The expression of Twist has an impact on survival in human bladder cancer and is influenced by the smoking status

Fondrevelle, Marie E.; Kantélip, B.; Reiter, Robert E.; Chopin, Dominique; Thiery, Jean Paul; Monnien, Franck; Bittard, Hugues; Wallerand, Hervé

doi:10.1016/j.urolonc.2007.12.012

Cited by 69 publications

(55 citation statements)

References 19 publications

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“…For example, Yoshino and coworkers (54) found that benzo[a]pyrene induced EMT-related genes in lung cancer cells; while fibronectin and Twist were induced, E-cadherin expression was deceased. In support of these findings, and in the context of another tobaccoinduced malignancy, Fondrevelle and colleagues (55) found that the expression of Twist was influenced by smoking status in patients with bladder cancer. Tobacco-specific carcinogen 4-(nmethyl-n-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) has also been found to promote EMT via induction of E-cadherin transcriptional repressors in human bronchial epithelial cells (56).…”

Section: Epithelial-mesenchymal Transitionmentioning

confidence: 70%

Smoking and Lung Cancer: The Role of Inflammation

Walser

Cui²,

Yanagawa³

et al. 2008

Proceedings of the American Thoracic Society

275

158

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Worldwide over 1 million people die due to lung cancer each year. It is estimated that cigarette smoking explains almost 90% of lung cancer risk in men and 70 to 80% in women. Clinically evident lung cancers have multiple genetic and epigenetic abnormalities. These abnormalities may result in activation of oncogenes and inactivation of tumor-suppressor genes. Chronic inflammation, which is known to promote cancer, may result both from smoking and from genetic abnormalities. These mediators in turn may be responsible for increased macrophage recruitment, delayed neutrophil clearance, and increase in reactive oxygen species (ROS). Thus, the pulmonary environment presents a unique milieu in which lung carcinogenesis proceeds in complicity with the host cellular network. The pulmonary diseases that are associated with the greatest risk for lung cancer are characterized by abundant and deregulated inflammation. Pulmonary disorders such as chronic obstructive pulmonary disease (COPD)/emphysema are characterized by profound abnormalities in inflammatory and fibrotic pathways. The cytokines and growth factors aberrantly produced in COPD and the developing tumor microenvironment have been found to have deleterious properties that simultaneously pave the way for both epithelialmesenchymal transition (EMT) and destruction of specific host cellmediated immune responses. Full definition of these pathways will afford the opportunity to intervene in specific inflammatory events mediating lung tumorigenesis and resistance to therapy.

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Section: Epithelial-mesenchymal Transitionmentioning

confidence: 70%

Smoking and Lung Cancer: The Role of Inflammation

Walser

Cui²,

Yanagawa³

et al. 2008

Proceedings of the American Thoracic Society

275

158

View full text Add to dashboard Cite

show abstract

“…In human tumor cell lines the forced expression of E-cadherin was not sufficient to reverse the process of EMT in Twist-expressing cells, showing that Twist might be responsible for modulating other important signaling pathways. For example, it can be involved in tumor progression and metastasis development independently of E-cadherin expression [17].…”

Section: Discussionmentioning

confidence: 99%

CD99 correlates with low cyclin D1, high topoisomerase 2 status and triple negative molecular phenotype but is prognostically irrelevant in breast carcinoma

Czapiewski¹,

Wełnicka-Jaśkiewicz²,

Seroczyńska³

et al. 2015

pjp

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CD99 is a protein initially described in the Ewing sarcoma family of tumors, but growing evidence has shown its expression in other tumors of mesenchymal, hematopoietic and even epithelial origin. Some articles report CD99 in metaplastic carcinoma of the breast, a subtype of breast carcinoma (BC) with pronounced epithelial to mesenchymal (EMT) phenotype. Our aim was to analyse the potential relationship between CD99 and selected EMT (vimentin, E-cadherin, Twist) and proliferation markers (Ki-67, c-myc, cyclin D1, topoisomerase 2α), molecular subtypes of BC, as well as overall survival (OS) and progression-free survival (PFS). In a group of 122 cases CD99 membrane expression was seen in 14 (11.5%) cases: strong in 11 (9%) and moderate in 3 (2.5%). Expression of CD99 correlated with low cyclin D1 index, high level of topoisomerase 2α expression and lack of progesterone receptor (PR) but not with EMT characteristics. Additionally, strong expression of CD99 correlated with triple negative molecular BC phenotype. CD99 was prognostically irrelevant for OS and PFS. CD99 correlates with selected proliferative markers and low ER/PR receptor status but not with patients' outcome in BC. Further studies are required to explain precisely its role in molecular pathogenesis of BC.

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“…Twist can promote malignant tumor development and metastasis, and Twist activation in human cancers might both be a prognostic and/or predictive factor as well as a novel therapeutic target (11)(12)(13). Twist CpG methylation is a useful biomarker in breast cancer diagnosis (14,15).…”

Section: Introductionmentioning

confidence: 99%

Differential methylation of CpG islands within the dermo1 gene promoter in several cancer cell lines

Mao

Toh²,

Ding³

et al. 2010

Oncol Rep

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Abstract. Inactivation of tumor-related genes by promoter hypermethylation is a common epigenetic event in the development of variety of tumors. Dermo1 (also called twist2) is a novel cancer-related gene which belongs to the basic helixloop-helix (bHLH) transcription factor family. Herein, we report that dermo1 expression was sporadically abrogated in human cancer cells by transcriptional silencing associated with CpG island promoter hypermethylation. Direct sequencing of bisulfite-modified DNA from a panel of seven human cancer cell lines (HL60, Molm14, MV4-11, RS4:11, MDM-BA231, H358, and H1299) revealed that CpG dinucleotides in the dermo1 promoter were methylated. RT-PCR results demonstrated that dermo1 CpG island hypermethylation was accompanied by a low basal dermo1 expression level. Our data implicate dermo1 as a tumor suppressor gene and a valuable molecular marker for human cancer.

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The expression of Twist has an impact on survival in human bladder cancer and is influenced by the smoking status

Cited by 69 publications

References 19 publications

Smoking and Lung Cancer: The Role of Inflammation

Smoking and Lung Cancer: The Role of Inflammation

CD99 correlates with low cyclin D1, high topoisomerase 2 status and triple negative molecular phenotype but is prognostically irrelevant in breast carcinoma

Differential methylation of CpG islands within the dermo1 gene promoter in several cancer cell lines

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