Characterization of Androgen Receptor Complex Associated Protein (ARCAP) in hepatocellular carcinoma and liver.

BACKGROUND: Hepatocellular carcinoma (HCC) ranks many tasks in clinical oncology due to possibly developing a general tumor in men and, usually lead to malignant to death within years. Researches had reported about major factors for being HCC was male sex and HCC associated with cirrhosis in childhood was found more common in males than females. In certain mouse strains as studied, breeding with testosterone significantly increases the development of HCC. Furthermore, castration of male mice diminished the frequency of the development of liver tumors. Meanwhile male hepatitis B virus transgenic mice have a greater occurrence of HCC than females. METHODS: We apply degenerate priming PCR to observe the expression of various steroid receptors in livers. Yeast-two hybrid screening to search a novel RNA fragment helps to find a new full-length gene by RACE experiment. RT-PCR is applied to detect various expressions in tissues and cell lines. In situ hybridization detects DNA in Chromosome mapping. GFP-constructs transfection proves the gene localization in cells. Immunoprecipitation pulldown assay verifies protein interaction. Gene transfection followed with luciferase assay demonstrates the interaction of genes within cellular signaling. Genomic alignment analysis for observing sequences data perform from NCBI database website (http://www.ncbi.nim.nih.gov/genebank/). RESULTS: The androgen receptor (AR) expression level is found at the highest level among the steroid receptors families detected in liver tumors. By yeast-two hybrid screening, we cloned an Androgen Receptor Complex Associated Protein (ARCAP), of 95 Kd in molecular weight and its cDNA. ARCAP locates at Chromosome 1. Our findings indicate ARCAP is highly expressed in hepatoma cell lines and liver tumors and their adjacent tumors as observed. Yeast two-hybrid assay and in vitro immunoprecipitation assays demonstrated an interaction between AR and ARCAP. CONCLUSION: We aim to search for different types and levels of steroid receptors expressed within human HCCs and in the adjacent liver tissues. To verify possible molecular mechanisms by which AR might affect hepatoma cells, we had characterized a novel protein ARCAP which functions as a coregulator to interact with AR within liver. The ligand-dependent AR with its cofactor, ARCAP, can induce a signal cascade by transactivation.

Frontier review of the roles of exosomes in osteoarthritis.

Osteoarthritis (OA) is a common degenerative disease; however, its exact pathophysiology and early diagnosis are still a challenge. Growing attention to the exosomes may inspire innovations that would make the current management of OA more effective. The exosomes in synovial fluid are relatively stable, and they can be easily isolated by the relatively noninvasive procedure of liquid biopsy to provide diagnostic and monitoring value. Some miRNAs (miR-504, miR-146a, miR-26a, miR-200c, and miR-210) have been known to be secreted in exosomes of OA patients. On the other hand, intraarticular injection of platelet-rich plasma (PRP) is becoming a popular therapy for OA patients. PRP is also a source of exosomes and their numerous contents. It is evident from the literature that PRP-derived exosomes can induce chondrogenic gene expression in OA chondrocytes. Here, we review the latest findings on the roles of exosomes in OA with the emphasis on PRP-derived exosomes and their potential applications for treating OA.

A PRISMA-compliant meta-analysis of apolipoprotein C3 polymorphisms and nonalcoholic fatty liver disease.

BACKGROUND: The relationship between apolipoprotein C3 (APOC3) gene polymorphisms and nonalcoholic fatty liver disease (NAFLD) risk has been investigated in many studies, with inconclusive findings. This meta-analysis evaluated the effect of APOC3 promoter region polymorphisms (-455T/C and -482C/T) on NAFLD susceptibility. METHODS: A comprehensive search of eligible studies up to October 2020 was performed on Medline, Embase, Web of Science, and Google Scholar databases. No restriction was imposed on language, publication date, or publication status. Odds ratios (ORs) with their 95% confidence intervals (CIs) were calculated to assess the combined effect sizes. The levels of heterogeneity, sensitivity, subgroup, and publication bias were analyzed subsequently. RESULTS: This meta-analysis included eight studies, consisting of 1,511 patients with NAFLD and 1,900 controls fulfilling the inclusion criteria and exclusion criteria. The pooled analysis showed significant associations between APOC3 -455T/C polymorphism and NAFLD risk in allelic (OR = 1.33; 95% CI = 1.05-1.67), dominant (OR = 1.34; 95% CI = 1.04-1.72), and recessive (OR = 1.60; 95% CI = 1.06-2.40) models. Ethnicity-based stratification showed that -455T/C polymorphism was significantly associated with NAFLD risk in the non-Asian but not in the Asian population. No association was evident between -482C/T polymorphism and NAFLD risk. CONCLUSION: Our findings suggest that APOC3 promoter region polymorphism -455T/C may be associated with NAFLD risk in the non-Asian but not in the Asian population. Additional studies with other functional polymorphisms are needed to discover APOC3 gene effects on NAFLD.

Pandemic analysis of infection and death correlated with genomic open reading frame 10 mutation in severe acute respiratory syndrome coronavirus 2 victims.

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues the pandemic spread of the coronavirus disease 2019 (COVID-19), over 60 million people confirmed infected and at least 1.8 million dead. One of the most known features of this RNA virus is its easiness to be mutated. In late 2020, almost no region of this SARS-CoV-2 genome can be found completely conserved within the original Wuhan coronavirus. Any information of the SARS-CoV-2 variants emerged through as time being will be evaluated for diagnosis, treatment, and prevention of COVID-19. METHODS: We extracted more than two million data of SARS-CoV-2 infected patients from the open COVID-19 dashboard. The sequences of the 38-amino acid putative open reading frame 10 (Orf10) protein within infected patients were gathered output through from National Center for Biotechnology Information and the mutation rates in each position were analyzed and presented in each month of 2020. The mutation rates of A8 and V30 within Orf10 are displayed in selected counties: United States, India, German, and Japan. RESULTS: The numbers of COVID-19 patients are correlated to the death numbers, but not with the death rates (stable and <3%). The amino acid positions locating at A8(F/G/L), I13, and V30(L) within the Orf10 sequence stay the highest mutation rate; N5, N25, and N36 rank at the lowest one. A8F expressed highly dominant in Japan (over 80%) and German (around 40%) coming to the end of 2020, but no significant finding in other countries. CONCLUSION: The results demonstrate via mutation analysis of Orf10 can be further combined with advanced tools such as molecular simulation, artificial intelligence, and biosensors that can practically revealed for protein interactions and thus to imply the authentic Orf10 function of SARS-CoV-2 in the future.