BackgroundMicroRNAs have been reported to play significant roles in pathogenesis of colorectal cancer (CRC). In the present study, we aimed to investigate the functional role of microRNA-455-3p (miR-455-3p) in CRC, as well as its underlying mechanisms.Material/MethodsHuman colon cancer cell line HCT116 cells were transfected with miR-455-3p mimics, inhibitors, or controls. After transfection, the effects of miR-455-3p mimics or inhibitors on cell proliferation were analyzed by 3-(4, 5-dimethyl-2- thiazolyl)-2, 5-diphenyl -2-H-tetrazolium bromide (MTT) assay and BrdU assay, and the effects of miR-455-3p mimics or inhibitors on cell apoptosis were determined. In addition, the underlying mechanisms of cell proliferation and apoptosis were explored by assessing the protein levels of cell cycle regulators and apoptosis-related protein.ResultsThe results showed that overexpression of miR-455-3p significantly inhibited the cell proliferation (P<0.05 or <0.01) in HCT116 cells compared with the control group, but significantly increased the apoptosis (P<0.01). On the contrary, suppression of miR-455-3p significantly increased the cell proliferation but decreased the apoptosis. Moreover, we found that overexpression of miR-455-3p significantly elevated the protein levels of p27 kinase inhibition protein (KIP) 1, Bax, pro-caspase-3, and active caspase-3, and markedly downregulated the levels of B-cell lymphoma-2 (Bcl-2). Contrary results were found by suppression of miR-455-3p. However, there were no significant differences in p21 expression.ConclusionsMiRNA-455-3p functions as an anti-oncogene in HCT116 cells by inhibiting cell proliferation and inducing of apoptosis.

The aberrant expression of tumor suppressor Smad4 often occurs in colorectal cancer (crc), and this phenomenon is believed to be associated with drug resistance. The present study aimed to investigate the effects of Smad4 on the sensitivity of crc cells to cetuximab, and the possible mechanism underlying such an effect. a total of 629 colorectal adenocarcinoma cases were downloaded from The cancer Genome atlas (TcGa) database, and a Smad4 mutation rate of ~21% was demonstrated among the cases. low expression of Smad4 was present in crc tissues analyzed by TcGa and in four crc cell lines, as determined by reverse transcription-quantitative Pcr (rT-qPcr) and western blot analysis. cell counting kit-8 (ccK-8) was used to measure the effects of different concentrations of cetuximab on SW480 cell viability at 24 and 48 h. The results demonstrated that treatment of SW480 cells with 20 µg/ml cetuximab for 48 h markedly reduced cell viability. in addition, plasmids were transfected into SW480 cells to induce Smad4 silencing or overexpression. Silencing Smad4 attenuated the sensitivity of SW480 crc cells to cetuximab; this effect was reflected in increased cell viability and slightly increased migration and invasion, as determined by ccK-8, wound scratch and Transwell analyses. rT-qPcr and western blotting was performed to assess the expression levels of apoptosis-and epithelial-mesenchymal transition (eMT)-related genes. Silencing Smad4 partly reversed the effects of cetuximab on the mrna and protein expression levels of vimentin, Bax/Bcl-2 and e-cadherin. However, Smad4 overexpression enhanced SW480 cell sensitivity to cetuximab. in conclusion, Smad4 may serve a vital role in the sensitivity of crc cells to chemotherapeutic drugs by promoting eMT.

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Objective: The aim of the study is to determine the role of nuclear receptor coactivator 2 in cell proliferation and invasion ability of gastric cancer cells and to explore its possible mechanisms. Methods: Immunohistochemical staining was used to determine NCOA2 gene expression in gastric cancer. Western blotting was used to detect Wnt signal pathways–related protein expression. Colony formation assays, Cell Counting Kit-8 assays, and transwell assays were used to determine cell proliferation, metastasis, and invasion ability of gastric cancer cells. A flow cytometric apoptosis tests determine gastric cancer cell apoptosis ability after inhibition of the expression of nuclear receptor coactivator 2. Subcutaneous mouse models were used to determine the gastric cancer growth and peritoneal metastasis differences after inhibition the expression of nuclear receptor coactivator 2. Results: The expression of nuclear receptor coactivator 2 in gastric cancer cells is high ( P < .01), including lymph node metastasis, TNM staging, and gender differences in nuclear receptor coactivator 2 expression were statistically significant ( P < .01). Short interfering nuclear receptor coactivator 2 could inhibit the proliferation and invasion ability of gastric cancer cells. Short interfering nuclear receptor coactivator 2 promotes the apoptosis of gastric cancer cells. Animal experiments showed that short interfering nuclear receptor coactivator 2 could inhibit the growth and invasion of gastric cancer-transplantable tumors. Knockdown of the expression of nuclear receptor coactivator 2 inhibited the Wnt/β-catenin signaling pathway in the gastric cancer cells. Conclusions: Knockdown of the expression of nuclear receptor coactivator 2 can inhibit the proliferation and invasion of human gastric cancer in vitro and in vivo. The underlying mechanism of NOCA2 affects the Wnt signaling pathway.

Background COVID-19 pandemic has forced physicians to quickly determine the patient’s condition and choose treatment strategies. This study aimed to build and validate a simple tool that can quickly predict the deterioration and survival of COVID-19 patients. Methods A total of 351 COVID-19 patients admitted to the Third People’s Hospital of Yichang between 9 January to 25 March 2020 were retrospectively analyzed. Patients were randomly grouped into training (n = 246) or a validation (n = 105) dataset. Risk factors associated with deterioration were identified using univariate logistic regression and least absolute shrinkage and selection operator (LASSO) regression. The factors were then incorporated into the nomogram. Kaplan-Meier analysis was used to compare the survival of patients between the low- and high-risk groups divided by the cut-off point. Results The least absolute shrinkage and selection operator (LASSO) regression was used to construct the nomogram via four parameters (white blood cells, C-reactive protein, lymphocyte≥0.8 × 109/L, and lactate dehydrogenase ≥400 U/L). The nomogram showed good discriminative performance with the area under the receiver operating characteristic (AUROC) of 0.945 (95% confidence interval: 0.91–0.98), and good calibration (P = 0.539). Besides, the nomogram showed good discrimination performance and good calibration in the validation and total cohorts (AUROC = 0.979 and AUROC = 0.954, respectively). Decision curve analysis demonstrated that the model had clinical application value. Kaplan-Meier analysis illustrated that low-risk patients had a significantly higher 8-week survival rate than those in the high-risk group (100% vs 71.41% and P < 0.0001). Conclusion A simple-to-use nomogram with excellent performance in predicting deterioration risk and survival of COVID-19 patients was developed and validated. However, it is necessary to verify this nomogram using a large-scale multicenter study.