Analysis of S100A11 in DNA Damage Repair

Foertsch, Franziska; Melle, Christian

doi:10.1007/978-1-4939-9030-6_28

Cited by 2 publications

(1 citation statement)

References 25 publications

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“…Some specific S100 proteins were also described to act as gatekeepers of the cell integrity by stimulating the repair of damaged cellular membranes or nuclear DNA. Such activities are promoted for example by S100A10 and S100A11, which form membrane repair complexes with other key factors such as ANXA2 and AHNAK [ 55 , 103 ], or by S100A11 interaction with RAD51 in the nucleus, which helps maintain genomic stability [ 104 ].…”

Section: General Overview Of S100 Proteins Functionsmentioning

confidence: 99%

S100 Proteins in Fatty Liver Disease and Hepatocellular Carcinoma

Delangre

Oppliger

Berkcan

et al. 2022

IJMS

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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.

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Section: General Overview Of S100 Proteins Functionsmentioning

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

Dual effects of targeting S100A11 on suppressing cellular metastatic properties and sensitizing drug response in gastric cancer

Cui

et al. 2021

Cancer Cell Int

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Background S100A11 is a member of the S100 family of proteins containing two EF-hand calcium-binding motifs. The dysregulated expression of the S100A11 gene has been implicated in tumour metastasis. However, the role of S100A11 protein in tumour cell response to chemotherapeutic drugs has not been characterised. Methods Transcript levels of S100A11 in gastric cancer were evaluated using an in-house patient cohort. Protein expression of S100A11 in gastric cancer was estimated by immunohistochemistry of a tissue microarray. The stable gastric cancer cell lines were established using lentiviral shRNA vectors. The knockdown of S100A11 was validated by qRT-PCR, PCR, and Western blot. The cellular function of S100A11 was estimated by assays of cell adhesion, migration, and invasion. The cell cytotoxic assay was performed to investigate the response to chemotherapeutic drugs. An unsupervised hierarchical clustering and principal component analysis (HCPC) was applied to unveil the dimensional role of S100A11 among all S100 family members in gastric cancer. Results High expression of S100A11 is associated with poor survival of gastric cancer patients (p < 0.001, HR = 1.85) and is an independent prognostic factor of gastric cancer. We demonstrate that S100A11 plays its role as a tumour promoter through regulating the MMP activity and the epithelial-mesenchymal transition (EMT) process. The stable knockdown of S100A11 suppresses the metastatic properties of gastric cancer cells, which include enhancing cell adhesion, but decelerating cell migration and invasion. Furthermore, the knockdown of S100A11 gene expression dramatically induces the cellular response of gastric cancer cells to the first-line chemotherapeutic drugs fluoropyrimidine 5-fluorouracil (5-FU) and cisplatin. Conclusion The present study identifies S100A11 as a tumour promoter in gastric cancer. More importantly, the S100A11-specific targeting potentially presents dual therapeutic benefits by not only controlling tumour progression but also sensitising chemotherapeutic cytotoxic response.

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Analysis of S100A11 in DNA Damage Repair

Cited by 2 publications

References 25 publications

S100 Proteins in Fatty Liver Disease and Hepatocellular Carcinoma

S100 Proteins in Fatty Liver Disease and Hepatocellular Carcinoma

Dual effects of targeting S100A11 on suppressing cellular metastatic properties and sensitizing drug response in gastric cancer

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