22 overexpression tumor xenografts. h The protein levels of CDK4, PTEN, P21, P16, MTHFR, MTHFD2, and MeCP2 in vivo. i qRT-PCR of MiR-22, P16, PTEN, P21, and RASSF1A expressions in MeCP2 knockdown tumor xenografts. The results are shown as the mean±SD. n = 3, *p < 0.05, **p < 0.01, Student’s t test.

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