The therapeutic effect of combined drugs on cervical cancer has been confirmed. Whether anti-PD-1 antibody combined with paclitaxel mediates the PI3K-Akt pathway to regulate cervical cancer still requires further research. 20 nude mice received subcutaneous administration of Hela cells to establish cervical cancer model which was then assigned into blank control group, control group A (PD-1 antibody (5 mg/ kg) administration), control group B (paclitaxel), and observation group (PD-1 antibody combined with paclitaxel) followed by analysis of cell proliferation, apoptosis, expression of PI3K-Akt signaling proteins and mRNAs. Observation group had lowest tumor size, highest cell proliferation inhibition rate and apoptosis, which were all reversed in blank group with a largest tumor size, lowest cell proliferation inhibition rate and cell apoptosis. There were no differences between control group A and control group B (P > 0.05). The expressions of PI3K, Akt, p53, and p21 proteins were lowest in observation group and highest in blank group. In addition, control group showed no difference to control group B (P > 0.05). In conclusion, anti-PD-1 antibody combined with paclitaxel inhibits PI3K-Akt signaling activity, thereby downregulating PI3K, Akt, p53, and p21 protein, controlling cervical cancer cell division, promoting cell apoptosis, and exerting anti-tumor effects.

This study assesses the mechanism of Apatinib gene carried with CNT in regulating the growth and chemosensitivity of HPV through inducing AMPK/TSC2/mTOR signal pathway. SiHa cells were divided into blank set, empty carrier set, Apatinib set and Apatinib set carried with CNT randomly. Cell cycle of SiHa cells was detected through CCK-8 test, clone formation test and FCM. The mRNA presentation of Cyelin D3 was detected with Reverse Transcription-Polymerase Chain Reaction (RT-PCR). The protein expression of Cyelin D3, presentation and activation of AMPK, TSC2 and mTOR was detected with Western Blot assay. Expression of VEGFR-2 in Apatinib set and Apatinib set carried with Carbon nanotube (CNT) was reduced. The proliferative rate in Apatinib set was lower than in control set notably. The rate of clone formation in Apatinib set carried with CNT was declined notably compared with control set. The cell cycle was restrained in Apatinib set carried with CNT. The IC50 concentration of TAX in Apatinib set carried with CNT was lower than in control set. The expression of p-AMPK in Apatinib set and Apatinib set carried with CNT was elevated compared with control set. The active expression of AMPK was prompted in Apatinib set. And phosphorylation of mTOR was restrained. The growth of HPV was restrained and chemosensitivity of HPV was improved by Apatinib gene carried with CNT through inducing AMPK/TSC2/mTOR signal pathway.