TWIST1 is a molecular marker for a poor prognosis in oral cancer and represents a potential therapeutic target

Silva, Sabrina Daniela da; Alaoui‐Jamali, Moulay A.; Soares, Fernando Augusto; Carraro, Dirce Maria; Brentani, Helena; Hier, Michael P.; Rogatto, Sílvia Regina; Kowalski, Luiz Paulo

doi:10.1002/cncr.28404

Cited by 52 publications

(55 citation statements)

References 36 publications

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“…Dysregulation of Twist1 expression and function was also related with tumor invasion and metastasis in several solid cancers, such as oral cancer [30], esophageal squamous cell carcinoma [31], prostate cancer [32], as well as HCC [33,34]. In the present study, the ectopic expression or targeted knock down of SOX5 resulted in increased or decreased expression of Twist1.…”

Section: Discussionmentioning

confidence: 69%

SOX5 promotes epithelial–mesenchymal transition and cell invasion via regulation of Twist1 in hepatocellular carcinoma

et al. 2015

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The transcription factor sex determining region Y-box protein 5 (SOX5) plays important roles in various types of cancers. However, the expression and function of SOX5 in hepatocellular carcinoma (HCC) have not been elucidated. Here, we found that SOX5 is significantly up-regulated in HCC tissues and cell lines. Gain- and loss-of-function studies demonstrated that SOX5 promoted HCC cell migration and invasion. In addition, we revealed that SOX5 is linked to epithelial-mesenchymal transition (EMT) by regulation of Twist1. Our results indicate for the first time that SOX5 is a novel regulator of EMT in HCC and may be a potential therapeutic target for HCC metastasis.

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Section: Discussionmentioning

confidence: 69%

SOX5 promotes epithelial–mesenchymal transition and cell invasion via regulation of Twist1 in hepatocellular carcinoma

et al. 2015

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“…Apart from physical alterations, E-cadherin could induce EMT by induction of transcription factor such as Twist [21]. Twist is usually associated with the advanced cancers and linked with the positive lymph node, lung metastasis, and poor survival of oral squamous cell carcinoma patients [22]. …”

Section: Epithelial-mesenchymal Transition (Emt) and E-cadherinmentioning

confidence: 99%

Interactions between E-Cadherin and MicroRNA Deregulation in Head and Neck Cancers: The Potential Interplay

Wong

Gao

Chan

2014

BioMed Research International

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E-cadherin expression in the head and neck epithelium is essential for the morphogenesis and homeostasis of epithelial tissues. The cadherin-mediated cell-cell contacts are required for the anchorage-dependent growth of epithelial cells. Further, survival and proliferation require physical tethering created by proper cell-cell adhesion. Otherwise, the squamous epithelial cells will undergo programmed cell death. Head and neck cancers can escape from anoikis and enter into the epithelial-mesenchymal transition stages via the modulation of E-cadherin expression with epigenetic mechanisms. At epigenetic level, gene expression control is not dependent on the DNA sequence. In the context of E-cadherin regulation in head and neck cancers, 2 major mechanisms including de novo promoter hypermethylation and microRNA dysregulation are most extensively studied. Both of them control E-cadherin expression at transcription level and subsequently hinder the overall E-cadherin protein level in the head and neck cancer cells. Increasing evidence suggested that microRNA mediated E-cadherin expression in the head and neck cancers by directly/indirectly targeting the transcription suppressors of E-cadherin, ZEB1 and ZEB2.

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“…The classical subtype is characterized by overexpression of genes related to oxidative stress response and xenobiotic metabolism, and is most strongly associated with tobacco exposure. Deregulation of the KEAP1/NRF2 oxidative stress pathway appears to be a critical element of carcinogenesis in the classical subtype, and there is growing evidence to suggest that the KEAP1‐NRF2 mediated oxidative stress response plays a role in resistance to radiation in several human cancers . The atypical subtype is characterized by elevated expression of CDKN2A, LIG1 , and RPA2 , and has also been associated with low EGFR expression …”

Section: Introductionmentioning

confidence: 99%

Gene Expression Subtype Predicts Nodal Metastasis and Survival in Human Papillomavirus–Negative Head and Neck Cancer

et al. 2018

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Objective/Hypothesis Gene expression analyses of head and neck cancer have revealed four molecular subtypes: basal (BA), mesenchymal (MS), atypical (AT), and classical (CL). We evaluate whether gene expression subtypes in oral cavity (OCSCC) and laryngeal (LSCC) can be used to predict nodal metastasis and prognosticate survival. Level of Evidence 2b Study Design Retrospective cohort study and genomic analysis Methods OCSCC and LSCC cases were identified from the TCGA head and neck cancer cohort. RNA-Seq by Expected Maximization (RSEM) was used to quantify gene expression levels from TCGA RNA-seq data and to assign each case to one of four subtypes. Descriptive statistics were used to describe patient, disease and treatment characteristics in each subtype. Cox regression and Kaplan Meier analyses were used to determine associations with survival. Results OCSCC cases were comprised primarily of the MS and BA subtypes, while LSCC was comprised primarily of CL and AT subtypes. In OCSCC, the MS subtype was significantly associated with higher risk of nodal metastasis. In a subset analysis of clinically T1-2N0M0 OCSCC, we demonstrate that the MS subtype was predictive of occult nodal metastasis (RR=3.38, 95% CI 1.08–10.69). In LSCC, the CL subtype was associated with significantly worse overall survival (HR=4.32, 95% CI 1.77–10.54, p=0.001). Conclusions Gene expression analysis reveals potential novel markers of nodal metastasis and survival in HPV (−) head and neck cancer. Future studies will continue to refine and validate these markers, with the goal of providing molecular risk assessments that guide therapy and improve patient outcomes.

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TWIST1 is a molecular marker for a poor prognosis in oral cancer and represents a potential therapeutic target

Cited by 52 publications

References 36 publications

SOX5 promotes epithelial–mesenchymal transition and cell invasion via regulation of Twist1 in hepatocellular carcinoma

SOX5 promotes epithelial–mesenchymal transition and cell invasion via regulation of Twist1 in hepatocellular carcinoma

Interactions between E-Cadherin and MicroRNA Deregulation in Head and Neck Cancers: The Potential Interplay

Gene Expression Subtype Predicts Nodal Metastasis and Survival in Human Papillomavirus–Negative Head and Neck Cancer

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