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In Silico, In Vitro, and Clinical Investigations of Cathepsin B and Stefin A mRNA Expression and a Correlation
Magdalena Rudzinska-Radecka1,2, Anastasia S Frolova1,3, Anastasia V Balakireva1,4
1Institute of Molecular Medicine, Sechenov First Moscow State Medical University, 119991 Moscow, Russia.
Abstract:
The cysteine protease Cathepsin B (CtsB) plays a critical role in multiple signaling pathways, intracellular protein degradation, and processing. Endogenous inhibitors regulate its enzymatic activity, including stefins and other cystatins. Recent data proved that CtsB is implicated in tumor extracellular matrix remodeling, cell invasion, and metastasis: a misbalance between cathepsins and their natural inhibitors is often considered a sign of disease progression. In the present study, we investigated CtsB and stefin A (StfA) expression in renal cell carcinoma (RCC). mRNA analysis unveiled a significant CTSB and STFA increase in RCC tissues compared to adjacent non-cancerogenic tissues and a higher CtsB expression in malignant tumors than in benign renal neoplasms. Further analysis highlighted a positive correlation between CtsB and StfA expression as a function of patient sex, age, tumor size, grade, lymph node invasion, metastasis occurrence, and survival. Alternative overexpression and silencing of CtsB and StfA confirmed the correlation expression between these proteins in human RCC-derived cells through protein analysis and fluorescent microscopy. Finally, the ectopic expression of CtsB and StfA increased RCC cell proliferation. Our data strongly indicated that CtsB and StfA expression play an important role in RCC development by mutually stimulating their expression in RCC progression.
Insights
Cathepsin B (CtsB) and stefin A (StfA) are upregulated in renal cell carcinoma (RCC), correlating with tumor progression and patient outcomes. Their mutual expression drives RCC development and proliferation.
Area of Science:
- Oncology
- Biochemistry
- Molecular Biology
Background:
- Cathepsin B (CtsB) is a cysteine protease involved in cellular processes and implicated in tumor progression.
- Endogenous inhibitors like stefins regulate CtsB activity; an imbalance is linked to disease progression.
- CtsB's role in extracellular matrix remodeling, invasion, and metastasis highlights its oncogenic potential.
Purpose of the Study:
- To investigate the expression of Cathepsin B (CtsB) and stefin A (StfA) in renal cell carcinoma (RCC).
- To determine the correlation between CtsB and StfA expression and clinicopathological features of RCC.
- To elucidate the functional role of CtsB and StfA in RCC development and progression.
Main Methods:
- Quantitative mRNA analysis of CTSB and STFA in RCC tissues versus adjacent non-cancerogenic tissues.
- Protein analysis and fluorescent microscopy to confirm CtsB and StfA expression and correlation in RCC cells.
- Overexpression and silencing experiments to assess the functional impact of CtsB and StfA on RCC cells.
Main Results:
- Significant upregulation of CTSB and STFA mRNA in RCC tissues, with higher CtsB levels in malignant tumors.
- Positive correlation between CtsB and StfA expression and patient sex, age, tumor size, grade, lymph node invasion, metastasis, and survival.
- Ectopic expression of CtsB and StfA enhanced RCC cell proliferation, confirming their mutual stimulation in RCC progression.
Conclusions:
- CtsB and StfA are significantly overexpressed in RCC and are associated with adverse clinicopathological features.
- A positive correlation exists between CtsB and StfA expression, suggesting a mutual regulatory mechanism in RCC.
- CtsB and StfA play a crucial role in RCC development and progression, potentially serving as therapeutic targets.
