SOX9 is an atypical intestinal tumor suppressor controlling the oncogenic Wnt/ß-catenin signaling

Prévostel, Corinne; Rammah-Bouazza, Cyrine; Trauchessec, Hélène; Canterel-Thouennon, Lucile; Busson, Muriel; Ychou, Marc; Blache, Philippe

doi:10.18632/oncotarget.10573

Cited by 43 publications

(70 citation statements)

References 37 publications

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“…Moreover, miR-101-3p targets SOX9 which bridges the pathway to Wnt/β-catenin. Several studies in different types of cancer showed the connection between SOX9 and the Wnt/β-catenin [72][73][74]. As a result, the oncogenic lncRNAs NEAT1 promotes NSCLC progression by activating the miR-101-3p/SOX9/Wnt/β-catenin axis.…”

Section: The Pi3k/akt Pathwaymentioning

confidence: 99%

Hypoxia: Overview on Hypoxia-Mediated Mechanisms with a Focus on the Role of HIF Genes

Tirpe

Gulei

Ciortea

et al. 2019

IJMS

274

183

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Hypoxia represents a frequent player in a number of malignancies, contributing to the development of the neoplastic disease. This review will discuss the means by which hypoxia powers the mechanisms behind cancer progression, with a majority of examples from lung cancer, the leading malignancy in terms of incidence and mortality rates (the frequent reference toward lung cancer is also for simplification purposes and follow up of the global mechanism in the context of a disease). The effects induced by low oxygen levels are orchestrated by hypoxia-inducible factors (HIFs) which regulate the expression of numerous genes involved in cancer progression. Hypoxia induces epithelial-to-mesenchymal transition (EMT) and metastasis through a complex machinery, by mediating various pathways such as TGF-β, PI3k/Akt, Wnt, and Jagged/Notch. Concomitantly, hypoxic environment has a vast implication in angiogenesis by stimulating vessel growth through the HIF-1α/VEGF axis. Low levels of oxygen can also promote the process through several other secondary factors, including ANGPT2, FGF, and HGF. Metabolic adaptations caused by hypoxia include the Warburg effect—a metabolic switch to glycolysis—and GLUT1 overexpression. The switch is achieved by directly increasing the expression of numerous glycolytic enzymes that are isoforms of those found in non-malignant cells.

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Section: The Pi3k/akt Pathwaymentioning

confidence: 99%

Hypoxia: Overview on Hypoxia-Mediated Mechanisms with a Focus on the Role of HIF Genes

Tirpe

Gulei

Ciortea

et al. 2019

IJMS

274

183

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“…As an atypical tumor suppressor, SOX9 has been shown to interact with nuclear β-catenin. Inactivation of SOX9 causes loss of inhibition of the oncogenic Wnt/β-catenin signalling pathway and is associated with patient survivals (54). Some novel TSGs harbor mutational hotspots.…”

Section: Application To Tcga Datamentioning

confidence: 99%

Contextual Classifications of Cancer Driver Genes

Chandrashekar

Ahmadinejad

Wang

et al. 2019

Preprint

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Functions of cancer driver genes depend on cellular contexts that vary substantially across tissues and organs. Distinguishing oncogenes (OGs) and tumor suppressor genes (TSGs) for each cancer type is critical to identifying clinically actionable targets. However, current resources for context-aware classifications of cancer drivers are limited. In this study, we show that the direction and magnitude of somatic selection of missense and truncating mutations of a gene are suggestive of its contextual activities. By integrating these features with ratiometric and conservation measures, we developed a computational method to categorize OGs and TSGs using exome sequencing data. This new method, named genes under selection in tumors (GUST) shows an overall accuracy of 0.94 when tested on manually curated benchmarks. Application of GUST to 10,172 tumor exomes of 33 cancer types identified 98 OGs and 179 TSGs, >70% of which promote tumorigenesis in only one cancer type. In broad-spectrum drivers shared across multiple cancer types, we found heterogeneous mutational hotspots modifying distinct functional domains, implicating the synchrony of convergent and divergent disease mechanisms. We further discovered two novel OGs and 28 novel TSGs with high confidence.The GUST program is available at https://github.com/liliulab/gust. A database with pre-computed classifications is available at https://liliulab.shinyapps.io/gust

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“…Although most studies showed that SOX9 played an oncogenic role in cancer development. Excopic expression of SOX9 was found to suppress cell growth, clonal capacity and colonosphere formation by inhibiting Wnt/ß-catenin signaling pathway and c-myc expression in colorectal cancer, suggesting that SOX9 might be a tumor suppressor in colorectal cancer [81]. SOX9 expression was progressively decreased in cervical carcinoma in situ and especially in invasive cervical carcinoma, compared with normal cervix tissue.…”

Section: Sox9 and Cancermentioning

confidence: 96%

SOX Genes and Cancer

Cui¹,

Zhao²,

Hu³

2018

Gene Expression and Regulation in Mammalian Cells - Transcription From General Aspects

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Transcription factors play a critical role in regulating the gene expression programs that establish and maintain specific cell states in humans. Deregulation of these gene expression programs can lead to a broad range of diseases including cancer. SOX transcription factors are a conserved group of transcriptional regulators that mediates DNA binding by a highly conserved high-mobility group (HMG) domain. Numerous evidence has recently demonstrated that SOX transcription factors critically control cell fate and differentiation in major developmental processes, and that their upregulation may be important for cancer progression. In this review, we discuss recent advances in our understanding of the role of SOX genes in cancer.

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SOX9 is an atypical intestinal tumor suppressor controlling the oncogenic Wnt/ß-catenin signaling

Cited by 43 publications

References 37 publications

Hypoxia: Overview on Hypoxia-Mediated Mechanisms with a Focus on the Role of HIF Genes

Hypoxia: Overview on Hypoxia-Mediated Mechanisms with a Focus on the Role of HIF Genes

Contextual Classifications of Cancer Driver Genes

SOX Genes and Cancer

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