Our findings demonstrate that tumor-suppressor proteins Oct4 and SOX2 have a prominent expression profile in the primary stage of cancer, but, in the metastatic stage, their expression is downregulated, leading to the failure to prevent metastatic cancer.
Reduction in tumor weight and volume following treatment with CL-siSOX2 was associated with reduced protein expression of SOX2 and markers of tumor initiation, inflammation, invasion and metastasis in mice tumor xenografts.
Polyoxometalates (POMs) have been revealed as interesting antitumor agents inhibiting the action of Sox2 transcription factor, which reduces the risk of metastasis during hormonal therapies.
Multivariate analyses of our validation-cohort revealed that high SOX2 expression represents a major risk-factor for poor survival (HR = 3·19; 95%CI 1·74-5·84; p < 0·01) that is independent from metastasis and other known clinical risk-factors at the time of diagnosis.
On the other hand, dysregulation of SOX2 expression is associated with a multitude of cancer types and it has been shown that SOX2 positively affects cancer cell traits such as the capacity to proliferate, migrate, invade and metastasize.
In addition, upregulated SOX2 was associated with advanced and metastatic tumors in OSCC patients and was responsible for the drug-resistance property of OSCC cells.
lncRNA SOX2-OT upregulated by IRF4 promotes cell proliferation and metastasis in cholangiocarcinoma via upregulating SOX2 and activating PI3K/AKT signaling pathway.
In orthotopic and subcutaneous lung cancer xenograft models, inhibition of FGFR1 suppressed tumor growth, SOX2 expression, EMT, and metastasis in vivo; however, these processes caused by SOX2-overexpressing stable cell lines were not suppressed by FGFR1 inhibition.
Further analysis of exosomal DNA sequences of NANOG and other embryonic stemness genes (OCT3/4, SOX2, etc.) may establish a robust collection of exosome based diagnostic markers, and further elucidate the mechanisms of cancer formation, progression, and metastasis.
The high expression of cancer stem cell transcription factors (Oct4, Sox2 and Nanog) is a valuable prognostic factor, suggesting a higher risk of tumor recurrence and metastasis.
These findings provide evidence that ECM1 regulates GC cell metastasis and glucose metabolism by inducing ITGB4/FAK/SOX2/HIF-1α signal pathway and have important implications for the development of therapeutic target to prevent tumor metastasis and recurrence.
Moreover, Sema4C-overexpressing luminal breast cancer cells upregulated the transcription factors Snail, Slug and SOX-2, and formed estrogen-independent metastatic tumors in mice.
This article will discuss the role of SOX2 in breast cancer, including its occurrence, invasion and metastasis, diagnosis and treatment, relapse, resistance, and prognosis.
The over-expression of tumour suppressor genes such as RB and SOX17 and down-regulation of an oncogene such as SOX2 were in accordance to the inhibitory role of miR-340 that causes blockage of breast cancer metastasis which should be further investigated.
Increased RAD6 levels cause histone 2B ubiquitination-mediated epigenetic changes that stimulate transcription of stem cell genes, including ALDH1A1 and SOX2, leading to a cancer stem cell phenotype, which is implicated in disease recurrence and metastasis.