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Updated: Jun 11, 2025

Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
Published on: February 6, 2015
Downregulation of RhoB Inhibits Cervical Cancer Progression and Enhances Cisplatin Sensitivity
Weijiao Wang1,2, Yubin Jia1,2, Yuhuan Liu1,2
1Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Abstract:
RhoB, a member of the Rho GTPase family, has been implicated in the malignant progression of various cancer types. However, its role in cervical cancer (CC) remains unclear. Therefore, this study aims to elucidate the biological function of RhoB in CC and its relationship with cisplatin sensitivity. We analyzed data from the TCGA, GTEx, and GEO databases, revealing that RhoB mRNA expression is downregulated in CC tissues compared to normal cervical tissues. The further analysis of the TCGA database and Tongji samples showed that CC patients with a high RhoB expression had a shorter overall survival (OS). Subsequently, we found that the knockdown of RhoB inhibited the proliferation, migration, and invasion of cancer cells, while increasing apoptosis. Through Western blot (WB) analysis, we found that knocking down RhoB resulted in an increased expression of the epithelial marker E-cadherin, while the levels of N-cadherin, MMP2, MMP9, Vimentin, and Snail1 were reduced. Additionally, RhoB mRNA expression was upregulated in CC tissues after chemotherapy compared to CC tissues before chemotherapy. In CC cells, RhoB expression increased with cisplatin concentration, and the IC50 value decreased following RhoB knockdown. Moreover, the knockdown of RhoB could enhance the cellular apoptosis triggered by cisplatin. This study demonstrated that RhoB plays an oncogenic role in CC and that its knockdown could enhance the sensitivity of CC cells to cisplatin.
Insights
RhoB is downregulated in cervical cancer (CC) but promotes its progression. Reducing RhoB inhibits CC growth and enhances cisplatin sensitivity, offering a potential therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- RhoB, a Rho GTPase, is linked to cancer progression, but its role in cervical cancer (CC) is not well understood.
- Understanding RhoB's function in CC is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the biological role of RhoB in cervical cancer.
- To determine the relationship between RhoB expression and cisplatin sensitivity in CC.
Main Methods:
- Analysis of public databases (TCGA, GTEx, GEO) and patient samples.
- RhoB knockdown experiments in CC cells.
- Assessment of cell proliferation, migration, invasion, apoptosis, and epithelial-mesenchymal transition (EMT) markers.
- Western blot analysis.
- Evaluation of cisplatin sensitivity and IC50 values.
Main Results:
- RhoB mRNA expression was downregulated in CC tissues.
- High RhoB expression correlated with shorter overall survival in CC patients.
- RhoB knockdown suppressed CC cell proliferation, migration, and invasion, while increasing apoptosis.
- RhoB knockdown altered EMT markers, increasing E-cadherin and decreasing N-cadherin, MMP2, MMP9, Vimentin, and Snail1.
- RhoB expression increased post-chemotherapy and with cisplatin concentration.
- RhoB knockdown enhanced CC cell sensitivity to cisplatin and increased cisplatin-induced apoptosis.
Conclusions:
- RhoB plays an oncogenic role in cervical cancer progression.
- Downregulation of RhoB inhibits CC cell growth and metastasis.
- Targeting RhoB can enhance the efficacy of cisplatin chemotherapy in cervical cancer.
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