Loading
SOX2 (Transcription factor SOX-2) is a protein that switches other genes on and off. In the public catalogues the evidence so far is association rather than a proven role. Tied to Colorectal cancer, Skin cancer and Lung cancer.
Transcription factor that forms a trimeric complex with OCT4 on DNA and controls the expression of a number of genes involved in embryonic development such as YES1, FGF4, UTF1 and ZFP206. Binds to the proximal enhancer region of NANOG. Critical for early embryogenesis and for embryonic stem cell pluripotency.
Open Targets scores its association with cancer at 0.70 (direct and indirect evidence; datatypes literature 1.00, affected pathway 0.62, animal model 0.69, somatic mutation 0.96).
In plain words · SOX2 (Transcription factor SOX-2) is a protein that switches other genes on and off. In the public catalogues the evidence so far is association rather than a proven role. Tied to Colorectal cancer, Skin cancer and Lung cancer.
SOX2 (Transcription factor SOX-2) is a protein that switches other genes on and off. In the public catalogues the evidence so far is association rather than a proven role. Tied to Colorectal cancer, Skin cancer and Lung cancer.
Transcription factor that forms a trimeric complex with OCT4 on DNA and controls the expression of a number of genes involved in embryonic development such as YES1, FGF4, UTF1 and ZFP206. Binds to the proximal enhancer region of NANOG.
No product in this corpus aims at SOX2 yet. Transcription factors have no pocket to plug, so drugs either degrade them or block the partner protein they need to dock on DNA.
First described 1992. Earliest sequence paper UniProt cites for the protein: Sadler L.A. et al, 1992. Source.
Sources: HGNC HGNC:11195 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P48431 (protein name, function text, keywords and locations (REST API)); Open Targets ENSG00000181449 (association with cancer (MONDO_0004992) 0.70; per-cancer scores at or above 0.5: colorectal cancer 0.55, skin cancer 0.53, lung cancer 0.51 (GraphQL API, CC0))
Transcription factor that forms a trimeric complex with OCT4 on DNA and controls the expression of a number of genes involved in embryonic development such as YES1, FGF4, UTF1 and ZFP206. Binds to the proximal enhancer region of NANOG. Critical for early embryogenesis and for embryonic stem cell pluripotency. Downstream SRRT target that mediates the promotion of neural stem cell self-renewal. Keeps neural cells undifferentiated by counteracting the activity of proneural proteins and suppresses neuronal differentiation. May function as a switch in neuronal development. Location: Nucleus speckle; Cytoplasm; Nucleus (UniProt). Locus 3q26.33 (HGNC).
| Cancer | Prevalence | Measure | Note | Source |
|---|---|---|---|---|
| Non-small-cell lung cancer | 29-43% | High-level amplification of the squamous lineage programme | cBioPortal high-level amplification: SOX2 194 of 487, 39.8%, and TP63 154 of 487, 31.6%, in lusc_tcga_pan_can_atlas_2018; SOX2 76 of 178, 42.7%, and TP63 51 of 178, 28.7%, in lusc_tcga_pub; SOX2 220 of 1,144, 19.2%, and TP63 176, 15.4%, in the combined nsclc_tcga_broad_2016. In adenocarcinoma the same genes are amplified in 10 of 511 (2.0%) and 10 of 511 (2.0%). The founding paper counted squamous differentiation genes altered in 44% of tumours (Cancer Genome Atlas Research Network 2012). | cBioPortal (TCGA) |
Approximate, population-level figures; the measure column says what was counted. Ranges show the midpoint as a bar.
It turned neuroendocrine transformation from a pathological curiosity into a mechanism with a genotype and a candidate intervention, and it is the reason EZH2 inhibitors are in prostate cancer trials at all.
A mechanism for the most feared form of treatment resistance in prostate cancer, and the reason combined TP53 and RB1 loss is worth knowing about before a man starts an androgen receptor drug rather than after his biopsy comes back neuroendocrine. Reversibility in the laboratory is also an argument that the switch is a target and not just a prognosis.
It explained why squamous lung cancer has no equivalent of an EGFR inhibitor: its commonest alterations are a transcription factor amplicon, a tumour suppressor deletion and an antioxidant switch, none of which is a drug target in the way a mutant kinase is.
Query for this target: (TITLE:"SOX2" OR ABSTRACT:"SOX2" OR TITLE:"SRY-box transcription factor 2" OR ABSTRACT:"SRY-box transcription factor 2" OR TITLE:"Transcription factor SOX-2" OR ABSTRACT:"Transcription factor SOX-2") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about SOX2, not a curated reading list.
Shares Neuroendocrine and small-cell prostate cancer, Transcriptional machinery & addiction, Lineage plasticity & neuroendocrine transformation, Metastatic castration-resistant prostate cancer.
Shares Comprehensive genomic characterization of squamous cell lung cancers, Skin cancer (all types), Lung cancer (all types), Open Targets Platform.
Shares SOX2 promotes lineage plasticity and antiandrogen resistance in TP53- and RB1-deficient prostate cancer, Neuroendocrine and small-cell prostate cancer, Prostate cancer.
Shares SOX2 promotes lineage plasticity and antiandrogen resistance in TP53- and RB1-deficient prostate cancer, Neuroendocrine and small-cell prostate cancer, Lineage plasticity & neuroendocrine transformation, Metastatic castration-resistant prostate cancer.
Shares Neuroendocrine and small-cell prostate cancer, Lineage plasticity & neuroendocrine transformation, Metastatic castration-resistant prostate cancer, Prostate cancer.
Shares Comprehensive genomic characterization of squamous cell lung cancers, Open Targets Platform, Non-small-cell lung cancer.
Shares Metastatic castration-resistant prostate cancer, Open Targets Platform, Prostate cancer.
Shares Neuroendocrine and small-cell prostate cancer, Lineage plasticity & neuroendocrine transformation, Prostate cancer.