Significance of TWIST and E‐cadherin expression in the metastatic progression of prostatic cancer

Hf, Yuen; Chua, Chee Wai; Yp, Chan; Wong, YC; Wang, X; Chan, Kwong‐Yau

doi:10.1111/j.1365-2559.2007.02665.x

Cited by 117 publications

(114 citation statements)

References 33 publications

(73 reference statements)

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“…another study also showed nuclear immunoreaction with Twist in high-grade squamous cell carcinoma (12). according to invasive behavior of adCC, our results support previous studies that have shown a relationship between nuclear Twist expression and increasing tumor invasiveness (10,19).…”

supporting

confidence: 81%

“…Twist includes two proteins: Twist1 and Twist2, which have shown similar expression in tumors (8). Twist expression was previously shown in some normal tissues such as prostate and breast (11,19). it was also demonstrated that this protein showed higher expression in malignant tumors compared to benign tumors such as prostate, parathyroid and lung (19)(20)(21).…”

mentioning

confidence: 92%

“…adCC is a high-grade tumor with a high ability of metastasis (29). it was demonstrated that nuclear expression of Twist was related to tumor metastasis (19). Previous studies have demonstrated higher expression of Twist in high grade adCC and its relationship with perineural invasion (13,14).…”

mentioning

confidence: 99%

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Twist expression in pleomorphic adenoma, adenoid cystic carcinoma and mucoepidermoid carcinoma of salivary glands

Pardis

Zare²,

Jaafari‐Ashkavandi³

et al. 2016

TJPATH

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Objective: Twist is an important transcription factor that induces epithelial-mesenchymal transition and therefore plays an important role in tumor progression. There are a few studies on Twist expression in salivary gland carcinomas. The aim of this study was to evaluate and compare the expression of Twist in the most common benign and malignant salivary gland tumors and to determine whether its expression was correlated with any tumor characteristics.Material and Method: in this retrospective cross-sectional study, 45 cases including 11 cases of normal salivary gland, 12 pleomorphic adenomas, 12 adenoid cystic carcinomas and 10 mucoepidermoid carcinomas were enrolled. The mean and intensity of Twist expression were evaluated immunohistochemically and were compared using statistical analysis. Results:The expression of Twist was higher in malignant salivary gland tumors in comparison with normal glands and benign tumors (p= 0.03). it was also higher in pleomorphic adenomas in comparison with normal tissue. adenoid cystic carcinomas and mucoepidermoid carcinomas showed no significant difference in Twist expression (p= 0.50). There was no correlation with the size, stage or grade of tumor. Conclusion:The findings showed that Twist might play a role in the formation of salivary gland neoplasm and also may affect malignant transformation and tumoral invasion. The exact mechanism of this marker and the possibility of using it as a therapeutic target require further investigation.

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supporting

confidence: 81%

mentioning

confidence: 92%

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Twist expression in pleomorphic adenoma, adenoid cystic carcinoma and mucoepidermoid carcinoma of salivary glands

Pardis

Zare²,

Jaafari‐Ashkavandi³

et al. 2016

TJPATH

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“…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]. These studies clearly demonstrate that TWIST is a master transcription factor that controls EMT, cancer progression and metastasis and a useful molecular target for treatment of cancer metastasis.…”

Section: Introductionmentioning

confidence: 65%

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, a helix-loop-helix transcription factor, is highly expressed in many types of human cancers (44). Recently, TWIST1 was suggested to be an oncogene (23,45,46) and confers prostate cancer cells with an enhanced metastatic potential through promoting EMT, and a high TWIST1 expression in human prostate cancer is associated with an increased metastatic potential (47). However, we did not find dihydrotestosterone to effect the TWIST1-regulated and/or EMT-related genes such as CDH1, SNAIL, and vimentin expression in LNCaP cells ( Fig.…”

Section: Discussionmentioning

confidence: 99%

Indole-3-Carbinol and 3′,3′-Diindolylmethane Modulate Androgen's Effect on C-C Chemokine Ligand 2 and Monocyte Attraction to Prostate Cancer Cells

Kim

Milner

et al. 2013

Cancer Prevention Research

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Inflammation has a role in prostate tumorigenesis. Recruitment of inflammatory monocytes to the tumor site is mediated by C-C chemokine ligand 2 (CCL2) through binding to its receptor CCR2. We hypothesized that androgen could modulate CCL2 expression in hormone-responsive prostate cancer cells and thereby promote recruitment of monocytes. Given the inhibitory effect of broccoli-derived compounds indole-3-carbinol (I3C) and 3,3 0 -diindolylmethane (DIM) on androgen-dependent pathways, we also reasoned that I3C and DIM could modulate the effect of androgen on CCL2-mediated pathways. Dihydrotestosterone was found to induce a time-dependent (0-72 hours) and concentration-dependent (0-1 nmol/L) increase in CCL2 mRNA levels in androgen-responsive human prostate cancer cells (LNCaP). This increase in CCL2 mRNA corresponded with increased secretion of CCL2 protein. The effect of dihydrotestosterone was mediated through an androgen receptor (AR)-dependent pathway as small inhibitor RNA against AR negated the induction of CCL2. Although dihydrotestosterone also induced TWIST1 mRNA, an epithelialmesenchymal transition-related factor, and purported inducer of CCL2, blocking its expression with small inhibitor RNA did not inhibit dihydrotestosterone induction of CCL2 mRNA. Moreover, conditioned media from androgen-treated cells promoted human monocyte THP-1 cell migration and this effect was blocked by antibody against CCL-2. Both I3C and DIM inhibited promotional effects of dihydrotestosterone on CCL2 and migration. These results show that androgen may regulate CCL2 and promote inflammatory microenvironment in prostate tumors and that this process can be blocked by broccoli-derived compounds.Cancer Prev Res; 6(6); 519-29. Ó2013 AACR.

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Significance of TWIST and E‐cadherin expression in the metastatic progression of prostatic cancer

Abstract: These results suggest that TWIST may serve as a prognostic marker for high-grade prostatic cancer. In addition, up-regulation of TWIST in combination with aberrant E-cadherin expression in primary prostatic cancer specimens may predict development of distal metastatic disease.

Cited by 117 publications

References 33 publications

Twist expression in pleomorphic adenoma, adenoid cystic carcinoma and mucoepidermoid carcinoma of salivary glands

Twist expression in pleomorphic adenoma, adenoid cystic carcinoma and mucoepidermoid carcinoma of salivary glands

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

Indole-3-Carbinol and 3′,3′-Diindolylmethane Modulate Androgen's Effect on C-C Chemokine Ligand 2 and Monocyte Attraction to Prostate Cancer Cells

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