BackgroundGrowing evidence has implicated the important role of the long non-coding RNAs (lncRNAs) in gastric cancer progression. In this study, we examined the expression of lncRNA zinc finger E-box-binding homeobox 2 antisense RNA 1 (ZEB2-AS1) in gastric cancer tissues and elucidated the molecular mechanisms underlying ZEB2-AS1-mediated gastric cancer progression.MethodsQuantitative real-time PCR measured the gene expression level; CCK-8, colony formation and cell invasion assays determined gastric cancer cell proliferation, growth and invasion, respectively; the xenograft nude mice model was used to determine in vivo tumor growth; Bioinformatics analysis and luciferase reporter assay determined the downstream targets of ZEB2-AS1 and miR-143-5p. The expression of ZEB2-AS1 was upregulated in gastric cancer cell lines.ResultsKnockdown of ZEB2-AS1 suppressed gastric cancer cell proliferation, growth and invasion, and also suppressed in vivo tumor growth in the nude mice. Overexpression of ZEB2-AS1 potentiated gastric cancer cell proliferation, growth and invasion. Bioinformatics analysis and luciferase reporter assay showed that miR-143-5p was a direct target of ZEB2-AS1 and was negatively regulated by ZEB2-AS1. Furthermore, hypoxia-inducible factor-1α (HIF-1α) was found to be a target of miR-143-5p and was negatively regulated by miR-143-5p. The rescue in vitro assays showed that the effects of ZEB2-AS1 overexpression on gastric cancer cell proliferation, growth and invasion was mediated via miR-143-5p/HIF-1α. ZEB2-AS1 and HIF-1α was upregulated in gastric cancer tissues, while miR-143-5p was down-regulated; and ZEB2-AS1 expression level was inversely correlated with miR-143-5p expression level, and positively correlated with HIF-1α mRNA expression level; while miR-143-5p expression level was inversely correlated with HIF-1α expression level. High ZEB2-AS1 expression level was correlated with poor differentiation, lymph node metastasis and distant metastasis.ConclusionCollectively, our results indicated that ZEB2-AS1 was up-regulated in gastric cancer tissues and cells and promoted cell proliferation and metastasis through miR-143-5p/HIF-1α pathway, which may provide a promising target for treatment of gastric cancer.

GERD is highly prevalent in adult in Urumqi, especially in Uygur. Male, civil servant, smoking, strong tea, alcohol drinking, meat diet and BMI are risk factors correlated to GERD.

Aberrant activation of Wnt/β-catenin signaling is observed in >90% of colorectal cancer cases. microRNAs (miRNAs) regulate the expression of key genes in Wnt/β-catenin signaling. As a result, abnormal expression of miRNAs regulates the activation of Wnt/β-catenin signaling in several types of cancer. In the current study, it was demonstrated that miR-501-3p was overexpressed in colorectal tumor tissues compared to the adjacent normal tissues. Downregulation of miR-501-3p inhibited cell proliferation and sphere formation, while it induced cell cycle arrest at the G1 phase in colorectal cancer cells. Bioinformatics analysis results predicted that adenomatous polyposis coli (APC), a negative regulator of Wnt/β-catenin signaling, was a potential target gene of miR-501-3p. Inhibition of miR-501-3p increased APC expression in colorectal cancer cells. Additionally, β-catenin was destabilized following miR-501-3p inhibition; immunofluorescence analysis revealed that β-catenin translocated from nucleus to cytoplasm. In addition, cyclin D1 and c-Myc, two well-characterized target genes of Wnt/β-catenin signaling, were downregulated following miR-501-3p inhibition. Transfection of APC small interfering RNA re-activated β-catenin and stimulated the expression of cyclin D1 and c-Myc. Furthermore, silencing of APC reversed the miR-501-3p inhibitor-induced cell cycle disruption, and the inhibition of cell proliferation and sphere formation in colorectal cancer cells. In conclusion, the present study identified miR-501-3p as a novel regulator of Wnt/β-catenin signaling in colorectal cancer cells via targeting APC, suggesting that miR-501-3p may act as a novel oncogenic miRNA in colorectal cancer.

