Skip to main content
Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: M6A associated TSUC7 inhibition contributed to Erlotinib resistance in lung adenocarcinoma through a notch signaling activation dependent way

Fig. 5

TUSC7 sensitized Erlotinib treatment and formed feedback loop with miR-146/Notch signaling cascade. A Notch signaling inhibition resulted in cMYC promoter activity decreasing, and TUSC7 inhibition strongly increased the activity. B Inhibition of TUSC7 increased miR-146a expression, and then stimulated the DICER1 activity. C The scheme image represented the cMYC promoter detection modes. D Western blotting confirmed that in PC9ER and HCC827ER cells, miR-146 and TUSC7 acted the opposite way to promote the DICER1/CCND1 expression. E TUSC7 and miR-146a was sustained by cMYC (Left) and DICER1 (Right) respectively. F The regulative signaling pathways were drafted and illustrated for detailed exhibition. G In vivo study confirmed the effective inhibition of TUSC7 exhibited on tumor growth, and the Notch signaling inactivation by using FLI-06 also suppressed the in vivo tumor expansion

Back to article page