S100A8/A9 Activate Key Genes and Pathways in Colon Tumor Progression

Ichikawa, Mie; Williams, Roy; Wang, Ling; Vogl, Thomas; Srikrishna, Geetha

doi:10.1158/1541-7786.mcr-10-0394

Cited by 300 publications

(315 citation statements)

References 80 publications

(116 reference statements)

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“…These data indicate that p38 MAPK mediates the NF-κB activation induced by S100A8/A9. These results are consistent with reports that S100A8/A9 promotes activation of MAP kinase and NF-κB signaling pathway in breast cancer, leukemia, neuroblastoma, prostate cancer and colon cancer cells (Ghavami et al, 2008b;Hermani et al, 2006;Ichikawa et al, 2011). In addition, we found that activation of p38 MAPK and NF-κB was associated with the S100A8/ A9-induced cell migration and invasion as evidenced by attenuation of the migration and invasion by the SB203580 and Bay (Fig.…”

Section: A B Csupporting

confidence: 93%

“…This is consistent with the finding that S100A8/A9 provoked p38 MAPK while JNK phosphorylation was unaffected in human prostate and breast cancer cells (Ghavami et al, 2008b;Hermani et al, 2006). In contrast, S100A8/A9 activates ERK and JNK but not p38 MAPK in colon cancer cells (Ichikawa et al, 2011). Therefore, the effect of S100A8/A9 on MAPK signaling may depend on the cancer cell types.…”

Section: A B Csupporting

confidence: 90%

“…Stromal S100A8-and S100/A9-positive myeloid cells in a cancer microenvironment have been characterized (Ichikawa et al, 2011;Sheikh et al, 2007;Turovskaya et al, 2008). Previously, we have also observed the enhanced S100A8 and S100A9 expression in infiltrating cells in the stroma of gastric cancers (Choi et al, 2012).…”

Section: A B C D E Fmentioning

confidence: 58%

“…S100A8/A9 activates p38 MAPK and NF-κB signaling We next determined S100A8/A9-activated signaling pathways in gastric cancer cells. Mitogen-activated protein kinase (MAPK) is a key mediator of intracellular signaling pathway in response to different stimuli and has been reported to be activated by S100A8/A9 in various cancers (Hermani et al, 2006;Ichikawa et al, 2011). To investigate activation of MAPK, the phosphorylation of MAPK subfamilies was estimated by Western blotting in gastric cancer cells.…”

Section: Resultsmentioning

confidence: 99%

“…sion and invasion of disseminating malignant cells in lung cancer (Hiratsuka et al, 2006) and colon cancer (Ichikawa et al, 2011). However, we previously demonstrated that endogenous S100A8 and S100A9 might be negative role on migration and invasion (Choi et al, 2012), indicating that endogenous S100A8/ A9 play a role that is different to that of exogenous S100A8/A9.…”

Section: A B Cmentioning

confidence: 96%

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S100A8 and S100A9 Promotes Invasion and Migration through p38 Mitogen-Activated Protein Kinase-Dependent NF-κB Activation in Gastric Cancer Cells

Kwon

Moon

Park

et al. 2013

Molecules and Cells

107

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S100A8 and S100A9 (S100A8/A9) are low-molecular weight members of the S100 family of calcium-binding proteins. Recent studies have reported S100A8/A9 promote tumorigenesis. We have previously reported that S100A8/A9 is mostly expressed in stromal cells and inflammatory cells between gastric tumor cells. However, the role of environmental S100A8/A9 in gastric cancer has not been defined. We observed in the present study the effect of S100A8/A9 on migration and invasion of gastric cancer cells. S100A8/ A9 treatment increased migration and invasionat lower concentrations that did not affect cell proliferation and cell viability. S100A8/A9 caused activation of p38 mitogenactivated protein kinase (MAPK) and nuclear factor-κB (NF-κB). The phosphorylation of p38 MAPK was not affected by the NF-κB inhibitor Bay whereas activation of NF-κB was blocked by p38 MAPK inhibitor SB203580, indicating that S100A8/A9-induced NF-κB activation is mediated by phosphorylation of p38 MAPK. S100A8/A9-induced cell migration and invasion was inhibited by SB203580 and Bay, suggesting that activation of p38 MAPK and NF-κB is involved in the S100A8/A9 induced cell migration and invasion. S100A8/A9 caused an increase in matrix metalloproteinase 2 (MMP2) and MMP12 expression, which were inhibited by SB203580 and Bay. S100A8/A9-induced cell migration and invasion was inhibited by MMP2 siRNA and MMP12 siRNA, indicating that MMP2 and MMP12 is related to the S100A8/A9 induced cell migration and invasion. Taken together, these results suggest that S100A8/A9 promotes cell migration and invasion through p38 MAPKdependent NF-κB activation leading to an increase of MMP2 and MMP12 in gastric cancer.

