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RTKN2 knockdown alleviates the malignancy of breast cancer cells by regulating the Wnt/β-catenin pathway
Xiaomei Zhang1, Jian Wang2, Haiying Li3
1Department of Radiotherapy, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.
Abstract:
RTKN2 is a new effector protein of Rho GTPase, and has been indicated to be a tumor inhibitor in colon cancer. In this article, we explored the function of RTKN2 in BC cell development. RTKN2 expression in BC tissues and BC cell lines was evaluated by RT-qPCR and Western blot assay. CCK-8, Wound-healing and Transwell assays were carried out to examine the role of RTKN2 knockdown on proliferation, the migratory ability and the invasive ability of BC cells. FCM and Western blot assay were performed to measure the function of RTKN2 silencing on BC cell apoptosis. In addition, the regulatory effect of RTKN2 on Wnt/β-catenin pathway was studied via Western blot assay. RTKN2 expression was elevated in BC tissues and BC cells. Down-regulation of RTKN2 restrained BC cell progression by suppressing cell proliferation, migratory ability, invasive ability, and inducing apoptosis. In addition, reduced of RTKN2 sharply reduced the expressing levels of Wnt3A, β-catenin, C-Myc, and Cyclin D1, suggesting that RTKN2 silencing blocked the motivation of Wnt/β-catenin pathway in BC development. The in vivo experiment also confirmed the inhibitory effect of RTKN2 on BC tumors. Our study confirmed that RTKN2 was highly expressed in BC. Moreover, RTKN2 knockdown suppressed the development of BC through affecting the Wnt/β-catenin pathway. Hence, we deduced that RTKN2 was a possible treatment target for BC.
Insights
Rhotekin 2 (RTKN2) is highly expressed in bladder cancer (BC) and promotes tumor growth. Reducing RTKN2 inhibits BC cell proliferation, migration, and invasion, offering a potential new treatment target.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- RTKN2, a Rho GTPase effector, shows potential as a tumor suppressor in colon cancer.
- Its role in bladder cancer (BC) development requires further investigation.
Purpose of the Study:
- To investigate the function of RTKN2 in bladder cancer (BC) cell progression.
- To explore the underlying molecular mechanisms, including the Wnt/β-catenin pathway.
Main Methods:
- RT-qPCR and Western blot for RTKN2 expression analysis.
- Cell proliferation (CCK-8), migration (Wound-healing), invasion (Transwell), and apoptosis (FCM) assays.
- Analysis of Wnt/β-catenin pathway components via Western blot.
Main Results:
- RTKN2 expression is significantly elevated in BC tissues and cell lines.
- RTKN2 knockdown suppressed BC cell proliferation, migration, and invasion, while inducing apoptosis.
- Silencing RTKN2 downregulated Wnt3A, β-catenin, C-Myc, and Cyclin D1, inhibiting the Wnt/β-catenin pathway.
- In vivo studies confirmed RTKN2's tumor-promoting role in BC.
Conclusions:
- RTKN2 is highly expressed in BC and promotes tumor development.
- RTKN2 knockdown inhibits BC progression by modulating the Wnt/β-catenin pathway.
- RTKN2 represents a potential therapeutic target for bladder cancer.
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