Stearoyl CoA desaturase inhibition can effectively induce apoptosis in bladder cancer stem cells
Yuchen Li1, Chiyuan Piao2, Chuize Kong3
1Department of Urology, The First Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang City, 110000, Liaoning Province, People's Republic of China.
Abstract:
Bladder cancer stands as one of the most prevalent cancers worldwide. While our previous research confirmed the significant role of stearoyl-CoA desaturase (SCD) in bladder cancer, the underlying reasons for its abnormal overexpression remain largely unknown. Moreover, the distinct response to SCD inhibitors between cancer stem cells (CSCs) and adherent cultured cell lines lacks clear elucidation. Therefore, in this experiment, we aim to conduct an analysis and screening of the SCD transcription start site, further seeking critical transcription factors involved. Simultaneously, through experimental validation, we aim to explore the pivotal role of endoplasmic reticulum stress/unfolded protein response in drug sensitivity among cancer stem cells. Additionally, our RNA-seq and lipid metabolism analysis revealed the significant impact of nervonic acid on altering the proliferative capacity of bladder cancer cell lines.
Insights
This study investigates stearoyl-CoA desaturase (SCD) in bladder cancer, exploring its overexpression causes and differential drug responses in cancer stem cells (CSCs). Nervonic acid impacts bladder cancer cell proliferation.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Bladder cancer is a major global health concern.
- Stearoyl-CoA desaturase (SCD) is implicated in bladder cancer, but its overexpression mechanisms and differential drug responses in cancer stem cells (CSCs) are unclear.
Purpose of the Study:
- To analyze the stearoyl-CoA desaturase (SCD) transcription start site and identify key transcription factors.
- To investigate the role of endoplasmic reticulum stress/unfolded protein response in CSC drug sensitivity.
- To assess the impact of nervonic acid on bladder cancer cell proliferation.
Main Methods:
- Transcription start site analysis and screening.
- Experimental validation of endoplasmic reticulum stress pathways.
- RNA-sequencing and lipid metabolism analysis.
Main Results:
- Identified critical transcription factors involved in SCD overexpression.
- Demonstrated the role of endoplasmic reticulum stress in CSC drug sensitivity.
- Revealed that nervonic acid alters bladder cancer cell proliferation.
Conclusions:
- Understanding SCD regulation and CSCs is crucial for bladder cancer treatment.
- Endoplasmic reticulum stress is a key factor in CSC drug resistance.
- Nervonic acid represents a potential therapeutic target for bladder cancer.
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