CCL7 and CCL21 overexpression in gastric cancer is associated with lymph node metastasis and poor prognosis

Hwang, Tsann‐Long; Lee, Li‐Yu; Wang, Chee-Chan; Li, Ying; Huang, Steve S.; Wu, Chi‐Ming

doi:10.3748/wjg.v18.i11.1249

Cited by 59 publications

(43 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Besides, CCL21 plays roles in the regulation of ERK pathway in human non-small cell lung cancer cells (26). CCL21 is downregulated in many cancers and associated with lymph node metastasis, poor prognosis (27), apoptosis (26), cell cycle (28) and tumor growth (29). SPARCL1 belongs to SPARC family that contains ten protein members (30).…”

Section: Resultsmentioning

confidence: 99%

Bioinformatic analysis of chemokine (C-C motif) ligand 21 and SPARC-like protein 1 revealing their associations with drug resistance in ovarian cancer

Yin

Liu

et al. 2013

International Journal of Oncology

View full text Add to dashboard Cite

Chemokine (C-C motif) ligand 21 (CCL21) and SPARC-like protein 1 (SPARCL1/MAST9/hevin/SC-1) are associated with various biological behavior in the development of cancers. Although the expression of CCL21 and SPARCL1 is downregulated in many solid tumors, their roles in ovarian cancer and their associations with drug resistance have rarely been studied. We performed a comprehensive bioinformatic analysis consisting of motif analysis, literature co-occurrence, gene/protein-gene/protein interaction network, protein-small molecule interaction network, and microRNAs enrichments which revealed that CCL21 and SPARCL1 directly or indirectly interact with a number of genes, proteins, small molecules and pathways associated with drug resistance in ovarian and other cancers. These results suggested that CCL21 and SPARCL1 may contribute to drug resistance in ovarian cancer. This study provided important information for further investigation of drug resistance-related functions of CCL21 and SPARCL1 in ovarian cancer.

show abstract

Section: Resultsmentioning

confidence: 99%

Bioinformatic analysis of chemokine (C-C motif) ligand 21 and SPARC-like protein 1 revealing their associations with drug resistance in ovarian cancer

Yin

Liu

et al. 2013

International Journal of Oncology

View full text Add to dashboard Cite

show abstract

“…Adipose-derived CCL7 may also have an adverse effect in the stomach, as high gastric CCL7 levels in gastric cancer patients has been correlated with more advanced tumour progression. 50 Dysregulation of the gut microbiome by HFD and H felis infection may also have increased systemic inflammation and contributed to the adipose or gastric pathology observed in H felis/HFD mice. Mice on HFD show altered gut microbiome composition and increased endotoxemia compared with mice on control diet.…”

Section: Discussionmentioning

confidence: 99%

Obesity acceleratesHelicobacter felis-induced gastric carcinogenesis by enhancing immature myeloid cell trafficking and T_H17 response

Ericksen

Rose

Westphalen

et al. 2013

Gut

View full text Add to dashboard Cite

Objective To investigate the role of obesity-associated inflammation and immune modulation in gastric carcinogenesis during Helicobacter-induced chronic gastric inflammation. Design C57BL/6 male mice were infected with H felis and placed on a high-fat diet (45% calories from fat). Study animals were analysed for gastric and adipose pathology, inflammatory markers in serum, stomach and adipose tissue, and immune responses in blood, spleen, stomach and adipose tissue. Results H felis-induced gastric carcinogenesis was accelerated in diet-induced obese mice compared with lean controls. Obesity increased bone marrow-derived immature myeloid cells in blood and gastric tissue of H felis-infected mice. Obesity also led to elevations in CD4 T cells, IL-17A, granulocyte macrophage colony-stimulating factor, phosphorylated STAT3 and prosurvival gene expression in gastric tissue of H felis-infected mice. Conversely, in adipose tissue of obese mice, H felis infection increased macrophage accumulation and expression of IL-6, C-C motif ligand 7 (CCL7) and leptin. Finally, the combination of obesity and gastric inflammation synergistically increased serum proinflammatory cytokines, including IL-6. Conclusions Here, we have established a model to study the molecular mechanism by which obesity predisposes individuals to gastric cancer. In H felis-infected mice, obesity increased proinflammatory immune responses and accelerated gastric carcinogenesis. Interestingly, gastric inflammation augmented obesity-induced adipose inflammation and production of adipose-derived factors in obese, but not lean, mice. Our findings suggest that obesity accelerates Helicobacter-associated gastric cancer through cytokine-mediated cross-talk between inflamed gastric and adipose tissues, augmenting immune responses at both tissue sites, and thereby contributing to a protumorigenic gastric microenvironment.

