| The data identify Sox2 as a context-dependent tumor suppressor protein that is dispensable for normal tissue regeneration, but restrains stomach adenoma formation through modulation of Wnt-responsive and intestinal genes. | gastric, |
| The molecular mechanism governing the oncogenic potential of SOX2 in breast cancer. | breast, |
| SOX2 is an amplified lineage-survival oncogene in lung and esophageal squamous cell carcinomas. | esophageal,lung, |
| results indicate that the SOX2 transcription factor, a major regulator of stem cell function, is also an oncogene and a driver gene for the recurrent 3q26.33 amplifications in lung SCC | lung, |
| SOX2 is an oncogene activated by recurrent 3q26.3 amplifications in human lung squamous cell carcinomas. | lung, |
| Evidence that SOX2 overexpression is oncogenic in the lung. | lung, |
| Targeted silencing of the oncogenic transcription factor SOX2 in breast cancer. | breast, |
| results present evidence that SOX2 may regulate the expression of oncogenes in cancer stem cells to promote the development of human lung cancer | lung, |
| show that IGF-IR-mediated POU5F1 expression to form a complex with beta-catenin and SOX2 is crucial for the self-renewal and oncogenic potentials of lung adenocarcinoma stem-like cells | lung, |
| The emerging role of SOX2 in cell proliferation and survival and its crosstalk with oncogenic signaling in lung cancer. | lung, |
| SOX2 is a critical oncogene linked to cancer stemness properties in urothelial carcinoma of the bladder. | bladder, |
| findings support that cytokine-induced stem cell factor SOX2 possesses oncogenic properties, with the potential to serve as a prognostic biomarker in endometrial carcinoma. | endometrial, |
| SOX2 acted as a target of miR-7-5p. SOX2 was an oncogene in breast cancer through promoting cell proliferation, migration and invasion. | breast, |
| SOX2 in squamous cell carcinoma: amplifying a pleiotropic oncogene along carcinogenesis. | None |
| Results demonstrate that SOX2 is a critical oncogene associated with arsenic-induced malignant stemness properties of urothelial cells. In addition, SOX2 regulated the expressions of various stemness-related molecules. | None |
| The mRNA and protein expression level of SOX2 and Survivin was significantly higher in salivary adenoid cystic carcinoma tissues than in paracancerous normal salivary gland tissues, indicating that both of the two are tissue-specific and may become salivary adenoid cystic carcinoma oncogenes. | None |