scholarly journals Crosstalk between microRNA-122 and FOX family genes in HepG2 cells

2016 ◽  
Vol 242 (4) ◽  
pp. 436-440 ◽  
Author(s):  
Subodh Kumar ◽  
Ankita Batra ◽  
Shruthi Kanthaje ◽  
Sujata Ghosh ◽  
Anuradha Chakraborti
Keyword(s):  
Hepatocellular Carcinoma ◽  
Molecular Interactions ◽  
In Silico ◽  
Hepg2 Cells ◽  
Molecular Mechanisms ◽  
In Silico Analysis ◽  
Transcript Level ◽  
Forkhead Box ◽  
Fox Genes ◽  
Silico Analysis

MicroRNA-122 (miR-122) is liver specific and plays an important role in physiology as well as diseases including hepatocellular carcinoma (HCC). Downregulation of miR-122 in HCC modulates apoptosis. Similarly, the putative targets of miR-122, the forkhead box (FOX) family genes also play an important role in the regulation of apoptosis. Hence, an interplay between miR-122 and FOX family genes has been explored in this study. Initially, an augmentation of apoptosis was noticed in HepG2 cells after transfection with miR-122. Further, the predicted miR-122 targets, the FOX family genes ( FOXM1b, FOXP1, and FOXO4) were selected via in silico analysis based on their role in apoptosis. We checked the expression of all these genes at transcript level after the transfection of miR-122 and found that the relative expression of FOXP1 and FOXM1b was significantly downregulated (p < 0.005) and that of FOXO4 was upregulated (p < 0.005). Thus, the finding indicates deregulation of these FOX genes as a result of miR-122 augmentation might be involved in the modulation of apoptosis. Impact Statement Here, we have investigated the crosstalk between microRNA-122 (miR-122) and selective FOX family genes in HepG2 cells. miR-122 is a prominent miRNA in liver and has been reported to be downregulated in hepatocellular carcinoma (HCC). It has been speculated that diminished level of miR-122 during HCC might be one of the reasons for tumor progression. However, the exact molecular interactions are not clear yet. This study unravels one of the molecular mechanisms of miR-122 through which it might impact the tumorigenesis of HCC.

scholarly journals The pattern of gene copy number alteration (CNAs) in hepatocellular carcinoma: an in silico analysis

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Arman Shahrisa ◽  
Maryam Tahmasebi-Birgani ◽  
Hossein Ansari ◽  
Zahra Mohammadi ◽  
Vinicio Carloni ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
In Silico ◽  
Copy Number ◽  
Copy Number Alteration ◽  
Gene Copy Number ◽  
In Silico Analysis ◽  
Gene Copy ◽  
Sequencing Data ◽  
Silico Analysis

Abstract Background Hepatocellular carcinoma (HCC) is the most common type of liver cancer that occurs predominantly in patients with previous liver conditions. In the absence of an ideal screening modality, HCC is usually diagnosed at an advanced stage. Recent studies show that loss or gain of genomic materials can activate the oncogenes or inactivate the tumor suppressor genes to predispose cells toward carcinogenesis. Here, we evaluated both the copy number alteration (CNA) and RNA sequencing data of 361 HCC samples in order to locate the frequently altered chromosomal regions and identify the affected genes. Results Our data show that the chr1q and chr8p are two hotspot regions for genomic amplifications and deletions respectively. Among the amplified genes, YY1AP1 (chr1q22) possessed the largest correlation between CNA and gene expression. Moreover, it showed a positive correlation between CNA and tumor grade. Regarding deleted genes, CHMP7 (chr8p21.3) possessed the largest correlation between CNA and gene expression. Protein products of both genes interact with other cellular proteins to carry out various functional roles. These include ASH1L, ZNF496, YY1, ZMYM4, CHMP4A, CHMP5, CHMP2A and CHMP3, some of which are well-known cancer-related genes. Conclusions Our in-silico analysis demonstrates the importance of copy number alterations in the pathology of HCC. These findings open a door for future studies that evaluate our results by performing additional experiments.

A report of rifampin-resistant leprosy from northern and eastern India: identification and in silico analysis of molecular interactions

2014 ◽  
Vol 204 (2) ◽  
pp. 193-203 ◽  
Author(s):  
Sundeep Chaitanya Vedithi ◽  
Mallika Lavania ◽  
Manoj Kumar ◽  
Punit Kaur ◽  
Ravindra P. Turankar ◽  
...  
Keyword(s):  
Molecular Interactions ◽  
In Silico ◽  
In Silico Analysis ◽  
Eastern India ◽  
Silico Analysis

In silico analysis of molecular interactions between HIV-1 glycoprotein gp120 and TNF receptors

