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| Inflammatory factors and its sources | Role of EMT in tumor cells | References |
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| TNFα (secreted by macrophages) | It induces EMT in breast cancer cells through activation of NF-κB-dependent transcription factors (EMT-TFs) such as Twist1, Snail, Slug, and Zeb1/2 that drive inactivation of E-cadherin | [2] |
| It activates EMT in renal cell carcinoma through overexpression of chemokine receptors such as CXCR2 and CXCR3 | [49] |
| TGFβ (secreted by cancer-associated fibroblasts, leukocytes, endothelial cells, and immune-infiltrating cells) | It induces inactivation of CDH1 in human Panc1 cells through activation of Snail1 and Snail2 | [40] |
| It induces EMT of mammary epithelial cells through overexpression of SIRT1 deacetylase (NAD-dependent deacetylase sirtuin-1) that drives deacetylation of histone and inactivation of a promoter of the miR-200 gene | [42] |
| IL-1β (secreted by tumor-infiltrating immune effector cells and tumor stromal cells) | It also induces EMT through overexpression of stemness markers Bmi1 and Nestin which maintain self-renewal of cancer stem cells (CSCs) | [51] |
| It induces tamoxifen resistance in the breast cancer cell model through activation of Twist1 that drives methylation in the promoter region of ESR1 gene which in turn reduces the expression of ERα | [56] |
| It enhances EMT in oral squamous cell carcinoma and dysplastic oral keratinocytes through the production of proinflammatory cytokines such as IL-6, IL-8, and GROα | [63] |
| IL-6 (secreted by T cells, macrophages, and tumor cells) | It induces EMT via JAK-STAT3 or NF-kB pathways via activation of EMT-TFs such as Snail, Slug, Twist, and Zeb1 which reduces the expression of CDH1 that drive migration and invasion of the tumor. It induces STAT3-driven EMT, invasion, and metastasis in colorectal cancer through downregulation of miR-34a which prevents EMT through regulation of Snail1 | [2] |
| It induces EMT via activation of STAT3 which induces the development of chemoresistance in ovarian cancer | [69] |
| It triggers EMT in lung adenocarcinoma through activation of STAT3/Snail1 | [72] |
| IL-8 (secreted by T cells, macrophages, and tumor cells) | It induces EMT in breast, colon, thyroid, and nasopharyngeal cancer through activation of a Slug-Akt signaling pathway | [23] |
| It induces EMT in thyroid cancer cells and hepatocellular carcinoma through overexpression of the AKT/Slug and JAK2/STAT3/Snail1 pathways, respectively | [75, 76] |
| It triggers EMT in nasopharyngeal carcinoma through epigenetic silencing of E-cadherin | [77] |
| CCL2 (secreted by monocytes, macrophages, and dendritic cells) | It triggers EMT in lung cancer with IL-6 through activation of Twist/STAT3 | [79] |
| CCL5 (secreted by cancer stem cells) | It triggers EMT and metastasis of CD133-negative stem cells through activation of NF-κB in ovarian cancer | [86] |
| It triggers EMT in triple-negative breast cancer cells | [83] |
| CCL18 (secreted by macrophages) | It induces EMT in pancreatic cancer through activation of Snail1 | [86] |
| It triggers EMT and invasion of breast cancer cell lines through overexpression of vimentin and downregulation of E-cadherin | [33] |
| CCL20 (secreted by lymphocytes) | It triggers EMT in the colon and hepatocellular carcinoma | [88, 89] |
| CCL21 (secreted by lymphocytes) | It triggers EMT and invasion through overexpression of N-cadherin and MMP9 via the NF-κB-mediated pathway | [90] |
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