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Updated: Mar 22, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Twist2 promotes kidney cancer cell proliferation and invasion by regulating ITGA6 and CD44 expression in the
Hao-Jie Zhang1, Jing Tao2, Lu Sheng2
1Department of Urology, Huadong Hospital, Fudan University, Shanghai, People's Republic of China; Department of Urology, Zhongshan Hospital, Fudan University, Shanghai, People's Republic of China.
Abstract:
Twist2 is a member of the basic helix-loop-helix (bHLH) family and plays a critical role in tumorigenesis. Growing evidence has proven that Twist2 is involved in tumor progression; however, the role of Twist2 in human kidney cancer and its underlying mechanisms remain unclear. Real-time polymerase chain reaction and Western blot analysis were used to detect the expression of Twist2 in kidney cancer cells and tissues. Cell proliferation, cell cycle, apoptosis, migration, and invasion assay were analyzed using the Cell Count Kit-8, flow cytometry, wound healing, and Transwell analysis, respectively. In this study, we showed that Twist2 was upregulated in human kidney cancer tissues compared with normal kidney tissues. Twist2 promoted cell proliferation, inhibited cell apoptosis, and augmented cell migration and invasion in human kidney-cancer-derived cells in vitro. Twist2 also promoted tumor growth in vivo. Moreover, we found that the knockdown of Twist2 decreased the levels of ITGA6 and CD44 expression. This result indicates that Twist2 may promote migration and invasion of kidney cancer cells by regulating ITGA6 and CD44 expression. Therefore, our data demonstrated that Twist2 is involved in kidney cancer progression. The identification of the role of Twist2 in the migration and invasion of kidney cancer provides a potential appropriate treatment for human kidney cancer.
Insights
Twist2, a basic helix-loop-helix (bHLH) protein, is upregulated in kidney cancer. It promotes tumor growth, proliferation, and metastasis by regulating ITGA6 and CD44 expression, offering a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Twist2 is a basic helix-loop-helix (bHLH) protein implicated in tumorigenesis.
- The specific role and mechanisms of Twist2 in human kidney cancer progression are not well understood.
Purpose of the Study:
- To investigate the expression and function of Twist2 in human kidney cancer.
- To elucidate the underlying molecular mechanisms by which Twist2 influences kidney cancer development.
Main Methods:
- Real-time PCR and Western blot to assess Twist2 expression in kidney cancer tissues and cells.
- In vitro assays (Cell Count Kit-8, flow cytometry, wound healing, Transwell) to evaluate proliferation, apoptosis, migration, and invasion.
- In vivo studies to assess tumor growth.
- Analysis of ITGA6 and CD44 expression following Twist2 knockdown.
Main Results:
- Twist2 expression is significantly upregulated in human kidney cancer tissues compared to normal tissues.
- Twist2 overexpression promotes kidney cancer cell proliferation, inhibits apoptosis, and enhances migration and invasion in vitro.
- Twist2 promotes tumor growth in vivo.
- Knockdown of Twist2 reduces ITGA6 and CD44 expression, suggesting their involvement in Twist2-mediated effects.
Conclusions:
- Twist2 plays a crucial role in the progression of human kidney cancer.
- Twist2 promotes kidney cancer cell migration and invasion, potentially through the regulation of ITGA6 and CD44.
- Twist2 represents a potential therapeutic target for kidney cancer treatment.
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