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Section: A B Csupporting

confidence: 93%

Section: A B Csupporting

confidence: 90%

Section: A B C D E Fmentioning

confidence: 58%

Section: Resultsmentioning

confidence: 99%

Section: A B Cmentioning

confidence: 96%

See 3 more Smart Citations

S100A8 and S100A9 Promotes Invasion and Migration through p38 Mitogen-Activated Protein Kinase-Dependent NF-κB Activation in Gastric Cancer Cells

Kwon

Moon

Park

et al. 2013

Molecules and Cells

107

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S100A9‐Targeted Cowpea Mosaic Virus as a Prophylactic and Therapeutic Immunotherapy against Metastatic Breast Cancer and Melanoma

Chung

Park²,

Cai³

et al. 2021

Advanced Science

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Prognosis and treatment of metastatic cancer continues to be one of the most difficult and challenging areas of oncology. Treatment usually consists of chemotherapeutics, which may be ineffective due to drug resistance, adverse effects, and dose‐limiting toxicity. Therefore, novel approaches such as immunotherapy have been investigated to improve patient outcomes and minimize side effects. S100A9 is a calcium‐binding protein implicated in tumor metastasis, progression, and aggressiveness that modulates the tumor microenvironment into an immunosuppressive state. S100A9 is expressed in and secreted by immune cells in the pre‐metastatic niche, as well as, post‐tumor development, therefore making it a suitable targeted for prophylaxis and therapy. In previous work, it is demonstrated that cowpea mosaic virus (CPMV) acts as an adjuvant when administered intratumorally. Here, it is demonstrated that systemically administered, S100A9‐targeted CPMV homes to the lungs leading to recruitment of innate immune cells. This approach is efficacious both prophylactically and therapeutically against lung metastasis from melanoma and breast cancer. The current research will facilitate and accelerate the development of next‐generation targeted immunotherapies administered as prophylaxis, that is, after surgery of a primary breast tumor to prevent outgrowth of metastasis, as well as, therapy to treat established metastatic disease.

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The role of myeloid‐derived suppressor cells in gastrointestinal cancer

Cui

Lan

2021

Cancer Communications

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Gastrointestinal (GI) cancer encompasses a range of malignancies that originate in the digestive system, which together represent the most common form of cancer diagnosed worldwide. However, despite numerous advances in both diagnostics and treatment, the incidence and mortality rate of GI cancer are on the rise. Myeloid‐derived suppressor cells (MDSCs) are a heterogeneous population of immature myeloid cells that increase in number under certain pathological conditions, such as infection and inflammation, and this expansion is of particular relevance to cancer. MDSCs are heavily involved in the regulation of the immune system and act to dampen its response to tumors, favoring the escape of tumor cells from immunosurveillance and increasing both metastasis and recurrence. Several recent studies have supported the use of MDSCs as a prognostic and predictive biomarker in patients with cancer, and potentially as a novel treatment target. In the present review, the mechanisms underlying the immunosuppressive functions of MDSCs are described, and recent researches concerning the involvement of MDSCs in the progression, prognosis, and therapies of GI cancer are reviewed. The aim of this work was to present the development of novel treatments targeting MDSCs in GI cancer in the hope of improving outcomes for patients with this condition.

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S100A8/A9 Activate Key Genes and Pathways in Colon Tumor Progression

Cited by 300 publications

References 80 publications

S100A8 and S100A9 Promotes Invasion and Migration through p38 Mitogen-Activated Protein Kinase-Dependent NF-κB Activation in Gastric Cancer Cells

S100A8 and S100A9 Promotes Invasion and Migration through p38 Mitogen-Activated Protein Kinase-Dependent NF-κB Activation in Gastric Cancer Cells

S100A9‐Targeted Cowpea Mosaic Virus as a Prophylactic and Therapeutic Immunotherapy against Metastatic Breast Cancer and Melanoma

The role of myeloid‐derived suppressor cells in gastrointestinal cancer

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