Objective To investigate whether huaier can induce apoptosis of colorectal cancer (CRC) cells and its possible mechanism. Methods CCK8 assays detected the viability of HCT8 and HT29 cells with different concentration of huaier. Flow cytometry detected the apoptosis of HCT8 and HT29 cells, and the gene expression lever of P85α mRNA was detected by RT-qPCR assays. Western blot assays detected the expression lever of pathway protein P85α, p-AKT and AKT, apoptosis protein BAX, BCL-2, Cleaved caspase-3 and Cleaved caspase-9, and proliferating protein CDK4 and CyclinD1 on HCT8 and HT29 cells with different concentration of huaier. Results Huaier could reduce the viability of HCT8 and HT29 cells, and the viability were decreasing with the increasing concentration. The apoptosis rates of HCT8 and HT29 cells with different concentration of huaier were increased observably. It showed that huaier could increase the apoptosis rates of HCT8 and HT29 cells, and the apoptosis rates were increasing with the increasing concentration. The expression lever of P85α mRNA in HCT8 and HT29 cells were decreased observably. It showed that huaier could decrease the expression lever of P85α mRNA, and the expression lever of P85α mRNA were decreasing with the increasing concentration. Western blot assays showed that huaier can inhibit the expression lever of P85α, p-AKT/AKT, inhibit the expression of BCL-2, CDK4 and CyclinD1, and promote the expression lever of BAX, Cleaved caspase-3 and Cleaved caspase-9. Conclusion Huaier can inhibiting the proliferation and inducing the apoptosisof HCT8 and HT29 cells, and its mechanism may be related with PI3K/AKT signaling pathway.

Objective This study is aimed to verify whether vitexin can increase the sensitivity of colorectal cancer cells to chemotherapeutic drugs. Methods The cell-counting-kit-8 was applied to test the cell viability of HT29 cells. After HT29 cells being co-treated with vitexin and oxaliplatin, western blot was used to check the expression of P-gp, Bax, and Bcl-2 in these groups. The flowcytometry was employed to test the apoptosis rate and cell cycle of HT29 cells after being co-treated with vitexin and oxaliplatin. Results The viability of HT29 cells was decreased gradually via treated with vitexin at the concentration gradients of 30μmol, 60μmol, 90μmol and 120μmol. Western blot showed that compared to the single drug treated group, the relative expression of P-gp and BCL-2 was declined, the expression of Bax was increased in co-treated group. The flow cycometry showed that the G1 phase was significantly expanded and the apoptosis rate of Co-treated group was increased compared to the oxaliplatin single treated group(P<0.05). Conclusion The combination use of vitexin and oxaliplatin can increase the apoptosis of HT29 cells and further increase its sensitivity to the chemotherapeutic drug oxaliplatin.

Objective To investigate the efficacy and safety of Cinobufacini combined with chemotherapy in the treatment of colorectal cancer (CRC). Methods By searching the publicly published case-control studies on the combination of Cinobufacini in the treatment of colorectal cancer, RevMan 5.3 analysis software was used for systematic evaluation. Results A total of 10 research data were included. Meta-analysis showed that compared with conventional chemotherapy, the combination of cinobufagin and chemotherapy drugs could significantly improve the chemotherapy effect of patients (P=0.0001), the quality of patients life, KPS score (P<0.00001), and relieve pain (P<0.0003). In addition, a series of adverse reactions caused by chemotherapy were significantly reduced in colorectal patients (P<0.05). Conclusion Cinobufacini combined with chemotherapy has a more significant clinical effect than chemotherapy alone in the treatment of colorectal patients.

Objective To systematically evaluate the correlation between mTOR, p-mTOR and colorectal cancer and its clinicopathological characteristics. Methods Through searching domestic and foreign published articles on the relationship between mTOR, p-mTOR and colorectal cancer, the NOS scale was used to evaluate the risk of bias in the study, and the sensitivity and heterogeneity of the included literature were analyzed by Rev Man 5.3 software. Results Compared with normal or adjacent tissues, the expression of mTOR and p-mTOR was higher in colorectal cancer tissues (P<0.00001); compared with the infiltration depth T1 and T2 groups, mTOR and p-mTOR were in the infiltration depth T3, The expression of the T4 group was significantly increased (P<0.00001); compared with the clinical stage Ⅰ~Ⅱ group, the expression of mTOR and p-mTOR was higher in the clinical stage Ⅲ~Ⅳ group (P<0.00001); and no lymph node metastasis Compared with the group, the expression of mTOR and p-mTOR in the group with lymph node metastasis was significantly increased (P<0.0001); compared with the group without distant metastasis, the expression of mTOR and p-mTOR in the group with distant metastasis was significantly increased (P<0.0001); However, the expression of mTOR and p-mTOR was not statistically different between the poorly differentiated group and the middle-highly differentiated group. Conclusion The expression of mTOR and p-mTOR play an important role in the occurrence and development of colorectal cancer.