Fig 2: Inhibitory effects of TMPRSS11D knockdown were mediated by suppression of PI3K/Akt pathway in cervical cancer cells. (A) Expression levels of PI3K, p-PI3K, Akt, and p-Akt were measured using Western blot analysis at 24 h post transfection. (B) Cell proliferation of HeLa cells after IGF-1 treatment. (C) Cell migration of HeLa cells after IGF-1 treatment. n = 3. *p < 0.05 vs. si-NC group; #p < 0.05 vs. si-TMPRSS11D group.

Fig 3: Cell migration and invasion of cervical cancer cells were reduced after si-TMPRSS11D transfection. Cell migration and invasion were measured using transwell assays at 24 h post transfection. (A and B) Cell migration of cervical cancer cells. (C and D) Cell invasion of cervical cancer cells. n = 4. *p < 0.05.

Fig 4: Knockdown of TMPRSS11D promotes the apoptosis of cervical cancer cells. Cell apoptosis were detected through PI staining and the Annexin V method after transfection with si-TMPRSS11D or si-NC, followed by flow cytometry. (A) Figure was obtained from CaSki cells; (B) figure was obtained from HeLa cells. n = 4. *p < 0.05.

Fig 5: EMT phenotype of cervical cancer cells was prevented by si-TMPRSS11D transfection. After 24 h post transfection, the expression levels of EMT markers including E-cadherin, N-cadherin, and fibronectin in CaSki (A) and HeLa cells (B) were measured using Western blot analysis. n = 4. *p < 0.05.