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The aim of the present study was to investigate the effect of Forkhead box transcription factor M1 (FoxM1)-silencing on the growth, migration and invasion of K1 human papillary thyroid carcinoma (PTC) cells. The effect of FoxM1-small interfering RNA (siRNA) in K1 cells was detected by western blot analysis. FoxM1-siRNA and control siRNA were transfected into K1 cells using Lipofectamine® 2000 (transfection group, T) and the non-meaning sequence group (NM). K1 cells exposed to PBS solution comprised the blank control group (CON). Cell proliferation ability was detected using an MTT assay. Cell migration and invasion was detected by the single cell scratch test and Transwell invasion assay, respectively. Western blot analysis indicated that FoxM1 siRNA downregulated the expression of FoxM1 protein. Cell proliferation, migration and invasion were significantly lower in the T group compared with the NM and CON groups (P<0.05). These results indicated that silencing of FoxM1 expression could block growth, invasion and migration of K1 cells. This study may provide a novel target gene for targeted therapy of PTC.

To evaluate the clinical efficacy and safety of the rCCK96-104PE38 targeted drug in patients with colon cancer in general surgery, data of 80 patients with colon cancer who were admitted to the hospital from April 2019 to July 2021 were selected and randomly divided into the treatment group and the control group, with 40 cases in each group. Patients in the treatment group were treated with the rCCK96-104PE38 targeted drug, and those in the control group were treated with oxaliplatin. The treatment efficiency and incidence of adverse reactions were compared between the two groups. The inverse cholecystokinin (CCK96-104) was fused with pseudomonas aeruginosa exotoxin (PE38 toxin) through the gene amplification technique to construct a prokaryotic expression vector. Then, the rCCK96-104PE38 was purified by Ni-nitrilotriacetate (Ni-NTA) affinity chromatography, and the antitumor activity of rCCK96-104PE38 was verified. The results showed that the amplified rCCK96-104PE38 sequence was correct and the pET-28a prokaryotic expression system was adopted to successfully achieve active expression. The purified recombinant protein could induce the apoptosis of colon cancer cells in vitro and inhibit tumor growth in vivo. The total effective rate in the treatment group (80%, 32/40) was higher than that in the control group (60%, 24/40) ( P < 0.05 ). To sum up, the recombinant toxin rCCK96-104PE38 could not only specifically adsorb the colon cancer cells with high expression of CCK2R but also effectively inhibit tumor tissue growth and proliferation. Besides, the rCCK96-104PE38 protein had a good anticancer effect that helped effectively reduce the incidence of adverse reactions in patients, which was worthy of promoting.