S100 family members: potential therapeutic target in patients with hepatocellular carcinoma

Zhang, Cai; Yao, Ru; Chen, Jie; Zou, Qiong; Zeng, Linghai

doi:10.1097/md.0000000000024135

Cited by 15 publications

(12 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…S100 proteins have been linked to the development of many cancers [ 40 , 46 ], including HCC. Deregulated mRNA expression of many S100 isoforms, i.e., S100P , S100A2 , S100A5 , S100A6 , S100A7 , S100A7A , S100A8 , S100A9 , S100A10 , S100A11 , S100A12 , S100A13 , S100A14 , S100G and S100Z , has indeed been associated with HCC in patients [ 144 ]. In addition, upregulation of several S100 isoforms, i.e., S100P , S100A2 , S100A6 , S100A8 , S100A9 , S100A10 , S100A11 , S100A13 and S100A14 , correlates with poor survival in patients [ 65 , 144 ].…”

Section: Implication Of S100 Proteins In the Occurrence Of Hccmentioning

confidence: 99%

S100 Proteins in Fatty Liver Disease and Hepatocellular Carcinoma

Delangre

Oppliger

Berkcan

et al. 2022

IJMS

View full text Add to dashboard Cite

Non-alcoholic fatty liver disease (NAFLD) is a highly prevalent and slow progressing hepatic pathology characterized by different stages of increasing severity which can ultimately give rise to the development of hepatocellular carcinoma (HCC). Besides drastic lifestyle changes, few drugs are effective to some extent alleviate NAFLD and HCC remains a poorly curable cancer. Among the deregulated molecular mechanisms promoting NAFLD and HCC, several members of the S100 proteins family appear to play an important role in the development of hepatic steatosis, non-alcoholic steatohepatitis (NASH) and HCC. Specific members of this Ca2+-binding protein family are indeed significantly overexpressed in either parenchymal or non-parenchymal liver cells, where they exert pleiotropic pathological functions driving NAFLD/NASH to severe stages and/or cancer development. The aberrant activity of S100 specific isoforms has also been reported to drive malignancy in liver cancers. Herein, we discuss the implication of several key members of this family, e.g., S100A4, S100A6, S100A8, S100A9 and S100A11, in NAFLD and HCC, with a particular focus on their intracellular versus extracellular functions in different hepatic cell types. Their clinical relevance as non-invasive diagnostic/prognostic biomarkers for the different stages of NAFLD and HCC, or their pharmacological targeting for therapeutic purpose, is further debated.

show abstract

Section: Implication Of S100 Proteins In the Occurrence Of Hccmentioning

confidence: 99%

S100 Proteins in Fatty Liver Disease and Hepatocellular Carcinoma

Delangre

Oppliger

Berkcan

et al. 2022

IJMS

View full text Add to dashboard Cite

show abstract

“…Hepatocellular carcinoma (HCC) is a representative common hepatic cancer, and S100A2 is highly expressed and associated with advanced clinical features in HCC patients in vivo [ 10 , 61 ]. High S100A2 expression is associated with an unfavorable overall survival in vivo [ 10 , 62 ]. As S100A2 expression is upregulated, the hypomethylation status of the CpG island located at the S100A2 promoter site is correlated with the induction of S100A2 expression by HCC cells in vitro [ 10 ].…”

Section: Liver Diseasesmentioning

confidence: 99%

Influence of S100A2 in Human Diseases

Sugino

Sawada

2022

Diagnostics

View full text Add to dashboard Cite

S100 proteins are a family of low-molecular-weight proteins characterized by two calcium-binding sites with a helix-loop-helix (“EF-hand-type”) domain. The S100 family of proteins is distributed across various organs and can interact with diverse molecules. Among the proteins of the S100 family, S100 calcium-binding protein A2 (S100A2) has been identified in mammary epithelial cells, glands, lungs, kidneys, and prostate gland, exhibiting various physiological and pathological actions in human disorders, such as inflammatory diseases and malignant tumors. In this review, we introduce basic knowledge regarding S100A2 regulatory mechanisms. Although S100A2 is a tumor suppressor, we describe the various influences of S100A2 on cancer and inflammatory diseases.

show abstract

“…S100 family members have a broad range of intracellular and extracellular functions that encompass the regulation of cell apoptosis, proliferation, differentiation, migration, energy metabolism, calcium balance, protein phosphorylation, and inflammation [ 14 , 15 , 16 , 17 ]. In addition, S100 proteins may contribute to the development of many types of malignant tumors, autoimmune diseases, and chronic inflammatory diseases [ 18 ]. In the present study, we have shown that the family member S100z , located within the diabetes QTL Nidd13/NZO , is involved in β-cell proliferation as well as apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Identification of Novel Genes Involved in Hyperglycemia in Mice

Jonas

Kluth

Helms

et al. 2022

IJMS

View full text Add to dashboard Cite

Current attempts to prevent and manage type 2 diabetes have been moderately effective, and a better understanding of the molecular roots of this complex disease is important to develop more successful and precise treatment options. Recently, we initiated the collective diabetes cross, where four mouse inbred strains differing in their diabetes susceptibility were crossed with the obese and diabetes-prone NZO strain and identified the quantitative trait loci (QTL) Nidd13/NZO, a genomic region on chromosome 13 that correlates with hyperglycemia in NZO allele carriers compared to B6 controls. Subsequent analysis of the critical region, harboring 644 genes, included expression studies in pancreatic islets of congenic Nidd13/NZO mice, integration of single-cell data from parental NZO and B6 islets as well as haplotype analysis. Finally, of the five genes (Acot12, S100z, Ankrd55, Rnf180, and Iqgap2) within the polymorphic haplotype block that are differently expressed in islets of B6 compared to NZO mice, we identified the calcium-binding protein S100z gene to affect islet cell proliferation as well as apoptosis when overexpressed in MIN6 cells. In summary, we define S100z as the most striking gene to be causal for the diabetes QTL Nidd13/NZO by affecting β-cell proliferation and apoptosis. Thus, S100z is an entirely novel diabetes gene regulating islet cell function.

show abstract

S100 family members: potential therapeutic target in patients with hepatocellular carcinoma

Cited by 15 publications

References 60 publications

S100 Proteins in Fatty Liver Disease and Hepatocellular Carcinoma

S100 Proteins in Fatty Liver Disease and Hepatocellular Carcinoma

Influence of S100A2 in Human Diseases

Identification of Novel Genes Involved in Hyperglycemia in Mice

Contact Info

Product

Resources

About