WITHDRAWN: Anti-inflammatory role and mechanism of microRNA-92b-3p in the progression of hypoxic pulmonary hypertension.

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The long non-coding RNA SNHG4/microRNA-let-7e/KDM3A/p21 pathway is involved in the development of non-small cell lung cancer.

Non-small cell lung cancer (NSCLC) is a foremost cause of malignancy-associated mortality globally. Recent studies have emphasized long non-coding RNAs (lncRNAs) as important biomarkers with diagnostic and therapeutic potential in regard to NSCLC. This study aimed to elucidate the functional role of lncRNA small nucleolar RNA host gene 4 (SNHG4) in NSCLC. Initially, 50 paired cancerous and noncancerous tissues were obtained from NSCLC patients. Human NSCLC H1299 cells were assayed to evaluate viability, colony formation, invasion, migration, cycle arrest, and apoptosis via Cell Counting Kit-8 (CCK-8), plate clone formation, and transwell invasion assays, as well as a scratch test and flow cytometry. A dual-luciferase reporter gene assay was used to examine lncRNA SNHG4 binding with miR-let-7e and miR-let-7e binding with lysine demethylase 3A (KDM3A). H1299 cells were xenografted into nude mice. lncRNAs SNHG4 and KDM3A were both upregulated in NSCLC tissues. The knockdown of lncRNA SNHG4 or KDM3A inhibited H1299 cell viability, colony formation, invasion, migration, and cycle progression while inducing apoptosis. lncRNA SNHG4 was found to bind to miR-let-7e that negatively targeted KDM3A. KDM3A inhibited p53-K372me1, thus reducing p21 expression. The NSCLC development was inhibited by downregulating lncRNA SNHG4 in nude mice. Taken together, the key findings of the current study demonstrate a novel lncRNA SNHG4/let-7e/KDM3A/p21 axis in NSCLC, highlighting a promising therapeutic target for NSCLC.

Inhibited histone deacetylase 3 ameliorates myocardial ischemia-reperfusion injury in a rat model by elevating microRNA-19a-3p and reducing cyclin-dependent kinase 2.

OBJECTIVE: Over the years, the roles of microRNAs (miRNAs) and histone deacetylase 3 (HDAC3) in human diseases have been investigated. This study focused on the effect of miR-19a-3p and HDAC3 in myocardial ischemia-reperfusion (I/R) injury (MIRI) by targeting cyclin-dependent kinase 2 (CDK2). METHODS: The I/R rat models were established by coronary artery ligation, which were then treated with RGFP966 (an inhibitor of HDAC3), miR-19a-3p agomir or antagomir, or silenced CDK2 to explore their roles in the cardiac function, pathological changes of myocardial tissues, myocardial infarction area, inflammatory factors and oxidative stress factors in rats with MIRI. The expression of miR-19a-3p, HDAC3, and CDK2 was determined by RT-qPCR and western blot assay, and the interaction among which was also verified by online prediction, luciferase activity assay and ChIP assay. RESULTS: The results indicated that HDAC3 and CDK2 were upregulated while miR-19a-3p was downregulated in myocardial tissues of I/R rats. The inhibited HDAC3/CDK2 or elevated miR-19a-3p could promote cardiac function, attenuate pathological changes, inflammatory reaction, oxidative stress, myocardial infarction area and apoptosis of myocardial tissues. HDAC3 mediates miR-19a-3p and CDK2 is targeted by miR-19a-3p. CONCLUSION: Inhibited HDAC3 ameliorates MIRI in a rat model by elevating miR-19a-3p and reducing CDK2, which may contribute to the treatment of MIRI.

Roles of XRCC1/XPD/ERCC1 Polymorphisms in Predicting Prognosis of Hepatocellular Carcinoma in Patients Receiving Transcatheter Arterial Chemoembolization.

OBJECTIVE: To investigate the potential prognostic roles of polymorphisms in the X-ray repair cross-complementing group 1 (XPCC1), xeroderma pigmentosum group D (XPD) and excision repair cross-complementing group 1 (ERCC1) genes for patients with hepatocellular carcinoma (HCC) receiving transcatheter arterial chemoembolization (TACE). METHODS: Clinical data and blood samples from 308 HCC patients receiving TACE were collected between January 2010 and December 2013. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RLFP) analyses was used to determine the genotypes of the XPCC1 (rs25487), XPD (rs13181) and ERCC1 (rs11615) genes. The relationships between the genotypes and the efficacy of TACE treatment were analyzed. RESULTS: The XRCCI rs25487 polymorphism was associated with a favorable prognosis in HCC patients receiving TACE (p = 0.006), and patients carrying variant genotypes (A/A + G/A) were associated with significantly reduced risk of death compared with those with the wild genotype (G/G) (HR = 0.556; 95% CI = 0.354-0.874). These findings were supported by Kaplan-Meier survival curve analysis showing that median survival time for patients with A/A + G/A genotypes was significantly longer compared with those with the G/G genotype (11.2 month vs. 8.0 months; log rank p = 0.006). Stratified analyses revealed that A/A + G/A genotypes of XRCC1 rs25487 are associated with significantly reduced risk of death compared with the G/G genotype in patients grouped by tumor size, portal vein tumor thrombus (PVTT), alpha-fetoprotein (AFP) and TNM stage (all p < 0.05). The ERCC1 rs13181 and XPD rs11615 polymorphisms were not predictive of clinical outcome for HCC patients receiving TACE (both p > 0.05). CONCLUSION: The XRCC1 rs25487 polymorphisms are prognostic for HCC patients receiving TACE. The ERCC1 and XPD polymorphisms had no relationship to the clinical outcomes.