[High expression of twist is positively correlated with the differentiation of lung cancer.].

BACKGROUND Twist has been identified as a promoting factor for epithelialmesenchymal transition (EMT), which enhances the metastatic potential of cancer. The aim of this study is to detect the expression of Twist in lung cancer tissues and cell lines, and analyze its relationship with clinicopathologic characteristics and biological behavior of lung cancer. METHODS Twist expression was examined in 68 lung cancer specimens and 8 normal lung specimens using immunohistochemistry (S-P method). Expression levels of Twist1 and Twist2 mRNA were detected using transcription-polymerase chain reaction (RT-PCR) in HBE and 8 lung cancer cell lines. Immunofluorescence was used to detect the Twist protein expression levels and subcellular localization in lung cancer cells and HBE (human normal bronchi epithelium) cells. RESULTS Among 68 lung cancer specimens, 9 samples showed weak expression of Twist 13.24% (9 of 68), 75.00% (51 of 68) lung cancer specimens showed moderate to strong Twist staining whereas 8 corresponding normal lung specimens showed weak staining extent. Twist expression level was positively correlated with differentiation (P =0.002) and age (P =0.012). Twist1 and Twist2 mRNA expression levels were incompatible in different histology types. The fluorescence signal of Twist protein was conspicuous in lung squamous cell carcinoma cells and adencarcinoma cells, primarily in cytoplasm, but low in HBE. CONCLUSIONS High expression of Twist in lung cancer was associated with differentiation. Twist could be used as a valuable biomarker to evaluate the progression of lung cancer.

[1]  細野 覚代 Expression of Twist increases the risk for recurrence and for poor survival in epithelial ovarian carcinoma patients , 2009 .

[2]  R. Maestro,et al.  Induction of EMT by twist proteins as a collateral effect of tumor-promoting inactivation of premature senescence. , 2008, Cancer cell.

[3]  D. Xie,et al.  Significance of TWIST expression and its association with E-cadherin in bladder cancer. , 2007, Human pathology.

[4]  Tomokazu Yoshizaki,et al.  Twist and epithelial-mesenchymal transition are induced by the EBV oncoprotein latent membrane protein 1 and are associated with metastatic nasopharyngeal carcinoma. , 2007, Cancer research.

[5]  S. Law,et al.  Upregulation of Twist in oesophageal squamous cell carcinoma is associated with neoplastic transformation and distant metastasis , 2006, Journal of Clinical Pathology.

[6]  P. V. van Diest,et al.  Twist overexpression induces in vivo angiogenesis and correlates with chromosomal instability in breast cancer. , 2005, Cancer research.

[7]  D. Silbergeld,et al.  TWIST is expressed in human gliomas and promotes invasion. , 2005, Neoplasia.

[8]  Xiaomeng Zhang,et al.  Up-regulation of TWIST in prostate cancer and its implication as a therapeutic target. , 2005, Cancer research.

[9]  V. Raman,et al.  HOXA5-Twist Interaction Alters p53 Homeostasis in Breast Cancer Cells* , 2005, Journal of Biological Chemistry.

[10]  J. Massagué,et al.  Epithelial-Mesenchymal Transitions Twist in Development and Metastasis , 2004, Cell.

[11]  S. Ariyan,et al.  Expression Profiling Reveals Novel Pathways in the Transformation of Melanocytes to Melanomas , 2004, Cancer Research.

[12]  S. Ramaswamy,et al.  Twist, a Master Regulator of Morphogenesis, Plays an Essential Role in Tumor Metastasis , 2004, Cell.

[13]  L. R. Howe,et al.  Twist is up-regulated in response to Wnt1 and inhibits mouse mammary cell differentiation. , 2003, Cancer research.

[14]  L. Kedes,et al.  Regulation of Histone Acetyltransferases p300 and PCAF by the bHLH Protein Twist and Adenoviral Oncoprotein E1A , 1999, Cell.