The clinical significance of long non-coding RNAs MALAT1 and CASC2 in the diagnosis of HCV-related hepatocellular carcinoma.

BACKGROUND: Globally, hepatocellular carcinoma (HCC) is the second most common cause of cancer-related death due to a lack of early predictive and/or diagnostic tools. Thus, research for a new biomarker is important. LncRNAs play a functional role in target gene regulation and their deregulation is associated with several pathological conditions including HCC. OBJECTIVE: This study aimed to explore the diagnostic potential of two LncRNAs MALAT1 and CASC2 in HCC compared to the routinely used diagnostic biomarker. MATERIALS AND METHODS: The current study is a case-control study carried out at Fayoum University Hospital and conducted on 89 individuals. The study included three groups of 36 HCC patients on top of HCV(HCC/HCV), 33 HCV patients, and 20 healthy volunteers as a control group. All study subjects were subjected to radiological examinations. The determination of CBC was performed by the automated counter and liver function tests by the enzymatic method were performed. In addition, HCV RNA quantification and the expression level of two LncRNAs (MALAT1 and CASC2) were performed by qRT-PCR. RESULTS: The results revealed a statistically significant difference between study groups regarding liver function tests with a higher mean in HCC/HCV group. Also, serum MALAT1 significantly up-regulated in HCV (11.2±2.8) and HCC/HCV (4.56±1.4) compared to the control group. Besides, serum CASC2 levels in the HCV group were significantly upregulated (14.9±3.6), while, downregulated in the HCC group (0.16± 0.03). Furthermore, The ROC analysis for diagnostic efficacy parameters indicated that CASC2 has higher accuracy (94.6%) and sensitivity (97.2%) for HCC diagnosis than AFP with an accuracy of (90.9%), sensitivity (69.4%), and MALAT1 showed an accuracy of (56.9%), sensitivity (72.2%). CONCLUSION: Our study results indicated that CASC2 is a promising biomarker and is considered better and could help in HCC diagnosis on top of HCV than MALAT1 and the routine biomarker AFP.

Resveratrol and Dulaglutide ameliorate adiposity and liver dysfunction in rats with diet-induced metabolic syndrome: Role of SIRT-1 / adipokines / PPARγ and IGF-1.

BACKGROUND: Adiposity and non-alcoholic fatty liver disease (NAFLD) are common characteristics of metabolic syndrome (MS). Understanding the underlying pathogenesis is crucial for the development of new remedies. Resveratrol controls obesity and glycemic disorders in patients with MS. OBJECTIVES: This study aimed to evaluate the effect of resveratrol and dulaglutide on adipose tissues and liver in rats with MS, declaring their possible mechanisms. METHODS: Rats allocated as Control, MS (induced by a high fat/ high sucrose diet for eight weeks), MS + Resveratrol (30 mg/kg/day orally), and MS + Dulaglutide (0.6 mg/kg twice weekly SC); drugs administration was in the last four weeks. Serum biochemical measurements were done. Liver and visceral fat were processed for biochemistry, histopathology, and immunohistochemistry. RESULTS: MS results demonstrated significantly increased systolic and diastolic blood pressure, anthropometric measurements, serum levels of alanine aminotransferase (ALT), glycemic indices, and lipids with decreased HDL-C. Tissue levels of leptin, malondialdehyde (MDA), and TNF-α reactivity significantly increased. Expression of adiponectin, PPARγ, and insulin growth factor-1 (IGF-1) decreased. Also, Western blotting mRNA gene expression of liver SIRT-1 was down-regulated. Resveratrol and dulaglutide significantly and effectively reversed MS complexity, ameliorating all findings, particularly NAFLD and adiposity-induced inflammation. Resveratrol significantly appears superior to dulaglutide regarding the effects on hemodynamics, lipids, adipokines, IGF-1 levels, and adipocyte size. Parallel, dulaglutide has more influence on glycemic control. CONCLUSION: Protective effects of the drugs may be through correlations between SIRT-1/adipokines/IGF-1 and PPARγ, improving the cross-talk between insulin resistance, obesity markers, liver dysfunction, and TNF-α. Promising multi-beneficial therapies of resveratrol or dulaglutide in MS are recommended clinically for this purpose. Showing the Experimental Design.

Correlation between LincR-Gng2-5'and LincR-Epas1-3'as with the severity of multiple sclerosis in Egyptian patients.

Introduction: Multiple sclerosis (MS) is an immune-mediated disorder. Long noncoding RNAs (lncRNAs, LncR, Linc RNA) have role in many autoimmune and inflammatory disorders, including MS. LincR-Gng2-5 AS locus in T helper 1 cell (TH1) and LincR-Epas1-3AS in T helper 2 cell (TH2) cell were located in a genomic region rich in genes code for proteins with immune regulatory function. Our aim was to evaluate the LincR-Gng2-5' and LincR-Epas1-3'AS fold change in blood of MS patients versus healthy controls and correlate it with disease severity, assessed based on Expanded Disability Status Scale (EDSS).Material and Methods: Sixty MS patients 42 relapsing remitting (RR, RRMS), 18 Secondary progressive (SP, SPMS) and sixty controls (age-matched and sex-matched) were studied. Blood of patients and control group undergone the investigation of LincR-Gng2-5' and LincR-Epas1-3'AS fold change by real-time PCR. Fold change >2 and p < .05 represent significant result.Results: LincR-Gng2-5' was significantly upregulated in MS patients with mean fold change (2.559) and (p = .03). Meanwhile, LincR-Epas1-3'AS levels were significantly downregulated with mean fold change (0.5964) and (p < .004). Patients with SP showed a significantly higher level of LincR-Gng2-5-fold change (3.71 ± 0.7) than that of RR (1.33 ± 0.3). LincR-Epas1-3'AS was markedly reduced among SP (0.43 ± 0.2) than that of RR (0.66 ± 0.1) but with no significant difference. As regards disease severity (EDSS); there was a significant positive correlation with LincR-Gng2-5 and negative correlation with LincR-Epas1-3'AS. LincR- Gng2-5and LincR-Epas1-3'AS, both are dysregulated in MS patient suggesting a role in disease pathogenesis.Conclusion: LincR-Gng2-5 AS and LincR-Epas1-3'AS fold change are correlated to MS severity (EDSS).