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Published on: October 27, 2020
Expression and mutational analysis of TGF-beta/Smads signaling in human cervical cancers
Kyung-Do Ki1, Seo-Yun Tong, Chu-Yeop Huh
1Department of Obstetrics and Gynecology, East-West Neo Medical Center, Kyung Hee University, Seoul, Korea.
Objective:
To define the molecular basis of TGF-beta1 function in cervical carcinogenesis, we explored the expression and mutational status of TGF-beta1, TGF-beta1 receptors, and Smads, the regulators of the TGF-beta1 signaling pathway, in human cervical cancers.
Methods:
Expression of TGF-beta1, TGF-beta1 receptors, and Smads transcripts were determined by quantitative reverse transcription-polymerase chain reaction (RT-PCR), and sequence alteration was analyzed using RT-PCR-single-strand conformation polymorphism (SSCP) analysis. Genomic levels of TGF-beta1, TGF-beta1 receptors and Smads was also measured by quantitative genomic PCR.
Results:
Abnormal overexpression of TGF-beta1 and abnormal reduction of type II TGF-beta1 receptor were identified in 36% (18 of 50) and 20% (10 of 50) of cervical cancer tissues, respectively. 22% (11 of 50) in Smad2 and 14% (7 of 50) in Smad4 revealed tumor specific mRNA reduction less than a half of normal means. In addition, no evidence for sequence alterations of the gene was found by RT-PCR-SSCP analysis.
Conclusion:
Our study demonstrates that disruption of TGF-beta/Smad signaling pathway exist in human cervical cancer, suggesting that abnormal expressions of the member of TGF-beta/Smad signaling pathway might contribute to the malignant progression of human cervical tumors via suppressing the tumor suppression function of TGF-beta1 1's tumor suppression function.
Insights
Disrupted TGF-beta/Smad signaling is found in cervical cancer. Abnormal expression of pathway members may drive tumor progression by suppressing TGF-beta1
Area of Science:
- Oncology
- Molecular Biology
- Cell Signaling
Background:
- Cervical cancer is a significant global health issue.
- The transforming growth factor-beta (TGF-beta) signaling pathway plays a crucial role in tumor suppression.
- Dysregulation of TGF-beta signaling is implicated in various cancers, including cervical cancer.
Purpose of the Study:
- To investigate the molecular basis of TGF-beta1 function in cervical carcinogenesis.
- To analyze the expression and mutational status of TGF-beta1, its receptors, and Smad proteins in human cervical cancers.
Main Methods:
- Quantitative reverse transcription-polymerase chain reaction (RT-PCR) to determine transcript levels.
- RT-PCR-single-strand conformation polymorphism (SSCP) analysis for sequence alterations.
- Quantitative genomic PCR to measure genomic levels of key genes.
Main Results:
- Abnormal overexpression of TGF-beta1 (36%) and reduced type II TGF-beta1 receptor (20%) were observed.
- Tumor-specific mRNA reduction was noted for Smad2 (22%) and Smad4 (14%).
- No sequence alterations were detected in the analyzed genes.
Conclusions:
- Disruption of the TGF-beta/Smad signaling pathway is evident in human cervical cancer.
- Abnormal expression of TGF-beta/Smad pathway components may contribute to cervical tumor malignant progression.
- The findings suggest a loss of TGF-beta1's tumor suppressive function in cervical carcinogenesis.