Hepatocellular carcinoma (Hcc) was the third most common cause of cancer-associated mortality in china in 2015. early detection of Hcc and hepatic cirrhosis (Hc) can serve a crucial role in the prevention and therapeutic intervention of these diseases. current early detection methods rely on less sensitive imaging modalities compared with the pathological examination. in the present study, a total of 64 patients with Hcc, 44 patients with Hc and 298 individuals with no evidence of disease (ned) were recruited, and the ability of methylated septin 9 (mSePT9) in diagnosing Hcc and Hc was investigated. The overall detection sensitivity of mSePT9 for Hcc and Hc was 76.7 and 34.1%, respectively, with a 95.9% specificity (HCC vs. NED). The sensitivity of mSEPT9 for HCC was significantly higher than that of α-fetoprotein (aFP; χ 2 test; 56.7%; P<0.05). The areas under the curve from the receiver operating characteristic curves of mSePT9 for detection of Hcc vs. ned, Hc vs. ned and Hcc vs. Hc were 0.85, 0.77 and 0.66, respectively, while those of aFP for the same groups were 0.80, 0.55 and 0.77, respectively. although both markers exhibited stage-dependent sensitivity in Hcc, mSePT9 was demonstrated to be more sensitive than aFP. The net reclassification index of mSPeT9 for Hcc detection was 0.212 compared with aFP, suggesting an improved diagnostic performance of mSePT9 compared with aFP. in addition, Kaplan-Meier survival analysis revealed that mSePT9 is able to predict the long-term survival of patients with Hcc. Further analysis suggested that patients >50 years of age exhibited higher sensitivity compared with those <50 years old in mSEPT9, but not in AFP. No significant difference in sensitivity was observed between compensated and decompensated patients with Hc, and in patients with Hc with a history of hepatitis B or c virus infection. no difference was observed between male and female subjects in the Hc and Hcc groups for mSePT9 and aFP. in conclusion, mSePT9 may detect Hcc with an overall improved sensitivity compared with aFP and may help in predicting the long-term survival of patients with Hcc. The present clinical study was retrospectively registered to the chinese clinical Trial registry on april 4, 2020 (http://www.chictr.org.cn/enindex. aspx; registration no. chicTr2000031547).

Objectives Dysglycemia promotes the occurrence of fatty liver disease (FLD). However, the process is unclear. This study aimed to analyze the median time-to-onset, cumulative prevalence and influencing factors for the occurrence of FLD in people undergoing routine screening and evaluation. Methods Data from Karamay Central Hospital (September 2008–April 2017) were analyzed. Survival analysis was performed to calculate the median time and cumulative prevalence of FLD associated with normal and elevated fasting blood glucose (FBG) levels. Cox proportional hazards model was used to determine risk factors. Results A total of 31,154 participants were included in the two cohorts of this study, including 15,763 men. The mean age was 41.1 ± 12.2 years. There were 2230 patients (1725 male) in the elevated FBG group, the median age was 53 years (range 21–85 years), the median time-to-onset of FLD was 5.2 years. The incidence of FLD was 121/1000 person-years, and the 1-, 3-, 5-, and 7-year prevalence rates were 4%, 30%, 49%, and 64%, respectively. The normal FBG group included 28,924 participants (14,038 male), the median age was 40 years (range 17–87 years), and the corresponding values were as follows: 8.3 years, 66/1000 person-years, and 3%, 16%, 28%, and 41%, respectively. The Cox proportional hazards analysis revealed that age, blood pressure, FBG, body mass index and triglycerides were independent influencing factors for FLD in individuals (P < 0.05). Conclusions Elevated FBG levels increase the risk of FLD and should be treated promptly.