CircRNA fibroblast growth factor receptor 3 promotes tumor progression in non-small cell lung cancer by regulating Galectin-1-AKT/ERK1/2 signaling.

The dysregulation of circular RNA (circRNA) expression is involved in the progression of several cancers, including non-small cell lung cancer (NSCLC). However, the role and underlying molecular mechanisms of circRNA FGFR3 (circFGFR3) in NSCLC progression remains unknown. Here, we used quantitative real-time polymerase chain reaction to validate that circFGFR3 expression was higher in NSCLC tissues than in the paratumor tissues. Furthermore, our study indicated that the forced circFGFR3 expression promoted NSCLC cell invasion and proliferation. Mechanistically, we found that circFGFR3 promoted NSCLC cell invasion and proliferation via competitively combining with miR-22-3p to facilitate the galectin-1 (Gal-1), p-AKT, and p-ERK1/2 expressions. Clinically, we revealed that the high circFGFR3 expression correlates with the poor clinical outcomes in patients with NSCLC. Together, these data provide mechanistic insights into the circFGFR3-mediated regulation of both the AKT and ERK1/2 signaling pathways by sponging miR-22-3p and increasing Gal-1 expression.

Prevalence and risk factors associated with chronic kidney disease in a Zhuang ethnic minority area in China.

AIM: Numerous studies have examined and reported a high prevalence of chronic kidney disease (CKD) in the general population in various countries including China. However, the situation may be different in undeveloped rural minority regions in China because of China's economic diversity. The aim of the present study was to estimate the prevalence of CKD and to analyze its associated factors in a Zhuang ethnic minority area in Southwest China. METHODS: A cross-sectional survey of a rural minority area populated by people of Zhuang ethnicity in Southwest China using multistage, cluster random sampling methods was performed. The prevalence of indicators of kidney damage and CKD were calculated and risk factors associated with the presence of CKD were analyzed. RESULTS: In total, 7588 people participated in the study. After adjustment for age and gender, the prevalence of albuminuria, haematuria and reduced estimated glomerular filtration rate were 2.7%, 3.7%, and 2.2%, respectively. After adjustment for age and gender, the prevalence of CKD was 8.3%, while recognition of the disease was 3.6%. Independent risk factors associated with CKD were age, gender, and hypertension. Risk factors independently associated with kidney damage were age, gender, hyperuricaemia, and hypertension. CONCLUSION: Our data exhibited a lower prevalence and awareness of CKD in undeveloped rural minority regions, especially exhibited a low prevalence of albuminuria. This result attributed to the low prevalence of metabolic disorders in the local region. Risk factors associated with CKD in our study is similar to surveys in other regions of China.

[An epidemiology study on hypertension in the Zhuang nationality village from the Guangxi Zhuang Autonomous Region].

OBJECTIVE: To observe the risk factors and prevalence status of hypertension at the Guangxi Zhuang-rural region. METHODS: Through cross-sectional survey, Xinlan village (Ethnic-Zhuang tribe village) in Liangqing District of Nanning was chosen as survey site. Select Zhuang-ethnic villagers (age ≥ 18 years, living time ≥ 6 months per year) as survey subjects. Questionnaire survey and examinations including blood pressure measurement, blood tests, and urine test were made by trained medical professionals. Multivariate logistic regression analysis was used to analyze the risk factors of hypertension. RESULTS: Complete data were obtained in 2036 residents. The hypertension prevalence rate was 11.6% (237/2036) [12.5% (110/883) for male, 11.0% (127/1153) for female], adjusted prevalence rate was 10.7% (11.3% for male, 10.4% for female) based on the population of Guangxi in 2010. Hypertension awareness rate was 36.3% (86/237) , therapy rate was 22.8% (54/237) , and control rate was 11.0% (26/237) . Multivariate logistic regression analysis showed that age (OR = 1.06, 95%CI:1.05-1.08, P < 0.01), alcohol drinking habit (OR = 1.92, 95%CI:1.25-2.95, P < 0.01), high salt diet(OR = 1.48, 95%CI:1.04-2.10, P < 0.05), diabetes(OR = 7.03, 95%CI:1.94-25.44, P < 0.01), obesity(OR = 1.20, 95%CI: 1.15-1.25, P < 0.01) and hypertriglyceridemia(OR = 1.12, 95%CI:1.03-1.22, P < 0.01) were risk factors for hypertension in this cohort. CONCLUSIONS: Prevalence rate is slightly lower in adult of the Guangxi Zhuang-rural areas than national or Guangxi Zhuang Autonomous Region levels, but hypertension awareness, therapy and control rates in this cohort are not satisfactory. Targeted strategies are needed to improve the prevention and therapy of hypertension in this region.

