Arsenic Trioxide Affects the Proliferation of Gastric Cancer Cells through MiR-885-5p/CDC73 Axis.

Background: To explore Arsenic trioxide (As2O3) and its regulated miR-885-5p/CDC73 signaling pathway involved in the development of gastric cancer. Methods: Fifty-two healthy patients and patients with gastric cancer were enrolled 2019-2020 in He Xian Memorial Hospital, Guangzhou, China. The patients with gastric cancer were divided into control group and As2O3 administration group. After 2 courses of treatment, their peripheral blood was collected to analyze the therapeutic effect. miR-885-5p expression in peripheral blood was analyzed by qRT-PCR. As2O3 was added into MGC-803 gastric cancer cell line at 0, 10, 20, 40 and 80 µmol/L. The proliferation rate and 48h IC50 value of gastric cancer cells were investigated by CCK-8, and the effect of As2O3 on miR-885-5p expression in the cells was analyzed. Results: After 4 weeks of treatment, the objective efficiency of control group and As2O3 administration group was 17.3% and 13.4%, respectively, without significant statistical difference. The overall benefit rate of As2O3 administration group was significantly higher than that of the normal treatment group (P=0.049). qRT-PCR experiment results found that miR-885-5p significantly highly expressed in peripheral blood in the As2O3 administration group, while miR-885-5p in gastric cancer was lower compared with normal people. Adding As2O3 to the gastric cancer cells could significantly inhibit miR-885-5p expression, while miR-885-5p in gastric cancer cells affected cell expression by targeted regulation, affecting cell proliferation. Conclusion: As2O3 may be used as a drug treatment program for gastric cancer, and mainly regulates the proliferation of gastric cancer cells by affecting the miR-885-5p/CDC73 target axis to participate in the development of gastric cancer.

LncRNA SNHG7 inhibits proliferation and invasion of breast cancer cells by regulating miR-15a expression.

PURPOSE: To explore the inhibition of proliferation and invasion of breast cancer cells by LncRNA SNHG7 via regulating the expression of miR-15a and its mechanism. METHODS: The expression of SNHG7 in breast cancer and adjacent tissues and different breast cancer cells was measured by qRT-PCR and the relationship between SNHG7 and clinicopathological parameters of breast cancer patients was analyzed. The interaction of SNHG7 with miR-15a was explored by dual-luciferase reporter assay. The change in the proliferation of breast cancer cells after silencing SNHG7 was examined by cell proliferation assay. The change in the invasion of breast cancer cells after silencing SNHG7 was examined by Transwell invasion assay. Subcutaneous tumor formation in nude mice was detected to record the tumor size and volume of tumor cells. RESULTS: Compared with adjacent normal tissues, the expression of SNHG7 was significantly increased in breast cancer tissues; the expression of SNHG7 was the highest in breast cancer cells MCF7 and T47D; the expression level of SNHG7 was not notably different among breast cancer patients of different genders and age groups, and the difference was not statistically significant (p>0.05). The expression level of SNHG7 was higher in patients with a higher stage of breast cancer and patients with lymph node metastasis, and the difference was statistically significant. SNHG7 could specifically bind to the 3' UTR of miR-15a. The inhibition of SNHG7 led to constrained proliferation and invasion of breast cancer cells. The tumor volume and weight of the tumor-bearing mice in the si-SNHG7 group were significantly lower than those in the non-specific control (NC) group. CONCLUSION: SNHG7 plays an important role in the development of breast cancer. SNHG7 can affect the proliferation and invasion of breast cancer cells through its targeted regulation of miR-15a activity.

lncRNA MALAT1 regulates the expression level of miR-21 and interferes with the biological behavior of colon cancer cells.

