| the function of RON in tumors may be multidimensional, not just as a tumor suppressor or oncogene. | None |
| Targeted expression of the receptor tyrosine kinase RON in distal lung epithelial cells results in multiple tumor formation: oncogenic potential of RON in vivo. | lung, |
| The Ron proto-oncogene product is a phenotypic marker of renal oncocytoma. | kidney, |
| Expression of RON Proto-oncogene in Renal Oncocytoma and Chromophobe Renal Cell Carcinoma. | kidney, |
| The proto-oncogene, c-Cbl, which modulates ubiquitylation of RON, was increased in glia in both multiple sclerosis brains and experimental autoimmune encephalomyelitis spinal cords | brain, |
| Regulation of RON tyrosine kinase-mediated invasion of breast cancer cells. | breast, |
| RON has 2 alternative SRC-kinase-mediated modes of signaling that can contribute to oncogenic behavior in normal breast epithelial cells: an MSP-dependent increase in cell proliferation & migration and MSP-independent increased cell survival. | breast, |
| The expression of several oncogenic RON splice variants in malignant gliomas suggests that these could represent candidate targets for treatment with agents inhibiting RON activity | glioma, |
| Oncogenic MST1R activity in pancreatic and gastric cancer represents a valid target of HSP90 inhibitors. | pancreatic,gastric, |
| Data suggest that oncogenic RON160 is frequently expressed in primary invasive ductal, lobular, and lymph node-involved breast cancer tissues; RON160 overexpression is predominantly observed in invasive ductal and lymph node-involved cases. | breast, |
| the activated beta-catenin cascade is one of the pathways involved in tumorigenic activities mediated by the oncogenic RON variant | None |
| Pro-metastatic splicing of Ron proto-oncogene mRNA can be reversed: therapeutic potential of bifunctional oligonucleotides and indole derivatives. | None |
| macrophage stimulating 1 receptor is associated with invasive and oncogenic phenotypes such as tumor cell migration, invasion, resistance to apoptosis and cell cycle arrest | None |
| Identification of novel splicing variants from RON proto-oncogene pre-mRNA. | None |
| Knockdown of RON inhibited invasive growth & the activation of oncogenic signaling pathways including Akt, MAPK and beta-catenin. RON up-regulation was associated with tumor size, lymphatic metastasis, invasiveness, tumor stage and poor survival. | None |
| A 2-nt RNA enhancer on exon 11 promotes exon 11 inclusion of the Ron proto-oncogene. | None |
| Hypoxia promotes nuclear translocation and transcriptional function in the oncogenic tyrosine kinase RON. | None |
| SRSF2 promotes exon 11 inclusion of Ron proto-oncogene through targeting exon 11. | None |
| Aberrant glycosylation of the RON receptor was shown as an alternative mechanism of oncogenic activation. | None |
| the cis-regulatory landscape that determines alternative splicing of exon 11 in the proto-oncogene MST1R (RON), was examined. | None |