<i>Twist</i> is required for patterning the cranial nerves and maintaining the viability of mesodermal cells

Ota, Masato S.; Loebel, David A.F.; O'Rourke, Meredith P.; Wong, Nicole; Tsoi, Bonny; Tam, Patrick

doi:10.1002/dvdy.20047

Cited by 36 publications

(25 citation statements)

References 48 publications

(73 reference statements)

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“…However, the p53 protein levels were unchanged. These results agree with previous reports that upregulation of TWIST led to alterations of p53-responsive factors such as Bax, rather than p53 itself in an environment where p53 pathway is intact (4,25,26). However, unlike observed in DU145 and PC3 cells, we did not find any significant alterations of the Bcl-2 protein between the TWIST transfectants and the vector control.…”

Section: Resultssupporting

confidence: 61%

Up-Regulation of TWIST in Prostate Cancer and Its Implication as a Therapeutic Target

Kwok¹,

Ling²,

Lee³

et al. 2005

Cancer Research

417

394

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Androgen-independent metastatic prostate cancer is the main obstacle in the treatment of this cancer. Unlike a majority of solid cancers, prostate cancer usually shows poor response to chemotherapeutic drugs. In this study, we have shown a potential novel target, TWIST, a highly conserved bHLH transcription factor, in the treatment of prostate cancer. Using malignant and nonmalignant prostate tissues, we found that TWIST expression was highly expressed in the majority (90%) of prostate cancer tissues but only in a small percentage (6.7%) of benign prostate hyperplasia. In addition, the TWIST expression levels were positively correlated with Gleason grading and metastasis, indicating its role in the development and progression of prostate cancer. Furthermore, down-regulation of TWIST through small interfering RNA in androgen-independent prostate cancer cell lines, DU145 and PC3, resulted in increased sensitivity to the anticancer drug taxol-induced cell death which was associated with decreased Bcl/Bax ratio, leading to activation of the apoptosis pathway. More importantly, inactivation of TWIST suppressed migration and invasion abilities of androgen-independent prostate cancer cells, which was correlated with induction of E-cadherin expression as well as morphologic and molecular changes associated with mesenchymal to epithelial transition. These results were further confirmed on the androgen-dependent LNCaP cells ectopically expressing the TWIST protein. Our results have identified TWIST as a critical regulator of prostate cancer cell growth and suggest a potential therapeutic approach to inhibit the growth and metastasis of androgen-independent prostate cancer through inactivation of the TWIST gene. (Cancer Res 2005; 65(12): 5153-62)

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Section: Resultssupporting

confidence: 61%

Up-Regulation of TWIST in Prostate Cancer and Its Implication as a Therapeutic Target

Kwok¹,

Ling²,

Lee³

et al. 2005

Cancer Research

417

394

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“…Twist1 has been implicated in the differentiation of multiple cell lineages including muscle, cartilage and osteogenic cells (Bialek et al 2004, Lee et al 1999, Lee et al 2000, Ota et al 2004). In mice, Twist1 was shown to be required for proper development of the head mesenchyme, somites, and limb buds (Lee et al 2009).…”

Section: Introductionmentioning

confidence: 99%

TWISTing stemness, inflammation and proliferation of epithelial ovarian cancer cells through MIR199A2/214

et al. 2010

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Cancer stem cells are responsible for sustaining the tumor and giving rise to proliferating and progressively differentiating cells. However, the molecular mechanisms regulating the process of cancer stem cell differentiation is not clearly understood. Recently, we reported the isolation of the epithelial ovarian cancer (EOC) stem cells (Type I/CD44+). In this study we show that Type I/CD44+ cells are characterized by low levels of both miR-199a and miR-214, whereas mature EOC cells (Type II/CD44-) have higher levels of miR-199a and miR-214. Moreover, these two miRNAs are regulated as a cluster on pri-miR-199a2 within the human Dnm3os gene (GenBank FJ623959). This study identify Twist1 as a regulator of this unique miRNA cluster responsible for the regulation of the IKKβ/NFκB and PTEN/AKT pathways and its association of ovarian cancer stem cell differentiation. Our data suggest that Twist1 may be an important regulator of “stemness” in EOC cells. The regulation of MIR199A2/214 expression may be used as a potential therapeutic approach in EOC patients.

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“…Twist-null embryos show numerous cranial defects, including failure of neural tube closure at forebrain and midbrain levels and severe anomalies in the branchial arches. 173,177,179,180 In particular, NC cells populate inappropriate locations in the first brancial arch and display defective osteogenic and odontogenic differentiation. In addition, loss of Twist impacts on the patterning of cranial ganglia and nerves.…”

mentioning

confidence: 99%

“…Interestingly, defects in the neural tube and NC at the midbrain and anterior hindbrain levels result primarily from the abnormalities in the cranial mesenchyme. 180 However, other defects have been reported in cardiac NC cells, resulting in anomalies in the cardiac outflow tract, and have been in contrast attributed to defects in NC cell delamination at the posterior hindbrain level. 181 The mechanisms by which Twist controls NC cell delamination remain unknown.…”

mentioning

confidence: 99%

Diversity in the molecular and cellular strategies of epithelium-to-mesenchyme transitions: Insights from the neural crest

Duband

2010

Cell Adhesion & Migration

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Twist is required for patterning the cranial nerves and maintaining the viability of mesodermal cells

Cited by 36 publications

References 48 publications

Up-Regulation of TWIST in Prostate Cancer and Its Implication as a Therapeutic Target

Up-Regulation of TWIST in Prostate Cancer and Its Implication as a Therapeutic Target

TWISTing stemness, inflammation and proliferation of epithelial ovarian cancer cells through MIR199A2/214

Diversity in the molecular and cellular strategies of epithelium-to-mesenchyme transitions: Insights from the neural crest

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