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Updated: Apr 23, 2026

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition
Published on: October 9, 2014
A comparison of Twist and E-cadherin protein expression in primary non-small-cell lung carcinoma and corresponding
Guanghui Wang1, Wei Dong, Hongchang Shen
1Department of Thoracic Surgery, Provincial Hospital Affiliated to Shandong University, Jinan, PR China.
Objective:
The metastasis of solid tumors is directly or indirectly responsible for most cancer-related deaths. It has already been known that in non-small-cell lung carcinoma cells, up-regulation of Twist (a highly conserved basic helix-loop-helix transcription factor) can promote epithelial-mesenchymal transition through down-regulation of E-cadherin. The main aim of this study was to determine whether the expression of Twist and E-cadherin differs between primary and metastatic lung carcinoma and to correlate Twist and E-cadherin expression in primary and metastatic non-small-cell lung carcinoma.
Methods:
Thirteen patients with non-small-cell lung carcinoma and hematogenous metastases were studied in retrospect, and Twist and E-cadherin were detected by immunohistochemistry in 26 tissue samples from the 13 patients.
Results:
We demonstrated that the expression of Twist was higher in metastatic non-small-cell lung carcinoma tissues than in primary non-small-cell lung carcinoma (p=0.008) and discordance of Twist expression was observed in 11 (85%) patients. For E-cadherin, 12 cases (92%) showed discordance between primary tumor and metastasis (p=0.002): E-cadherin expressed higher in the primary tumor than in the metastasis in 12 cases. We also found that increased Twist expression was correlated with decreased membranous E-cadherin expression (p=0.009).
Conclusions:
Our data imply that Twist induces epithelial-mesenchymal transition in non-small-cell lung carcinoma by reducing E-cadherin, then promoting metastasis.
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