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Table 1 Summary of SOX2 amplification and functions in cancer

From: SOX2 and cancer: current research and its implications in the clinic

Cancer type

SOX2 gene amplification

SOX2 function

Pathway/Process

References

Breast

No

↑cell proliferation, ↑colony formation, ↑↓invasion, ↑metastasis

↑WNT/ β-CATENIN, ↑EMT, ↓AMPK/mTOR

[21–27]

Cervical

Unknown

↑cell proliferation, ↑clonogenicity, ↑tumorigenicity

Unknown

[28]

Colorectal

Unknown

↑↓cell proliferation, ↑metastasis, ↑senescence, ↑autophagy, ↑tumor growth, ↑invasion, ↑migration, ↑anchorage-dependent growth

↑BMP, ↓mTOR,↑MET, ↑WNT/ β-CATENIN

[29–33]

Esophageal SCC

Yes

↑cell proliferation, ↑tumor growth

↑Akt/mTORC1, ↑STAT3

[17, 34–36]

Gastric

Unknown

↑↓ apoptosis, ↑↓cell proliferation, ↑migration

↑AKT signaling

[37–41]

Glioblastoma, GBM, medulloblastoma, oligodendroglioma

Yes

↑promoter hypomethylation, ↑invasion, ↑migration, ↑self-renewal CSCs, ↑cell proliferation, ↑colony formation

Unknown

[14, 15, 42–46]

Hepatocellular carcinoma

Unknown

↑invasion, ↑sphere formation

↑EMT

[47]

Layngeal

Unknown

↑ invasion/migration

↑MMP-2 ↑PI3L/AKT/mTOR

[48]

Melanoma

Unknown

↑invasion, ↑tumor volume, ↑self-renewal CSCs

↑Hedegehog-GLI signaling

[49–53]

Oral SCC

Yes

Unknown

Unknown

[20]

Osteosarcoma

Unknown

↑self-renewal CSCs, ↑tumorigenicity, ↑dedifferentiation

↓WNT/ β-CATENIN

[54]

Ovarian

Unknown

↑migration, ↑invasion, ↑colony formation

Unknown

[55, 56]

Pancreatic

Unknown

↑cell proliferation, ↑stemness/dedifferentiation

↑EMT

[57]

Prostate

Unknown

↑self-renewal CSCs, ↑cell proliferation, ↑cell survival, ↑metastasis, ↑migration, ↓apoptosis, ↓store-operated Ca2+ entry

↓Ca2+ channels, ↑EMT, ↓Survivin, ↑WNT/β-CATENIN, ↑EGFR/PI3K/AKT

[27, 58–60]

SCLC, Lung SCC, lung adenocarcinoma, NSCLC

Yes

↑cell proliferation, ↑cell survival, ↓apoptosis, ↑migration, ↑anchorage-dependent growth, ↑self-renewal CSCs, ↑metastasis, ↓autophagy, ↑tumor formation

↑MAP4K4-Survivin, ↓EGFR/Src/Akt ↓BMP4

[12, 16, 19, 61–70]

Sinonasal

Yes

Unknown

Unknown

[71]

Transitional cell Carcinoma

Unknown

↑alternative splicing

Unknown

[72]

  1. SOX2 has been shown to be amplified and functionally relevant in various cancer types. SOX2 in cancer functions through multiple mechanisms that vary depending on the cancer type. However, in most cases, SOX2 has been shown to increase cell proliferation, invasion, migration, metastasis and self-renewal of CSCs. In addition, some of these phenotypes have been linked to particular oncogenic pathways, including WNT/β-CATENIN, EGFR, mTOR and HH signaling.
  2. ↑ = Promotes/Improves.
  3. ↓ = Suppresses/Inhibits.
  4. ↑↓ = Conflicting research.