Abstract
ADAM-17 is a type I transmembrane protein, and its abnormal expression affects the body development and tumor growth. BMSCs act as a target gene carrier in tumor tissues. This study mainly aims to explore the role of ADAM-17 and BMSCs in drug-resistant cervical cancer (CC). BMSCs were transfected with ADAM-17 or empty vectors and then co-cultured with cisplatin-resistant CC cells followed by analysis of cell morphology. The in vivo effect of ADAM-17-modified BMSC was evaluated using animal model of CC. The protein expression of ADAM-17, EGFR, PI3K, and Akt was detected using Western blot and RT-qPCR. Transfection of ADAM-17 significantly facilitated tumor growth at different time points (4 d, 7 d, 10 d, 14 d), accompanied with the upregulation of ADAM-17, EGFR, PI3K, and Akt expression (p < 0.05) without differences between empty vector group and blank group (p > 0.05). Mechanistically, ADAM-17 directly targets EGFR in CC. In conclusion, ADAM-17-modified BMSC enhances the growth of drug-resistant CC cell and tumor growth through EGFR/PI3K/Akt signaling pathway, which may contribute to a novel therapy for treating CC.
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