Aims: Several recent reports have shown irisin protects the heart against ischemia/ reperfusion injury. However, the effect of irisin on I/R injury in diabetic mice has not been described. The present study was designed to investigate the role of irisin in myocardial ischemia-reperfusion (MI/R) injury in diabetic mice. Methods: A mouse model of diabetes was established by feeding wild type or genemanipulated adult male mice with a high-fat diet. All the mice received intraperitoneal injection of irisin or PBS. Thirty minutes after injection, mice were subjected to 30 min of myocardial ischemia followed by 3h (for cell apoptosis and protein determination), 24 h (for infarct size and cardiac function). Results: Knockout of gene FNDC5 augmented MI/R injury in diabetic mice, while irisin treatment attenuated MI/R injury, improved cardiac function, cellular ATP biogenetics, mitochondria potential, and impaired mitochondrion-related cell death. More severely impaired AMPK pathway was observed in diabetic FNDC5-/mice received MI/R. Knockout of gene AMPK blocks the beneficial effects of irisin on MI/R injury, cardiac function, cellular ATP biogenetics, mitochondria potential, and mitochondrion-related cell death. Conclusions: Our present study demonstrated that irisin improves the mitochondria function and attenuates MI/R injury in diabetic mice through AMPK pathway.
Background: Ovarian cancer typically is diagnosed late because insensitivity and lack of specificity of current biomarkers prior to its clinical detection. Ribosomal protein S6 (RPS6) is a ribosomal protein involved in the ribosomal 40S subunit, but its biological role in epithelial ovarian cancer (EOC) is still unknown. Results: RPS6 was elevated in EOC compared to normal ovarian tissues and adenomas. Higher expression of RPS6 predicted worse prognosis in EOC. The level of RPS6 was correlated with clinical stage, histological type and pathological grade. Knockdown of RPS6 reduced the proliferation of ovarian cancer cell lines SKOV-3 and HO8910, and inhibit the migration and invasion ability. It revealed that cells arrested at G0G1 phase after knockdown of RPS6, and the expressions of CyclinD1, Cyclin E, CDK2, CDK4, CDK6 and pRb were also reduced. Conclusions: RPS6 is involved in EOC and knockdown of RPS6 could inhibit the proliferation, invasion and migration ability of EOC in vitro by inducing G0/G1 phase arrest. RPS6 is expected to be a novel biomarker and molecular target to the EOC.
Objectives Our goal was to investigate the effects of rucaparib on the proliferation of cervical cancer cells and sensitivity to radiotherapy. Methods We used the human cervical cancer cell lines Hela and Siha and evaluated their viability and activity using various methods. Cellular proliferation was assessed by CCK-8 and clonogenic assays after treatment with rucaparib. Cell cycle analysis was performed using propidium iodide staining. Western immunoblotting analysis was used to detect the expression of cyclin D1 and CDK4. Immunofluorescence staining assay was performed to detect the expression of the DNA injury marker ץ-H2AX after treatment with rucaparib and radiotherapy. Animal experiments were also performed to evaluate tumor size after treatment with rucaparib. Immunohistochemistry was performed to analyze the expression of Ki-67. Results Rucaparib suppressed proliferation, induced G2/M phase arrest, and reduced the expression of cyclin D1 and CDK4 in cervical cancer cells. When rucaparib was combined with radiotherapy in cervical cancer cells, clone formation decreased significantly and G2/M phase arrest was accentuated. The expression of the DNA-damage marker ץ-H2AX was increased significantly, and rucaparib suppressed tumor growth in vivo. Conclusions Rucaparib exerts significant anti-proliferative effects and can serve as an effective radiosensitizer in cervical cancer, suggesting its candidacy in cervical cancer treatment and worthiness for further investigation.
The aim of the present study was to investigate the influence of perineural invasion (PNI) on the prognosis of patients with early cervical cancer (stages IA2-IIA2). A retrospective analysis was conducted on 406 patients with early cervical cancer who underwent a radical hysterectomy and pelvic lymphadenectomy between January 2007 and December 2014 at the Affiliated Hospital of Jiangnan University (Wuxi, China). The clinicopathological data of the patients were obtained and follow-up assessments were performed. A statistical analysis of the association between PNI and each index was performed, and the effect of PNI and the clinicopathological parameters on the prognosis of the patients was evaluated. Among the 406 cases with early cervical cancer, 41 cases were lost, with a follow-up rate of 89.90%. Overall, 43 PNI-positive patients were observed, with an occurrence rate of 10.59%. PNI-positivity was associated with hypertension, lymph node metastasis, depth of cervical invasion, surgical margin and vascular invasion (P<0.05), but it was not associated with age, diabetes, clinical stage, histological type or tumor size (P>0.05). The overall survival (OS) and disease-free survival (DFS) times of PNI-positive patients were significantly lower compared with those of PNI-negative patients. A multivariate regression analysis revealed that age, tumor size, clinical stage and PNI were independent risk factors for OS and DFS times. PNI is a poor prognostic factor for patients with early cervical cancer.
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