Sox2 is highly expressed in concert with p63 in most squamous cell carcinomas, but may also influence tumor differentiation in both non-small cell lung carcinomas and pulmonary neuroendocrine tumors.

show that a peak of genomic amplification on chromosome 3q26.33 found in squamous cell carcinomas (SCCs) of the lung and esophagus contains the transcription factor gene SOX2.

Data show that SOX2 protein expression was greatly higher in lung SCCs compared to adenocarcinomas.

Sox2 seems to be an independent predictor of poor outcome in stage I lung adenocarcinomas and may help stratify patients at increased risk for recurrence.

SOX2 amplification and upregulation are frequent events in squamous cell carcinomas of the lung and are associated with indicators of favorable prognosis

role in maintenance of stemness and tumorigenicity of human lung adenocarcinoma cancer stem-like cells/cancer-initiating cells

In the hypoxic conditions, OCT4 and SOX2, both of which are induced by HIF1alpha/HIF2alpha. promote CD133 expression in the lung cancer cells via their direct interaction with the P1 promoter.

results present evidence that SOX2 may regulate the expression of oncogenes in cancer stem cells to promote the development of human lung cancer

Sox2 appears to be an important gene in lung squamous cell carcinogenesis that in particular drives the development of poorly differentiated tumors.

Data indicate that the stem cell markers, Nanog, Oct-4 and SOX-2, were significantly upregulated in cisplatin resistant (CisR) lung cancer cell lines.

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

SOX2 is an independent positive prognostic marker in non-small cell lung carcinomas.

The associations of serum SOX2 levels with clinical existing lung tumor markers.

Increased expression of SOX2 and FGFR1 indicate poor prognosis in small cell lung cancer patients.

BMP4 could act as a tumor suppressor; its downregulation by elevated SOX2 results in enhanced growth of lung squamous cell carcinoma cells

Increased SOX2 gene copy number is associated with FGFR1 and PIK3CA gene gain in non-small cell lung cancer and predicts improved survival in early stage disease

Immunohistochemistry staining was performed to test the expression of SOX2 and FOXA1 in human breast and lung carcinoma. The results showed that there is an inhibitory effect of SOX2 on the expression of FOXA1 gene.

our findings reveal a new mechanism by which SOX2-mediated transcription repression of TIF1gamma promotes TGF-beta-induced epithelial-mesenchymal transition in non-small-cell lung cancer

SOX2 overexpression could be used as a positive prognostic factor in patients with stage III lung squamous cell carcinoma receiving adjuvant radiotherapy

we showed that ectopic expression of Sox2 in A549 cells was sufficient to render them more resistant to rapamycin treatment in vitro. These data suggested that rapamycin inhibited the function of lung cancer stem cells via SOX2.

This prompts for further studies on the mechanisms behind the TP53-induced regulation of SOX2 expression and the possible importance of hsa-miR-145 in lung cancer.

The authors found that high/positive SOX2 alterations, either DNA amplification or protein expression, were favorable for overall survival (OS) in non-small cell lung cancer. On the contrary, high/positive Nestin protein expression was poor for OS.

cyclin D1 is a direct target of transcription factor SOX2 in human lung squamous cell carcinoma cells.

Sox2 may be an important regulator in development of chemoresistance of lung cancer cells.

NFATc2 enhances tumor-initiating phenotypes through the NFATc2/SOX2/ ALDH1A1 axis in lung adenocarcinoma.

Histone acetyltransferase EP300 is necessary for the transcription factor SOX2 activity in basal cells, including for induction of the squamous fate. EP300 copy number gains are common in squamous cell carcinoma SQCCs, including lung cancer SQCC cell lines.

BCL11A is integral to lung squamous cell carcinoma pathology and highlights the disruption of the BCL11A-SOX2 transcriptional programme as a novel candidate for drug development.

Overexpression of SOX2 is sufficient to mediate the transition from hyperplasia to dysplasia in lung squamous cancer (LUSC) spheroids, while the presence of cancer-associated fibroblasts (CAFs) makes them invasive. Unexpectedly, CAFs suppress the activity of high SOX2 levels, restore hyperplasia, and enhance the formation of acinar-like structures.

In this study, the authors identify VEGF165, a splice variant of VEGF-A, as a regulator of sVEGFR1-i13 expression in lung carcinoma, and further show that VEGF165 cooperates with the transcription factor SOX2 and the splicing factor SRSF2 to control sVEGFR1-i13 expression.

SOX2 was found to be significantly upregulated in lung adenocarcinoma tissues of patients with lymph node metastasis. Additional results suggested that SOX2 interacts with CtBP1.

The role of SOX2 signaling in the lung squamous cell carcinoma.

High SOX2 expression is associated with drug resistance in lung cancer.

Study investigated super-enhancer profiles in lung squamous cell carcinoma (LUSC) and identified a novel subtype in which SOX2 and a neural transcription factor BRN2 have key roles in determining its distinctive differentiation state. BRN2 serves as an interacting partner for SOX2 in this novel subtype, instead of p63 in the classical subtype of LUSC.

lung adenocarcinoma resistance to therapy with EGFRtyrosine kinase inhibitors is related to increased expression of cancer stem cell markers SOX2, OCT4 and NANOG.

Chromosome 3q26 Gain Is an Early Event Driving Coordinated Overexpression of the PRKCI, SOX2, and ECT2 Oncogenes in lung Squamous Cell Carcinoma.

SOX2-induced upregulation of lncRNA LINC01561 promotes non-small-cell lung carcinoma progression by sponging miR-760 to modulate SHCBP1 expression.

The FDA-Approved Anti-Asthma Medicine Ciclesonide Inhibits lung cancer Stem Cells through Hedgehog Signaling-Mediated SOX2 Regulation.

SOX2 mediates cisplatin resistance in small-cell lung cancer with downregulated expression of hsa-miR-340-5p.

Novel HDAC11 inhibitors suppress lung adenocarcinoma stem cell self-renewal and overcome drug resistance by suppressing Sox2.

CAMK2A supported tumor initiating cells of lung adenocarcinoma by upregulating SOX2 through EZH2 phosphorylation.

PAK5 promotes the cell stemness ability by phosphorylating SOX2 in lung squamous cell carcinomas.

Distinct transcriptional programs of SOX2 in different types of small cell lung cancers.

Cross-talk between SOX2 and TGFbeta Signaling Regulates EGFR-TKI Tolerance and lung cancer Dissemination.

Putative stemness markers octamer-binding transcription factor 4, sex-determining region Y-box 2, and NANOG in non-small cell lung carcinoma: A clinicopathological association.

SOX2 has an important role in maintaining stem cell properties and functions that may be a potential target for effective lung cancer therapy.

Sox2 expression and Lkb1 loss cooperate to promote lung squamous cell carcinoma.

the cell of origin of K-Ras-induced tumors in the lung depends on levels of Sox2 expression affecting Notch signaling