scholarly journals Adiponectin accounts for gender differences in hepatocellular carcinoma incidence

2019 ◽  
Vol 216 (5) ◽  
pp. 1108-1119 ◽  
Author(s):  
Elisa Manieri ◽  
Leticia Herrera-Melle ◽  
Alfonso Mora ◽  
Antonia Tomás-Loba ◽  
Luis Leiva-Vega ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Adipose Tissue ◽  
Liver Cancer ◽  
Cancer Therapeutics ◽  
Cancer Development ◽  
Cancer Type ◽  
Cancer Cell Proliferation ◽  
Amp Activated Protein Kinase ◽  
Common Cancer Type ◽  
Insight Into

Hepatocellular carcinoma (HCC) is the sixth most common cancer type and the fourth leading cause of cancer-related death. This cancer appears with higher incidence in men and during obesity; however, the specific mechanisms underlying this correlation are unknown. Adipose tissue, a key organ in metabolic syndrome, shows evident gender disparities in the production of adipokines. Levels of the important adipokine adiponectin decrease in men during puberty, as well as in the obese state. Here, we show that this decrease in adiponectin levels is responsible for the increased liver cancer risk in males. We found that testosterone activates the protein JNK in mouse and human adipocytes. JNK-mediated inhibition of adiponectin secretion increases liver cancer cell proliferation, since adiponectin protects against liver cancer development through the activation of AMP-activated protein kinase (AMPK) and p38α. This study provides insight into adipose tissue to liver crosstalk and its gender relation during cancer development, having the potential to guide strategies for new cancer therapeutics.

scholarly journals Association of lncRNA H19 Gene Polymorphisms with the Occurrence of Hepatocellular Carcinoma

Genes ◽  
2019 ◽  
Vol 10 (7) ◽  
pp. 506 ◽  
Author(s):  
Edie-Rosmin Wu ◽  
Ying-Erh Chou ◽  
Yu-Fan Liu ◽  
Kuan-Chun Hsueh ◽  
Hsiang-Lin Lee ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cancer ◽  
Gene Polymorphisms ◽  
Primary Liver Cancer ◽  
Common Type ◽  
Cancer Development ◽  
Inhibitory Effects ◽  
Non Coding Rna ◽  
H19 Gene ◽  
Long Non Coding Rna

Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer, whose diversified occurrence worldwide indicates a connection between genetic variations among individuals and the predisposition to such neoplasms. Mounting evidence has demonstrated that long non-coding RNA (lncRNA) H19 can have both promotive and inhibitory effects on cancer development, revealing a dual role in tumorigenesis. In this study, the link of H19 gene polymorphisms to hepatocarcinogenesis was assessed between 359 HCC patients and 1190 cancer-free subjects. We found that heterozygotes for the minor allele of H19 rs2839698 (T) and rs3741219 (G) were more inclined to develop HCC (OR, 1.291; 95% CI, 1.003–1.661; p = 0.047, and OR, 1.361; 95% CI, 1.054–1.758; p = 0.018, respectively), whereas homozygotes for the polymorphic allele of rs2107425 (TT) were correlated with a decreased risk of HCC (OR, 0.606; 95% CI, 0.410–0.895; p = 0.012). Moreover, patients who bear at least one variant allele (heterozygote or homozygote) of rs3024270 were less prone to develop late-stage tumors (for stage III/IV; OR, 0.566; 95% CI, 0.342–0.937; p = 0.027). In addition, carriers of a particular haplotype of three H19 SNPs tested were more susceptible to HCC. In conclusion, our results indicate an association between H19 gene polymorphisms and the incidence and progression of liver cancer.

Hepatocellular carcinoma: molecular interactions between hepatitis C virus and p53 in hepatocarcinogenesis

2003 ◽  
Vol 5 (28) ◽  
pp. 1-16 ◽  
Author(s):  
Mónica Anzola ◽  
Juan José Burgos
Keyword(s):  
Hepatocellular Carcinoma ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Cancer Type ◽  
Crucial Importance ◽  
Hepatitis Viruses ◽  
Common Cancer ◽  
Correct Function ◽  
P53 Tumour Suppressor Gene ◽  
Common Cancer Type

Hepatocellular carcinoma (HCC) is the most important primary hepatic cancer and is a common cancer type worldwide. Many aetiological factors have been related to HCC development, such as liver cirrhosis, hepatitis viruses and alcohol consumption. Inactivation of the p53 tumour suppressor gene is one of the most common abnormalities in many tumours, including HCC. p53 is of crucial importance for the regulation of the cell cycle and the maintenance of genomic integrity. In HCC, hepatitis B and C virus (HBV and HCV) effect carcinogenic pathways, independently leading to anomalies in p53 function. Several authors have reported that some HCV proteins, such as the core, NS5A and NS3 proteins, interact with p53 and prevent its correct function. The mechanisms of action of these HCV proteins in relation to p53 are not completely clear, but they might cause its cytoplasmic retention or accumulation in the perinuclear region where the protein is not functional. The identification of the interactions between p53 and HCV proteins is of great importance for therapeutic strategies aimed at reducing the chronicity and/or carcinogenicity of the virus.

scholarly journals Sphingolipids in Non-Alcoholic Fatty Liver Disease and Hepatocellular Carcinoma: Ceramide Turnover

