| Data show that inhibition of ATP binding cassette subfamily B member 1 (ABCB1) might be a novel therapeutic strategy for non-small cell lung cancer (NSCLC) patients with acquired resistance to proto-oncogene proteins c-met (MET) inhibitors. | lung, |
| Is c-Met oncoprotein expression an adverse prognosticator in extrahepatic bile duct cancer treated with curative resection followed by adjuvant chemoradiotherapy?. | liver, |
| PIK3CA and MET may play an important role in oncogenesis of certain specific subtypes of head and neck cancer | HNSC, |
| Results indicate that miR-329 played a pivotal role in lung cancer through inhibiting cell proliferation, migration, invasion, and promoting apoptosis by targeting oncogenic MET. | lung, |
| Results showed that miR-23b and miR-27b were frequently reduced in oral squamous cell carcinoma clinical specimens and appeared to act as tumor suppressors through targeting of the MET oncogene in this disease. | oral |
| Using an integrative genetic analysis of 53 pediatric glioblastomas and five in vitro model systems, we identified previously unidentified gene fusions involving the MET oncogene in approximately 10% of cases. These MET fusions activated mitogen-activated protein kinase (MAPK) signaling and, in cooperation with lesions compromising cell cycle regulation, induced aggressive glial tumors in vivo. | glioblastoma,pediatric, |
| miR-27b was frequently downregulated in NSCLC tissues and cell lines and could inhibit the malignant phenotypes of NSCLC cells by directly targeting the MET oncogene. The identification of miR-27b-mediated novel signaling pathways may help reveal the molecular mechanism underlying the development and malignant progression of this disease. | lung, |
| Data illustrateS a cooperative effect of the direct oncogenic signaling of mutant beta-catenin and MET in hepatocytes with hepatic tumor-promoting stroma induced by beta-catenin deficiency | liver, |
| Data show that Kruppel like factor 4 (KLF4) was overexpressed in met proto-oncogene protein (c-Met)-overexpressing non-small-cell lung cancer (NSCLC) cells and tissues. | lung, |
| Analysis of 918 lung cancer and normal lung tissues and lung cancer cell lines revealed that MIR22HG was significantly downregulated in lung cancer; this decreased expression was associated with poor patient survival. MIR22HG bound and stabilized the YBX1 protein. Silencing of MIR22HG triggered both cell survival and cell death signaling through dysregulation of the oncogenes YBX1, MET, and p21. | lung, |
| Mechanistic studies revealed that infiltrating T-cells stimulate bladder cancer (BCa) estrogen receptor beta (ERbeta) signaling and consequently increase the expression of MET proto-oncogene through either direct binding of ERbeta to its promoter or via modulation of IL-1 expression enhancing BCa metastases and cell proliferation. | bladder, |
| Proto-Oncogene Proteins c-met (MET) overexpression is associated with an increased risk of recurrence in the triple-negative breast cancers (TNBCs). MET overexpression is associated with an increased risk of mortality. MET is an adverse prognostic marker for TNBCs. | breast, |
| Activation of hepatocyte growth factor/MET signaling initiates oncogenic transformation and enhances tumor aggressiveness in the murine prostate. | prostate, |
| A constitutional mutation( pR988C, c2962C>T ) mutation of the MET oncogene was identified in a patient with breast cancer, polycythemia vera and rheumatoid arthritis. Using CRISPR-Cas9 technology, pR988C MET-mutated transgenic mice, exhibited the autoimmune diseases and myeloproliferation observed in patient. | breast, |
| The present work seeks to assess whether pancreatic carcinomas release exosomes which express c-Met (proto-oncogene mesenchymal-epithelial transition factor) and PD-L1 (programmed cell death 1 ligand 1), and whether the detection of such expression in serum has diagnostic or prognostic meaning for the affected patients. | pancreatic, |
| [Coexpression of hepatocyte growth factor-scatter factor (HGF-SF) and HGF-SF receptors (c-met proto-oncogene) in mammalian brain]. | brain, |
| c-met proto-oncogene expression in benign and malignant human prostate tissues. | prostate, |
| Expression and loss of heterozygosity of c-met proto-oncogene in primary breast cancer. | breast, |
| Detection of the c-met proto-oncogene product in normal skin and tumours of melanocytic origin. | skin, |
| Coexpression of the c-met proto-oncogene and hepatocyte growth factor in human pancreatic cancer. | pancreatic, |