PURPOSE: This study aimed to verify whether the regulation of miR-21 expression by lncRNA MALAT1 interferes with the biological behavior and mechanism of colon cancer cells. METHODS: RT-qPCR was used to detect the expression of MALAT1 in colon cancer and paracancerous tissues and different colon cancer cell lines (HT-29, SW480, SW620, CaCo-2). The relationship between MALAT1 and clinicopathological parameters of colon cancer patients and the interaction of MALAT1 and miR-21 by dual luciferase reporter gene detection were detected. Transwell invasion assay detected the invasive ability of colon cancer cells after MALAT1 inhibition and scratch assay detected the migration ability of colon cancer cells after MALAT1 inhibition. Subcutaneous tumor formation was detected in nude mice to measure the inhibition of the tumor size and volume of MALAT1 colon cancer cells. RESULTS: Compared with paracancerous tissues, MALAT1 expression was significantly increased in colon cancer tissues. MALAT1 expression was the highest in HT-29 colon cancer cell line. MALAT1 was specifically bound to miR-21 3' UTR. Inhibition of MALAT1 could inhibit colon cancer cell invasion and migration ability, and tumor formation in nude mice showed that the tumor volume and weight of the tumor-bearing mice were reduced after inhibiting the expression of MALAT1. CONCLUSION: In conclusion, lncRNA MALAT1 plays an important role in the development of colon cancer. MALAT1 can regulate miR-21 to regulate the migration and invasion of colon cancer cells.

ESCO2 inhibits tumor metastasis via transcriptionally repressing MMP2 in colorectal cancer.

BACKGROUND: Establishment of cohesion 1 homolog 2 (ESCO2) plays important roles in the regulation of cohesion and genomic stability and has been implicated in human cancers. Yet, its clinical significance and biological function in colorectal cancer (CRC) are unknown. METHODS: The expression of ESCO2 was examined by quantitative real-time PCR, Western blot, and immunohistochemistry. The role of ESCO2 in the tumor metastasis of CRC and the related mechanisms were investigated using in vitro and in vivo models. RESULTS: In this study, we show that low expression of ESCO2 in CRC was closely correlated with lymphatic and distant metastasis. Patients with low ESCO2 expression experienced shorter overall survival and disease-free survival in two independent cohorts containing a total of 587 CRC cases. ESCO2 overexpression suppressed, whereas ESCO2 knockdown promoted cell migration in vitro and tumor metastasis in vivo via modulation of epithelial-mesenchymal transition (EMT) process. Mechanistically, ESCO2 inhibited the transcriptional activity of MMP2 promoter to downregulate its expression. Reexpression of MMP2 partially attenuated the ESCO2-mediated malignant phenotypes. CONCLUSION: Collectively, our data suggest that ESCO2 serves as a potential prognostic factor and exerts antimetastatic activity in CRC.

A novel, intelligent, pressure-sensing colostomy plug for reducing fecal leakage.

This study aims to describe and report the effectiveness of a novel, pressure-sensing colostomy plug for reducing fecal leakage. Nine miniature Tibetan pigs, aged 6-8 months, were given colostomies and divided into three groups (n = 3 each group). A novel pressure-sensing colostomy plug was placed in each pig and set to indicate when intestinal pressures of either 5, 10, or 15 mm Hg, respectively, were reached. When the pressure thresholds were reached, the animals' bowels were examined for the presence of stool and/or stomal leakage, and the data were recorded at weeks 1, 4, and 8 after surgery. The colostomy plug calibrated to 15 mm Hg pressure demonstrated the greatest accuracy in predicting the presence of stool in the bowels of study animals, averaging >90% sensitivity. In general, the sensitivity for predicting the presence of stool did not vary significantly over time, though there was a slight increase in accuracy in the 5 mm Hg group at later time-points. The sensitivity for predicting stool in the bowel did not change significantly over time in any of the three groups. Stomal leakage was found to be inversely proportional to the pressure-sensor setting, in that the 15 mm Hg group exhibited the greatest amount of leakage. This difference, however, was found to be significant only at week 1 postsurgery. The intelligent, pressure-sensing colostomy plug was able to accurately predict the presence of stool in the bowel and maintain continence, allowing negligible leakage.