Introduction: Although the survival rate of colorectal cancer (CRC) patients can be improved by surgery, radiotherapy, and chemotherapy, the resistance to 5-fluorouracil (5-Fu) affects the effect of chemotherapy and the prognosis of patients. An increasing number of studies showed that 5-Fu resistance was the main reason for the failure of colorectal cancer treatment. The poor prognosis of colorectal cancer greatly harms people’s health. This study aimed to clarify the correlation between cyclin-dependent kinase 1 (CDK1) and 5-Fu-induced tumor resistance. Materials and Methods: Cell proliferation and invasion experiments showed that down-regulation of CDK1 inhibited fluorouracil-resistant CRC cell proliferation. The expression level of CDK1 was detected in 5-Fu-resistant CRC cells in vitro. Tumor growth was inhibited by down-regulation of CDK1 in tumor xenograft mouse models. Results: We found that CDK1 was highly expressed in tumor tissues, especially in fluorouracil-resistant tissues. We also confirmed that the differential expression of 5-Fu in tumor tissues was related to tumor site, lymph node metastasis and stage. CDK1 promoted migration, invasion and inhibited apoptosis in 5-Fu-resistant CRC cells. Down-regulation of CDK1 inhibited fluorouracil-resistant CRC cell proliferation and tumorigenesis in vivo. Conclusion: High expression of CDK1 may lead to poor clinical prognosis, and inhibition of CDK1 enhances 5-Fu sensitivity in CRC. Our research suggested that CDK1 may be used to predict 5-Fu efficacy and as a therapeutic target for CRC.

Background: MicroRNAs play an important role in the genesis and progression of tumours, including colorectal cancer (CRC), which has a high morbidity and mortality rate. In this research, the role of miR-495-3p and HMGB1 in CRC was investigated. Methods: We performed qRT-PCR to detect the expression of miR-495-3p in colorectal cancer tissues and cell lines. Functional experiments, such as CCK-8, EdU, Transwell and apoptosis assays, were conducted to explore the effects of miR-495-3p on the proliferation, migration and apoptosis of CRC cells in vitro. Then, database prediction, dual-luciferase reporter gene assays and functional experiments verified the role of the miR-495-3p target gene HMGB1 in CRC. Finally, rescue experiments were performed to investigate whether overexpression of HMGB1 could reverse the inhibitory effect of miR-495-3p on CRC cell proliferation in vivo and in vitro. Results: miR-495-3p was downregulated in colorectal cancer tissues and cell lines, inhibited the proliferation and migration of colorectal cancer cells and promoted cell apoptosis. Database prediction and dual-luciferase reporter gene assays showed that HMGB1 was the downstream target gene of miR-495-3p. We finally demonstrated that miR-495-3p inhibited CRC cell proliferation by targeting HMGB1 in vitro and in vivo. Conclusion: Our research shows that miR-495-3p inhibits the progression of colorectal cancer by downregulating the expression of HMGB1, which indicates that miR-495-3p may become a potential therapeutic target for colorectal cancer.

Background: Gastric cancer (GC) is one of the malignant tumors with high incidence in China. At present, the relationship between type 2 diabetes (T2DM) and the therapeutic effect of various malignant tumors has attracted more and more attention. This study aimed to investigate whether T2DM is a prognostic factor for patients with GC. Methods: Patients who had GC and who were admitted to our hospital from November 2008 to December 2015 were included in the study. Among these patients, 84 patients GC complicated with T2DM (GC + T2DM) were enrolled in the observation group, and 215 patients with normal blood glucose were enrolled in the control group. Patients’ general information was collected by referring to their electronic and paper medical records, and their living status was followed up by conducting a telephone survey, referring to their hospitalization record, and performing an outpatient review. A propensity score matching method was used to select a 1:1 matched control for each patient with GC and diabetes. An overall survival curve was established using the Kaplan-Meier method. The survival rate was compared via a log-rank test. A Cox proportional hazards regression model was used to the analyse single and multiple factors affecting patient outcomes. Results: Before matching was conducted, the differences in gender, stage, treatment, and comorbidity were found to be statistically significant (P>0.05). After matching was completed, the clinical data and pathological differences between the two groups were not statistically significant (P<0.05). A histogram matching the pre- and post-propensity scores showed that the matching was successful. The results of the Cox regression model revealed that grouping, pathological type, and treatment were the independent risk factors of the survival of patients with GC. Survival analysis found that the 3-year, 5-year, and overall survival rates of the observation group were significantly lower than those of the control group (P<0.05). Conclusions: T2DM plays an important role in the development of GC, and is a prognostic factor among patients with GC.