S100A4 in cancer progression and metastasis: A systematic review

Fei, Fei; Qu, Jie; Zhang, Mingqing; Li, Yuwei; Zhang, Shiwu

doi:10.18632/oncotarget.18016

Cited by 144 publications

(142 citation statements)

References 169 publications

(202 reference statements)

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“…In addition to markers specifically expressed by epithelial tumor cells, we also observed differential expression in markers associated with tumor microenvironment, such as S100A4, which was upregulated in CC H (x 10.82; p = 1.5e −4 ). S100A4 is a member of the S100 calcium‐binding protein family, also known as fibroblast‐specific protein (FSP1) . Of note, we confirmed previous data showing an upregulation of S100 proteins (A6 and A11) by MALDI imaging in CC H , predominantly in the stromal part of the tumor .…”

Section: Resultssupporting

confidence: 90%

Proteomic Landscape of Cholangiocarcinomas Reveals Three Different Subgroups According to Their Localization and the Aspect of Non‐Tumor Liver

Faouder

Gigante

Léger

et al. 2018

Proteomics Clinical Apps

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Purpose Cholangiocarcinomas (CCs) define a heterogeneous entity based upon their anatomic localization (intra versus extrahepatic) and, for the intrahepatic CCs, the aspect of background liver (normal versus cirrhosis). The aim of the study was to characterize the molecular heterogeneity of CCs by a global proteomic approach. Experimental design Thirty‐three tumor samples from 17 intrahepatic CCs (iCC) (9 developed on normal (iCCN) and 8 developed in cirrhotic liver (iCCC)); 5 hilar CCs (CCH); 5 pancreatic CCs (CCP) and 6 hepatocellular carcinomas (HCC), were submitted to label‐free quantitative proteomic analysis. Differential proteins were analyzed by immunohistochemistry in a validation set of 30 CCs. Results Unsupervised analysis revealed two main clusters: cluster 1 contained most of the iCCC while cluster 2 was divided in 2 subgroups, one containing most of the iCCN and the other regrouping CCH and CCP. Compared to iCCN, iCCC displayed upregulation of molecules involved in cell adhesion, motility and angiogenesis. Epithelial markers associated with secretory pathway and fibroblast markers were overexpressed in CCH compared to iCCN Conclusion and clinical relevance This study demonstrated that iCCC is a specific entity, suggesting a major impact of the background liver on tumor biology, and confirmed that extrahepatic CCs define a homogeneous subgroup.

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Section: Resultssupporting

confidence: 90%

Proteomic Landscape of Cholangiocarcinomas Reveals Three Different Subgroups According to Their Localization and the Aspect of Non‐Tumor Liver

Faouder

Gigante

Léger

et al. 2018

Proteomics Clinical Apps

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“…Similar to Gal1 and Opn, overexpression of the S100A4 protein in dKO liver could have different roles at different stages of CLI in mutant mice. On one hand, S100A4 may confer protection and show anti-inflammatory activity in response to aberrations of lipid metabolism (48), but on the other hand, it may favor tumor progression and metastasis in different cancers (49), including HCC (50). Furthermore, overexpression of the Ntrk2 (TrkB) protein in hepatocytes of the young dKO mice (Fig.…”

Section: Discussionmentioning

confidence: 99%

Lack of galectin‐1 exacerbates chronic hepatitis, liver fibrosis, and carcinogenesis in murine hepatocellular carcinoma model

et al. 2019

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Chronic liver inflammation (CLI) is a risk factor for development of hepatocellular carcinoma (HCC). Galectin‐1 (Gal1) is involved in the regulation of inflammation, angiogenesis, and tumorigenesis, exhibiting multiple anti‐inflammatory and protumorigenic activities. We aimed to explore its regulatory role in CLI and HCC progression using an established model of CLI‐mediated HCC development, Abcb4 [multidrug‐resistance 2 (Mdr2)]‐knockout (KO) mice, which express high levels of Gal1 in the liver. We generated double‐KO (dKO) Gal1‐KO/Mdr2‐KO mice on C57BL/6 and FVB/N genetic backgrounds and compared HCC development in the generated strains with their parental Mdr2‐KO strains. Loss of Gal1 increased liver injury, inflammation, fibrosis, and ductular reaction in dKO mice of both strains starting from an early age. Aged dKO mutants displayed earlier hepatocarcinogenesis and increased tumor size compared with control Mdr2‐KO mice. We found that osteopontin, a well‐known modulator of HCC development, and oncogenic proteins Ntrk2 (TrkB) and S100A4 were overexpressed in dKO compared with Mdr2‐KO livers. Our results demonstrate that in Mdr2‐KO mice, a model of CLI‐mediated HCC, Gal1‐mediated protection from hepatitis, liver fibrosis, and HCC initiation dominates over its known procarcinogenic activities at later stages of HCC development. These findings suggest that anti‐Gal1 treatments may not be applicable at all stages of CLI‐mediated HCC.—Potikha, T., Pappo, O., Mizrahi, L., Olam, D., Mailer, S. M., Rabinovich, G. A., Galun, E., Goldenberg, D. S. Lack of galectin‐1 exacerbates chronic hepatitis, liver fibrosis, and carcinogenesis in murine hepatocellular carcinoma model. FASEB J. 33, 7995–8007 (2019). http://www.fasebj.org

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“…In addition, it is also involved in a wide range of biological functions, such as fibrogenesis and particularly inflammation regulation [16,23,24]. Previous studies have shown that S100A4 stimulated the releasing of various cytokines and growth factors that favors the inflammation process [25]. On the other hand, inflammation state in tissues was tightly associated with the HFD-induced obesity and obesity-related metabolic syndromes [26,27].…”

Section: Introductionmentioning

confidence: 99%

S100A4 protects mice from high-fat diet-induced obesity and inflammation

Hou

Jiao

et al. 2018

Laboratory Investigation

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As a member from S100 calcium-binding protein family, S100A4 is ubiquitous and elevated in tumor progression and metastasis, but its role in regulating obesity has not been well characterized. In this study, we showed that S100A4 was mainly expressed by stromal cells in adipose tissue and the S100A4 level in adipose tissue was decreased after high-fat diet (HFD). S100A4 deficient mice exhibited aggravated symptoms of obesity and suppressed insulin signaling after 12 weeks of HFD. Aggravated obesity in S100A4 deficient mice were found to be positively correlated with higher inflammatory status of the liver. Then, we found that extracellular S100A4 or overexpressed S100A4 inhibited adipogenesis and decreased mRNA levels of inflammation gene in 3T3-L1 adipocytes in vitro; whereas small interfering RNA (siRNA)-mediated suppression of S100A4 displayed the opposite results. Additionally, the protective effect induced by S100A4 during HFD-induced obesity was tightly related with activation of Akt signaling in adipose tissues, as well as livers and muscles. Taken together, we demonstrate that S100A4 is an inhibitory factor for obesity and attenuates the inflammatory reaction, while activating the Akt signaling, which suggest that S100A4 is a potential candidate for the treatment of diet-induced obesity and its complications.

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S100A4 in cancer progression and metastasis: A systematic review

Cited by 144 publications

References 169 publications

Proteomic Landscape of Cholangiocarcinomas Reveals Three Different Subgroups According to Their Localization and the Aspect of Non‐Tumor Liver

Proteomic Landscape of Cholangiocarcinomas Reveals Three Different Subgroups According to Their Localization and the Aspect of Non‐Tumor Liver

Lack of galectin‐1 exacerbates chronic hepatitis, liver fibrosis, and carcinogenesis in murine hepatocellular carcinoma model

S100A4 protects mice from high-fat diet-induced obesity and inflammation

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