Tumor suppressor miR-192-5p targets TRPM7 and inhibits proliferation and invasion in cervical cancer.

Cervical cancer is the fourth highest mortality cancer among women worldwide. Many researchers have discovered the major anticancer role of miR-192-5p. However, no study has revealed the effect of miR-192-5p on cervical cancer and its molecular mechanism. Therefore, in this study, we aimed to explore the role of miR-192-5p in proliferation, invasion of cervical cancer, and its regulatory mechanism. Firstly, the expression level of miR-192-5p was examined by real-time quantitative polymerase chain reaction. Cell counting kit-8 analysis was applied to detect the proliferation of transfected Caski and SiHa cells. Flow cytometry assay was applied to detect the apoptosis of transfected Caski and SiHa cells. Our result showed that miR-192-5p restrained cervical cancer cell proliferation and induced apoptosis. Then we employed wound healing and transwell assays to analyze the migration and invasion abilities of Caski and SiHa cells in vitro. The results showed that miR-192-5p had an inhibitory effect on cervical cancer migration and invasion. The results of in vivo experiment demonstrated that miR-192-5p also inhibited tumor development in nude mice. We further detected that the binding of transient receptor potential melastatin-subfamily member 7 (TRPM7) to miR-192-5p using bioinformatic methods and dual-luciferase reporter assay. Finally, we found that TRPM7 overexpression reversed the inhibitory effects of miR-192-5p on proliferation, migration, and invasion on cervical cancer cells. In conclusion, the findings of the present study revealed that miR-192-5p performs an inhibitory role in cervical cancer proliferation and invasion by targeting TRPM7.

Consistency of postoperative pain assessments between nurses and patients undergoing enhanced recovery after gynaecological surgery.

AIMS AND OBJECTIVES: To explore the consistency of pain intensity and pain location assessed by nurses and patients in gynaecology undergoing enhanced recovery after surgery pathway. BACKGROUND: Several studies have shown that clinical nurses' assessment of patients' pain is not always accurate. Little is known about the accuracy of nurses' pain assessments for gynaecological patients. Postoperative pain assessment and management is an essential part of enhanced recovery after surgery. DESIGN: Comparative cross-sectional study. METHODS: A total of 160 patients were recruited and only 85 patients and 17 nurses participated. Patients and nurses recorded pain scores (using an 11-point Numeric Rating Scale) and pain location (incision pain, surgical area pain in the abdominal cavity, other pain or no pain) on Pain Assessment Forms at 4 hr after surgery and on the first and second postoperative days. We used the STROBE guidelines to report our study. RESULTS: The patients' pain score was higher than that of nurses from 4 hr to second day after laparoscopic surgery at rest. The pain scores of both nurses and patients decreased over this period of time. All the intraclass correlation coefficients were between 0.214-0.296. At the three time points, surgical area pain in the abdominal cavity and abdominal incision pain were the main pain areas. All the kappa coefficients were between 0.164-0.255. CONCLUSIONS: The consistency of postoperative pain assessment about pain score and pain location between nurses and patients was not high. We should attach importance to systematic pain assessment, and more detailed enhanced recovery after surgery pathways should be developed about pain assessment. RELEVANCE TO CLINICAL PRACTICE: Continuing education for nurses regarding pain assessment is necessary. Nurses should accept the patient's self-reported pain. There should be a step that gives more time for pain assessment in enhanced recovery after surgery pathways.

The cross talk between cervical carcinoma cells and vascular endothelial cells mediated by IL-27 restrains angiogenesis.

PROBLEM: To explore whether cervical carcinoma cell-derived interleukin-27 (IL-27) modulates the angiogenesis of vascular endothelial cells. METHOD OF STUDY: The expression of IL-27 in cervical cancer tissues and cervical cell lines was analyzed by immunohistochemistry, ELISA and flow cytometry. Then, the effects of IL-27 on the proliferation and apoptosis-related molecules and angiogenesis in vitro of human umbilical vein endothelial cells (HUVECs) were investigated. Finally, in vivo experiment was performed to further confirm the effects of IL-27. RESULTS: Compared with cervicitis, the cervical cancer tissues highly expressed IL-27. Both HeLa and CaSki cells secreted IL-27, and HUVECs expressed low levels of IL-27 receptors (IL-27R). However, the co-culture of cervical cell lines and HUVECs led to a significant elevation of IL-27R on HUVECs. Co-culturing with IL-27-overexpressed HeLa cells downregulated Ki-67 and Bcl-2 and upregulated Fas expression in HUVECs. In addition, overexpression of IL-27 in HeLa cells and CasKi cells secreted less IL-8 and could further restrict angiogenesis compared with control cells in vitro. In the subcutaneous tumorous model of C57/BL6 mouse, there were decreased vessel density and tumor volume when inoculation with IL-27-overexpressed TC-1 cells. CONCLUSION: This study indicates that IL-27 secreted by cervical carcinoma cells restricts the angiogenesis in a paracrine manner in the pathogenesis of cervical cancer.