|
| Proteomic platform(s) in EMT assessing | Cancer type/sample type | Evaluated EMT-related process | Comments regarding EMT-related proteins | Ref |
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| iTRAQ-based quantitative proteomics | Colorectal cancer/tumour tissue | Tumourigenesis | TME proteins—ECM-receptors, focal adhesion, PI3K-Akt signalling pathway, angiogenesis, HIF-1 signalling pathways | [53, 54] |
| Reverse phase protein array | Colorectal cancer/tumour tissue | Recurrence | Collagen VI, FOXO3a, INPP4B, LcK, phospho-PEA15, phospho-PRAS40, Rad51, phospho-S6 | [56] |
| Tissue microarray | Colorectal cancer/tumour tissue | Metastasis | Cdc42BPA highly correlated with metastasis | [65] |
| Yeast-2-hybrid system and 2D gel-based proteomics | Colorectal cancer | Therapy resistance | FBXW7-ZEB2 tandem involved in stemness, chemoresistance, metastasis | [112] |
| Two-dimensional fluorescence gel electrophoresis | Hepatocellular carcinoma | Metastasis | GnT-V-mediated N-glycosylation of marker CD147/basigin. Upregulated and controlled by PI3K/Akt pathway | [68] |
| Label-free quantitative proteomics | Hepatocellular carcinoma | Inflammation | Inflammatory milieu has integrin, Rho family GTPases, IL-8, and ILK signalling pathway deregulations | [96] |
| Quantitative proteomic analysis | Hepatocellular carcinoma | Therapy resistance | Metformin inhibits AKT/GSK-3β signalling | [94] |
| Quantitative (phospho)proteomics | Hepatocellular carcinoma resistance | Therapy resistance | Proteins related to EMT and cell adhesion were associated with sorafenib treatment resistance | [114] |
| Label-free quantitative proteomics | Gastric cancer | Therapy resistance | Wnt/β-catenin pathway sustains trastuzumab resistance | [115] |
| Micro-Western Array | Prostate cancer | Therapy resistance | Caffeic acid phenethyl ester reduced β-catenin, NF-κB, and PI3K-Akt signalling | [106] |
| Liquid chromatography tandem-mass spectrometry | Prostate cancer | Therapy resistance | Signalling pathways in therapy-resistant tumours | [126] |
| Liquid chromatography-selected reaction monitoring mass spectrometry | Breast cancer | Aggressiveness | Estrogen, progesterone receptors, HER2/Neu receptor correlated with Ki-67 and vimentin | [72] |
| 2D-differential gel electrophoresis, MALDI-MS, immunoblotting | Breast cancer | Aggressiveness | ECM pattern—fibrinogen-β chain, collagen α-1(VI) chain, and α-1B-glycoprotein | [73] |
| Flow cytometric surface proteomics | Breast cancer | Aggressiveness | Upregulated proteins CD200, CD51/CD61, CD26, CD165, and CD54 | [76] |
| Reverse phase protein arrays | Breast cancer | Subtyping | Immune-related subtype and a hormone-related subtype | [78] |
| Quantitative multiplexed proteomic tandem mass tags | Breast cancer | Therapy resistance | TACC3 inhibitor, suppresses cancer cell stemness | [91] |
| Western blot, colony formation, flow cytometry for cellular apoptosis | Breast cancer | Therapy resistance | Resveratrol and salinomycin reverse EMT | [93] |
| iTRAQ technology | Breast cancer | Therapy resistance | E-cadherin, vimentin, TGF-β receptor I/II, smad2/3, β-catenin, caveolin, dystroglycan overexpression | [118] |
| Mass spectrometry | High-grade serous ovarian cancer | Tumourigenesis | Alpha-enolase and vimentin overexpression | [80] |
| GEL-LC-MS/MS and SILAC | Ovarian adenocarcinoma | Tumourigenesis | Activated signalling pathways PI3K/Akt/mTOR and Ras/Erk MAPK | [81] |
| Mass spectrometry-based quantitative proteomic approaches | Cervical cancer | Tumourigenesis | Myoferlin regulates ADAM12 expression | [83] |
| Membrane proteomic methodology | Head and neck squamous cell carcinoma | Tumourigenesis | EGFR constitutively phosphorylated | [85] |
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