miRNAs have the potential to act on diverse downstream genes, and miRNA signatures of HPV-infected tissues may provide insight into HPV-related carcinogenesis. We set out to profile miRNA expression in HPV-infected samples and relate this to histological and grade-specific alterations in the spectrum of cervical carcinogenesis in vivo. A total of 31 miRNAs showed significant and continuous expression along with the progression from normal cervical tissue to cancer, and six of them were validated in 133 samples. By bioinformatics analyses, we established a putative HPV-associated miRNA-mRNA regulatory network, showing that miR-29 is the most highly enriched. We also found that YY1 and CDK6 were both positively correlated with E6/E7 RNA expression and targeted by tumour-suppressive miR-29. Evidence of miR-29 involvement in HPV infection was further verified in patient samples and by various experimental approaches. Taken together, our results suggest that HPVs have oncogenic properties at least in part by reshaping the milieu of cellular miRNAs. miR-29 restrains cell cycle progression and induces apoptosis via YY1 and CDK6 promoting malignant transformation induced by HPV, although the abnormality of miR-29 in HPV-infected cells might be regulated in an indirect way.

Pelvic lymph node metastases are regarded as the most important risk factor and a predictor of poor prognosis for patients with cervical cancer. Exploration of metastasis-related molecules is helpful toward improving the prognosis in cervical cancer. To identify the role of miR-375 in metastasis and progression of cervical cancer, we examined the expression of miR-375 in 170 cervical cancer tissues and 68 normal cervical tissues, using stem-loop quantitative PCR, and found that the expression of miR-375 in cervical cancer tissues was significantly decreased by 4.45-fold, compared with 68 normal tissues. A significant correlation existed between miR-375 expression and clinicopathologic parameters, including lymph node metastasis of cervical cancer. Overexpressed miR-375 suppressed cell proliferation, blocked G1-to-S cell-cycle transition, and inhibited cell migration and invasion in human cervical SiHa and CaSki cells. SP1, a potential target gene of miR-375, was inversely correlated with miR-375 expression in cervical cancer tissues. Moreover, SP1 was negatively regulated by miR-375, and knockdown of SP1 by siRNA inhibited cell malignant behaviors. Thus, our findings suggest that down-regulated miR-375 promotes cell malignant behaviors via the target gene SP1 and may consequently contribute to the progression of cervical cancer.

Background Workplace violence (WPV) is a serious issue for healthcare workers and leads to many negative consequences. Several studies have reported on the prevalence of WPV in China, which ranges from 42.2 to 83.3%. However, little information is available regarding the correlates of WPV among healthcare workers and the differences across the different levels of hospitals in China. This study aimed to explore the correlates of WPV and career satisfaction among healthcare workers in China. Methods A self-designed WeChat-based questionnaire was used that included demographic and occupational factors. The Chinese version of the Workplace Violence Scale was used to measure WPV. Career satisfaction was assessed using two questions about career choices. Descriptive analyses, chi-square tests and multivariate logistic regressions were used. Results A total of 3706 participants (2750 nurses and 956 doctors) responded to the survey. Among the 3684 valid questionnaires, 2078 (56.4%) reported at least one type of WPV in the last year. Multivariate logistic regressions revealed that male sex, shift work, bachelor’s degree education, a senior professional title, working more than 50 h per week and working in secondary-level hospitals were risk factors associated with WPV. Healthcare workers who had experienced higher levels of WPV were less likely to be satisfied with their careers. Conclusions WPV remains a special concern for the Chinese healthcare system. Interventions to reduce WPV should be implemented by health authorities to create a zero-violence practice environment.

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BackgroundIt is widely accepted that metabolic syndrome is associated with an increased risk of chronic kidney disease (CKD). To investigate whether coexisting metabolic syndrome is a necessary condition for CKD in overweight and obese.MethodsA cohort study of 6852 Chinese individuals from August 2007 to December 2012. Examinations included a questionnaire, physical measurements, and blood sampling. Hazard ratios for incident CKD were estimated according to combinations of BMI category and absence or presence of metabolic syndrome.ResultsFor CKD, multivariable adjusted hazard ratios vs. normal weight individuals without metabolic syndrome were 1.31 (95 % CI, 0.89–1.92) in overweight and 2.39 (95 % CI, 1.27–4.52) in obese without metabolic syndrome and 1.54 (95 % CI, 1.18–3.95) in normal weight, 2.06 (95 % CI, 1.27–3.36) in overweight, and 2.77 (95 % CI, 1.42–4.31) in obese with metabolic syndrome. There were no interactions between BMI and absence or presence of metabolic syndrome on risk of CKD when BMI was categorized (normal weight, overweight, obese) (P = 0.17). Among individuals both with and without metabolic syndrome there were increasing cumulative incidences of CKD from normal weight through overweight to obese individuals (log-rank trend P = 0.04 to P < 0.001). Although the multivariable adjusted hazard ratio for CKD in individuals with vs. without metabolic syndrome was 1.82 (95 % CI, 1.20–2.78) within overweight and obese individuals (log-rank P = 0.005), only 26.1 % of the increased risk observed for BMI is explained by metabolic syndrome.ConclusionsThese findings suggest overweight and obesity are risk factors for CKD regardless of the presence or absence of metabolic syndrome.Electronic supplementary materialThe online version of this article (doi:10.1186/s12882-015-0083-8) contains supplementary material, which is available to authorized users.

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Our results unraveled the possibility that HPV-16 E6/E7 could promote cell invasive potential via regulating cadherin switching, and consequently contribute to progression and metastasis of cervical cancer.