Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chemokines and their receptors play diverse roles in malignant tumor progression, particularly as key mediators of tumor stroma interactions. C-C motif chemokine ligand 2 (CCL2) also called monocyte chemoattractant protein-1 (MCP-1), belongs to the C-C motif chemokine sub-family and is currently believed to mediate its actions through one receptor, C-C motif chemokine receptor 2 (CCR2). CCL2 has been identified as a major chemokine inducing the recruitment of macrophages in human tumors, including those of the bladder, cervix, ovary, lung and breast. In this study of Turkish women, the association of CCL2 A2518G and CCR2 V64I polymorphisms with endometrial cancer was investigated using 50 endometrial cancer patients and 211 controls. In our study, individuals with CCL2 A2518G GG genotype showed a 6.7-fold increased risk for endometrial cancer (p<0.0001) and individuals with CCL2 A2518G A allele had a 7.14-fold lower risk of endometrium cancer (p<0.0001). Individuals carrying the CCR2 64I/64I genotype had a 4.13-fold increased risk for endometrial cancer (p<0.0001). We also found that individuals carrying the CCR2 wt allele had a 4.16-fold lower risk for endometrial cancer (p=0.005). We observed that the CCL2 G: CCR2 64I haplotype frequency was significantly higher in patients compared to controls (p=0.019). In conclusion, we state that there appears to be an association between polymorphism of CCL2 and its receptor CCR2 and endometrial cancer. To the best of our knowledge, this is the first study to show such an association.
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PMID:Association of CCL2 and CCR2 gene variants with endometrial cancer in Turkish women. 2036 4

Chemokine (C-C motif) ligand 4 (CCL4) and vascular endothelial growth factor-A (VEGF-A) are involved in the progression and metastasis of some tumors, including ovarian cancer, colon cancer and prostate cancer. However, the roles of CCL4 and VEGF-A in human endometrial cancer (EC) are still unclear. Here, we demonstrated that the production of CCL4 and VEGF-A was significantly higher in EC tissues than in normal tissues, and their expression profiles were associated with the clinical stage of EC. In addition, we found that CCL4 promoted the angiogenesis and invasive ability of EC tumors by increasing the production of VEGF-A. We further confirmed the effect of CCL4 in the growth of EC tumors by silencing the expression of CCL4 in EC cell lines. Finally, we found that CCL4 upregulated VEGF-A expression by activating STAT3, and it enhanced the progression and metastasis of EC. Our study showed that CCL4 promoted tumor growth by upregulating VEGF-A expression, which affected the STAT3 signal pathway in the EC cells.
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PMID:CCL4 promotes the cell proliferation, invasion and migration of endometrial carcinoma by targeting the VEGF-A signal pathway. 3196 83