2019 ◽  
Vol 21 (1) ◽  
pp. 40 ◽  
Author(s):  
Jorge Simon ◽  
Alberto Ouro ◽  
Lolia Ala-Ibanibo ◽  
Natalia Presa ◽  
Teresa Cardoso Delgado ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Cancer Type ◽  
Alcoholic Fatty Liver ◽  
Ceramide Content ◽  
Common Cancer Type ◽  
Support Tumor Growth ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) has emerged as one of the main causes of chronic liver disease worldwide. NAFLD comprises a group of conditions characterized by the accumulation of hepatic lipids that can eventually lead to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC), the fifth most common cancer type with a poor survival rate. In this context, several works have pointed out perturbations in lipid metabolism and, particularly, changes in bioactive sphingolipids, as a hallmark of NAFLD and derived HCC. In the present work, we have reviewed existing literature about sphingolipids and the development of NAFLD and NAFLD-derived HCC. During metabolic syndrome, considered a risk factor for steatosis development, an increase in ceramide and sphigosine-1-phosphate (S1P) have been reported. Likewise, other reports have highlighted that increased sphingomyelin and ceramide content is observed during steatosis and NASH. Ceramide also plays a role in liver fibrosis and cirrhosis, acting synergistically with S1P. Finally, during HCC, metabolic fluxes are redirected to reduce cellular ceramide levels whilst increasing S1P to support tumor growth.

scholarly journals Olfm4 Is Highly Expressed in HCC Patients and as a Biomarker and Therapeutic Target for HCC

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Yulong Wei ◽  
Qingzhu Song ◽  
Fenglan Zhang ◽  
Tian Yuan
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Liver Cancer ◽  
Cancer Cell Proliferation ◽  
Mrna Expression Level ◽  
Healthy Individuals ◽  
Predictive Capacity ◽  
Messenger Ribonucleic Acid ◽  
Novel Drugs ◽  
Key Genes

Hepatocellular carcinoma (HCC) is one of the primary types of cancer that claims many lives worldwide, and its incidence continues to increase. Conventional therapies against liver cancer are inadequate, and the pathogenesis of HCC remains unclear. Thus, not only are more effective therapies to treat HCC required but also identification of the key genes involved in its pathogenesis is important for developing such therapies. This study found that olfactomedin 4 (OLFM4) level is higher in HCC patients than in healthy individuals. Furthermore, HCC patients also have higher messenger ribonucleic acid (mRNA) expression level in HCC tissues than in liver paracancerous tissues. OLFM4 has high predictive capacity as a biomarker for HCC and closely correlates to tumor size. It is confirmed that OLFM4 contributes to cancer cell proliferation, and HIF1α is involved in this process. Thus, the OLFM4/HIF-1α axis might be a target signaling pathway for developing novel drugs to treat HCC.

FAT10: Function and Relationship with Cancer

2020 ◽  
Vol 13 (3) ◽  
pp. 182-191 ◽  
Author(s):  
Senfeng Xiang ◽  
Xuejing Shao ◽  
Ji Cao ◽  
Bo Yang ◽  
Qiaojun He ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Hepatocellular Carcinoma ◽  
Current Knowledge ◽  
Therapeutic Strategies ◽  
Functional Change ◽  
Cancer Development ◽  
Cancer Cell Proliferation ◽  
Biological Functions ◽  
Carcinoma Breast ◽  
Cancer Types

Posttranslational protein modifications are known to be extensively involved in cancer, and a growing number of studies have revealed that the ubiquitin-like modifier FAT10 is directly involved in cancer development. FAT10 was found to be highly upregulated in various cancer types, such as glioma, hepatocellular carcinoma, breast cancer and gastrointestinal cancer. Protein FAT10ylation and interactions with FAT10 lead to the functional change of proteins, including proteasomal degradation, subcellular delocalization and stabilization, eventually having significant effects on cancer cell proliferation, invasion, metastasis and even tumorigenesis. In this review, we summarized the current knowledge on FAT10 and discussed its biological functions in cancer, as well as potential therapeutic strategies based on the FAT10 pathway.

A curcumin derivative, WZ35, suppresses hepatocellular cancer cell growthviadownregulating YAP-mediated autophagy

2019 ◽  
Vol 10 (6) ◽  
pp. 3748-3757 ◽  
Author(s):  
Lihua Wang ◽  
Zheng Zhu ◽  
Lei Han ◽  
Liqian Zhao ◽  
Jialei Weng ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cancer Therapy ◽  
Liver Cancer ◽  
Hepatocellular Cancer ◽  
Cancer Type ◽  
Common Cancer ◽  
The World ◽  
Anti Tumor Activity ◽  
Common Cancer Type ◽  
Curcumin Derivative

HCC is a common cancer type in the world. Here, we found WZ35, a novel derivative of curcumin, could notably suppress HCC cell growthviainhibiting YAP controlled autophagy, highlighting the potent anti-tumor activity of WZ35 in liver cancer therapy.

CD5L is upregulated in hepatocellular carcinoma and promotes liver cancer cell proliferation and antiapoptotic responses by binding to HSPA5 (GRP78)

2018 ◽  
Vol 32 (7) ◽  
pp. 3878-3891 ◽  
Author(s):  
Gemma Aran ◽  
Lucía Sanjurjo ◽  
Cristina Barcena ◽  
Marina Simon‐Coma ◽  
Érica Téllez ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Liver Cancer ◽  
Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Liver Cancer Cell
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