Identification of a novel function of TWIST, a bHLH protein, in the development of acquired taxol resistance in human cancer cells

Wang, Xianghong; Ling, Ming-Tat; Guan, Xin Yuan; Tsao, Sai Wah; Cheung, Hiu Wing; Lee, Davy Tak; Wong, Yong Chuan

doi:10.1038/sj.onc.1207128

Cited by 206 publications

(183 citation statements)

References 35 publications

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“…14,36,37 Only 9 samples present an amplification of the gene, which is expected to result in higher amounts of gene products in malignant bone tissues, according to previous studies. 18,22 These results pointed also toward frequent heterozygous deletions at TWIST in the DNA of pediatric osteosarcomas.…”

Section: Discussionmentioning

confidence: 72%

Frequent genomic abnormalities at TWIST in human pediatric osteosarcomas

Entz‐Werlé

Stoetzel

Berard-Marec

et al. 2005

Intl Journal of Cancer

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The identification of genes as markers for chromosome aberrations in specific tumors might facilitate oncogenesis mechanism comprehension, cancer detection, prediction of clinical outcomes, and response to therapy. Previous physiologic and oncologic data identified the TWIST gene as a marker for mesodermal derivative and bone tissue differentiation, but its contribution to bone malignancies has not been investigated. In the present study, search for genomic alterations in high-grade pediatric osteosarcomas was focused on the 7p21 region, and more specifically on the TWIST gene. In a cohort of 74 patients, we observed by allelotyping that 31 of 68 informative tumors were rearranged at the TWIST locus. Among them, analysis by quantitative PCR (QPCR) revealed that, surprisingly, mostly deletions (22/68), but also amplifications (9/ 68), of the TWIST gene were detected. Furthermore, deletions at TWIST were statistically correlated to other molecular abnormalities, like alterations at the APC or c-kit loci, as well as to clinical features such as a poor outcome. This work shows that the TWIST gene seemed to be involved in high-grade pediatric osteosarcomas and is a new marker with a possible initial predictive value. ' 2005 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 72%

Frequent genomic abnormalities at TWIST in human pediatric osteosarcomas

Entz‐Werlé

Stoetzel

Berard-Marec

et al. 2005

Intl Journal of Cancer

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“…In the process of metastasis, TWIST represses E-cadherin and β-catenin expression, promotes EMT, cell motility and invasiveness, and permits the intravasation of tumor cells [3,[7][8][9]. TWIST also enhances AKT2 expression, inhib-its p53 function and cell apoptosis, mediates HIF-1α-enhanced cancer progression, promotes cell survival, and contributes to oncogenesis, angiogenesis and acquired Taxol resistance [7,[10][11][12][13][14]. In agreement with these critical roles in cancer cells, TWIST is overexpressed in breast, gastric, hepatocellular, prostate and bladder cancers, and its upregulation correlates with low E-cadherin expression, high cancer aggressiveness and poor survival rate [3,8,[15][16][17][18][19].…”

Section: Introductionmentioning

confidence: 99%

The TWIST/Mi2/NuRD protein complex and its essential role in cancer metastasis

et al. 2010

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The epithelial-mesenchymal transition (EMT) converts epithelial tumor cells into invasive and metastatic cancer cells, leading to mortality in cancer patients. Although TWIST is a master regulator of EMT and metastasis for breast and other cancers, the mechanisms responsible for TWIST-mediated gene transcription remain unknown. In this study, purification and characterization of the TWIST protein complex revealed that TWIST interacts with several components of the Mi2/nucleosome remodeling and deacetylase (Mi2/NuRD) complex, MTA2, RbAp46, Mi2 and HDAC2, and recruits them to the proximal regions of the E-cadherin promoter for transcriptional repression. Depletion of these TWIST complex components from cancer cell lines that depend on TWIST for metastasis efficiently suppresses cell migration and invasion in culture and lung metastasis in mice. These findings not only provide novel mechanistic and functional links between TWIST and the Mi2/NuRD complex but also establish new essential roles for the components of Mi2/NuRD complex in cancer metastasis.

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“…Twist1, which is a member of a large family of basic helix-loop-helix proteins, has been implicated in bone and cartilage development, 11,12 regulation of inflammation, 13,14 tumor progression and metastasis, [15][16][17] and resistance of tumor cells to apoptosis induced by chemotherapeutic agents. 16,18 Thus, we reasoned that Twist1 may play an analogous role in primary lung fibroblasts subjected to the harsh were performed by GenScript (Piscataway, NJ). We affinitypurified IgG using a peptide affinity column.…”

mentioning

confidence: 99%

Gene Expression Profiling of Pulmonary Fibrosis Identifies Twist1 as an Antiapoptotic Molecular “Rectifier” of Growth Factor Signaling

Bridges

Kass

Loh

et al. 2009

The American Journal of Pathology

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Idiopathic pulmonary fibrosis (IPF) is a progressive and typically fatal lung disease. To gain insight into IPF pathogenesis, we performed gene expression profiling of IPF lungs. Twist1, a basic helix-loop-helix protein, was found among the most consistently and highly up-regulated genes and was expressed in nuclei of type II epithelial cells, macrophages, and fibroblasts in IPF lungs. We studied the function of Twist1 in fibroblasts further, because they are the major effector cells in this disease and persist despite an ambient proapoptotic environment. Twist1 was induced by the profibrotic growth factors (GFs) basic fibroblast growth factor, platelet-derived growth factor, and epidermal growth factor in primary rat lung fibroblasts (RLFs). Suppression of Twist1 expression resulted in decreased RLF accumulation due to increased apoptosis, whereas Twist1 overexpression protected RLFs against several apoptotic stimuli. Addition of platelet-derived growth factor in combination with other GFs led to an increase in proliferation. When Twist1 was depleted, GFs continued to act as mitogens but caused a marked increase in cell death. The increase in apoptosis under basal or growth factorstimulated conditions was partly mediated by up-regulation of the proapoptotic Bcl-2 family members, Bim and PUMA. These findings indicate that Twist1 promotes survival and accumulation of fibroblasts by shaping their responsiveness to growth factor stimulation. We propose that Twist1 represents one of the factors that promotes pathogenic accumulation of fibroblasts in fibrotic lung disease. (Am J Pathol

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Identification of a novel function of TWIST, a bHLH protein, in the development of acquired taxol resistance in human cancer cells

Cited by 206 publications

References 35 publications

Frequent genomic abnormalities at TWIST in human pediatric osteosarcomas

Frequent genomic abnormalities at TWIST in human pediatric osteosarcomas

The TWIST/Mi2/NuRD protein complex and its essential role in cancer metastasis

Gene Expression Profiling of Pulmonary Fibrosis Identifies Twist1 as an Antiapoptotic Molecular “Rectifier” of Growth Factor Signaling

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