2021 ◽  
pp. 104837
Author(s):  
Neyla Maria Pereira Alves ◽  
Ronald Rodrigues de Moura ◽  
Lucas Coêlho Bernardo ◽  
Almerinda Agrelli ◽  
Ana Sofia Lima Estevão de Oliveira ◽  
...  
Keyword(s):  
Molecular Interactions ◽  
In Silico ◽  
In Silico Analysis ◽  
Tnf Receptors ◽  
Glycoprotein Gp120 ◽  
Silico Analysis ◽  
Hiv 1

scholarly journals In silico analysis suggests disruption of interactions between HAMP from hepatocytes and SLC40A1 from macrophages in hepatocellular carcinoma

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Liang Hu ◽  
Chao Wu
Keyword(s):  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
In Silico ◽  
Large Scale ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
In Silico Analysis ◽  
Hepatocyte Proliferation ◽  
Upregulated Genes ◽  
Silico Analysis

Abstract Background Identification of factors associated with proliferation in the hepatocellular carcinoma (HCC) microenvironment aids in understanding the mechanisms of disease progression and provides druggable targets. Gene expression profiles of individual cells in HCC and para-carcinoma tissues can be effectively obtained using the single-cell RNA sequencing (scRNA-Seq) technique. Here, we aimed to identify proliferative hepatocytes from HCC and para-carcinoma tissues, detect differentially expressed genes between the two types of proliferative hepatocytes, and investigate their potential roles in aberrant proliferation. Results Two respective gene signatures for proliferative cells and hepatocytes were established and used to identify proliferative hepatocytes from HCC and para-carcinoma tissues based on scRNA-Seq data. Gene expression profiles between the two types of proliferative hepatocytes were compared. Overall, 40 genes were upregulated in proliferative hepatocytes from para-carcinoma tissue, whereas no upregulated genes were detected in those from HCC tissue. Twelve of the genes, including HAMP, were specifically expressed in the liver tissue. Based on previous reports, we found that HAMP modulates cell proliferation through interaction with its receptor SLC40A1. Comprehensive analysis of cells in HCC and para-carcinoma tissues revealed that: (1) HAMP is specifically expressed in hepatocytes and significantly downregulated in malignant hepatocytes; (2) a subset of macrophages expressing SLC40A1 and genes reacting to various infections is present in para-carcinoma but not in HCC tissue. We independently validated the findings with scRNA-Seq and large-scale tissue bulk RNA-Seq/microarray analyses. Conclusion HAMP was significantly downregulated in malignant hepatocytes. In addition, a subset of macrophages expressing SLC40A1 and genes reacting to various infections was absent in HCC tissue. These findings support the involvement of HAMP-SLC40A1 signaling in aberrant hepatocyte proliferation in the HCC microenvironment. The collective data from our in silico analysis provide novel insights into the mechanisms underlying HCC progression and require further validation with wet laboratory experiments.

scholarly journals The associations between Toll-like receptor 4 gene polymorphisms and hepatitis C virus infection: a systematic review and meta-analysis

2019 ◽  
Vol 39 (2) ◽  
Author(s):  
Narttaya Chaiwiang ◽  
Teera Poyomtip
Keyword(s):  
Hepatocellular Carcinoma ◽  
Systematic Review ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
In Silico ◽  
Meta Analysis ◽  
In Silico Analysis ◽  
Hcv Infection ◽  
Toll Like Receptor ◽  
Silico Analysis

Abstract Background and objective: The hepatitis C virus (HCV) is able to cause a life-threatening disease relating to lethal hepatocellular carcinoma. Previous, Toll-like receptor polymorphisms were proposed as promising biomarker for HCV-related hepatocellular carcinoma and disease progression. This study aimed to summarize the association of TLR4 polymorphisms and HCV infection through meta-analysis. Methods: We applied a systematic review and meta-analysis performed by using PubMed, EMBASE and Web of Science searches. The Modified Newcastle-Ottawa scale was used for quality assessment. The odd-ratio (OR) and 95% confidence interval (CI) were calculated to assess the association. In silico analysis was applied for proposing the function as microRNA (miRNA) of non-coding polymorphism. Finally, the miRNA target was predicted and annotated to suggest the possible relationship between polymorphism and HCV infection. Results: Our meta-analysis incorporated seven studies involving rs4986791, rs4986790 and rs2149356. No association exists between rs4986791 and HCV infection. However, the heterozygous model (AG vs GG) of rs4986790 significantly associates with HCV infection (OR = 0.33, 95% CI = 0.21–0.49, P<0.0001). Moreover, the rs2149356 TG genotype also associates with HCV infection in the over-dominant model (TG vs TT+TG: OR = 0.54, 95% CI = 0.40–0.75). In silico analysis of rs2149356G allele showed that this mutation is siRNA, which targets the set of genes, especially in the autophagy pathway. Conclusion: We demonstrated that rs4986790 and rs2149356 are associated with HCV infection.

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