High level of H3K4 tri-methylation modification predicts poor prognosis in esophageal cancer.

Objectives: An increase in the trimethylation of lysine 4 of histone 3 (H3K4me3) has been reported to be involved in the development of several types of tumors. However, the level and role of H3K4me3 in human esophageal cancer (HEC) remain unknown. Here, we assessed the role and clinical significance of H3K4me3 in HEC. Methods: The level of H3K4me3 was determined in 15 pairs of HEC and paracancerous tissues by Western blotting. A tissue microarray including samples from 100 HEC patients was analyzed by immunohistochemistry to determine the relationship between the level of H3K4me3 and the clinicopathological features of HEC patients. Then, the levels of H3K4me3 in HEC cells were elevated via knockdown of inhibitor of growth family member 4(Ing4) expression. Finally, the prognostic significance of H3K4me3 levels in HEC patients was further analyzed. Results: We found that H3K4me3 levels were frequently elevated in HEC tissues compared with adjacent esophageal tissues, and elevated H3K4me3 was significantly associated with poor tumor differentiation (p =1.39×10-5) and advanced tumor stage (p=8.5×10-5). After Ing4 knockdown in HEC cells, we found that the cell proliferation, metastasis, invasion and colony formation abilities were enhanced compared to those in the control cells. Notably, we found that HEC patients with a high level of H3K4me3 exhibited an unfavorable 5-year survival rate compared to those with a low level of H3K4me3 (p=6.8×10-5). The univariate analysis showed that the tumor differentiation, TNM stage, and H3K4me3 level were predictors of the overall survival rate of HEC patients. In the multivariate analysis, tumor stage (p=0.015) and H3K4me3 level (p=0.034) were revealed to be independent parameters for predicting the prognosis of HEC patients. Conclusions: Thus, high levels of H3K4me3 may be used as a meaningful biomarker for HEC prognosis evaluation.

Long non-coding RNA PSMA3-AS1 promotes malignant phenotypes of esophageal cancer by modulating the miR-101/EZH2 axis as a ceRNA.

BACKGROUNDS: Emerging evidences has demonstrated that dysregulation of long non-coding RNAs (lncRNAs) is critically involved in esophageal squamous cell carcinoma (ESCC) progression. However, the function of lncRNA PSMA3-AS1 in ESCC is unclear. Therefore, we aimed to explore the functions and potential mechanisms of PSMA3-AS1 in ESCC cells progression. RESULTS: Here, we found that PSMA3-AS1 expression was significantly up-regulated in ESCC tissues. Forced PSMA3-AS1 expression was correlated with tumor size, distant metastasis, and poor prognosis in ESCC patients. Functionally, PSMA3-AS1-overexpression promoted ESCC cells proliferation, invasion, and migration in vitro. Mechanistically, PSMA3-AS1 up-regulated EZH2 expression by competitively binding to miR-101. CONCLUSION: PSMA3-AS1 is significantly up-regulated in ESCC tissues, and the PSMA3-AS1/miR-101/EZH2 axis plays a critical role in ESCC progression. Taken together, our results may provide promising targets for ESCC therapy. METHODS: PSMA3-AS1 and miR-101 expression were explored using qRT-PCR in ESCC tissues and cell lines. Immunohistochemistry assays were carried out to analyze EZH2 (enhancer of zeste homolog) protein expression. RIP, dual-luciferase reporter, fluorescence in situ hybridization, and biotin pull-down assays were used to detect the interactions of PSMA3-AS1, miR-101 and EZH2. The biological functions of PSMA3-AS1 in PSMA3-AS1-altered cells were explored using CCK-8, colony formation, wound healing, and transwell assays in vitro.