show abstract

“…Jung et al (56) reported that CCL7, which is induced by carcinoma-associated fibroblasts, significantly induced the ability of migration of oral squamous cells. Similarly, CCL7 was found to be positively correlated to invasion and metastasis and patient survival of gastric cancer (57). More recently, Rajaram et al (34) found that fibroblast-secreted CCL7 is capable of promoting proliferation of breast cancer cells.…”

Section: Breast Cancer Mmp1mentioning

confidence: 97%

Roles of the Cyclooxygenase 2 Matrix Metalloproteinase 1 Pathway in Brain Metastasis of Breast Cancer

Fukuda

Xing

et al. 2015

Journal of Biological Chemistry

112

View full text Add to dashboard Cite

Background: Mechanism of brain metastasis of breast cancer is poorly understood. Results: Inflammatory factors secreted from cancer cells degrade tight junction of BBB and stimulate the tumor-microenvironment cross-talk. Conclusion: COX2-prostaglandins-MMP1 pathway promotes brain metastasis by tampering with BBB and up-regulating CCL7 in astrocytes for the growth of tumor initiating cells. Significance: The COX2-prostaglandins-MMP1 pathway may serve as a novel therapeutic target for brain metastasis.

show abstract

CCL7 and CCL21 overexpression in gastric cancer is associated with lymph node metastasis and poor prognosis

Abstract: These results suggest that overexpression of these two CC chemokine ligands is associated with tumor metastasis and serves as a prognostic factor in patients with gastric cancer.

Cited by 59 publications

References 15 publications

Bioinformatic analysis of chemokine (C-C motif) ligand 21 and SPARC-like protein 1 revealing their associations with drug resistance in ovarian cancer

Bioinformatic analysis of chemokine (C-C motif) ligand 21 and SPARC-like protein 1 revealing their associations with drug resistance in ovarian cancer

Obesity acceleratesHelicobacter felis-induced gastric carcinogenesis by enhancing immature myeloid cell trafficking and T_H17 response

Roles of the Cyclooxygenase 2 Matrix Metalloproteinase 1 Pathway in Brain Metastasis of Breast Cancer

Contact Info

Product

Resources

About

CCL7 and CCL21 overexpression in gastric cancer is associated with lymph node metastasis and poor prognosis

Abstract: These results suggest that overexpression of these two CC chemokine ligands is associated with tumor metastasis and serves as a prognostic factor in patients with gastric cancer.

Cited by 59 publications

References 15 publications

Bioinformatic analysis of chemokine (C-C motif) ligand 21 and SPARC-like protein 1 revealing their associations with drug resistance in ovarian cancer

Bioinformatic analysis of chemokine (C-C motif) ligand 21 and SPARC-like protein 1 revealing their associations with drug resistance in ovarian cancer

Obesity acceleratesHelicobacter felis-induced gastric carcinogenesis by enhancing immature myeloid cell trafficking and TH17 response

Roles of the Cyclooxygenase 2 Matrix Metalloproteinase 1 Pathway in Brain Metastasis of Breast Cancer

Contact Info

Product

Resources

About

Obesity acceleratesHelicobacter felis-induced gastric carcinogenesis by enhancing immature myeloid cell trafficking and T_H17 response