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Stearoyl-CoA Desaturase-1 Attenuates the High Shear Force Damage Effect on Human MG63 Osteosarcoma Cells
Kuo-Chin Huang1,2, Po-Yao Chuang1,3, Rong-Ze Hsieh4
1Department of Orthopaedics, Chiayi Chang Gung Memorial Hospital, Chiayi 613, Taiwan.
Abstract:
Mechanical regulation is known as an important regulator in cancer progression and malignancy. High shear force has been found to inhibit the cell cycle progression and result in cell death in various cancer cells. Stearoyl-CoA desaturase (SCD)-1, one of the important lipogenic enzymes, has recently been indicated as a potential pharmaceutical target in cancer therapy. In this study, we determined whether the cell fate control of shear force stimulation is through regulating the SCD-1 expression in cancer cells. Human MG63 osteosarcoma cells were used in this study. 2 and 20 dynes/cm2 shear forces were defined as low and high intensities, respectively. A SCD-1 upregulation in human MG63 osteosarcoma cells under 20, but not 2, dynes/cm2 shear force stimulation was shown, and this induction was regulated by Smad1/5 and peroxisome proliferator-activated receptor δ (PPARδ) signaling. Moreover, gene knockdown of PPARδ and SCD-1 in human MG63 osteosarcoma cells attenuated the differentiation inhibition and resulted in much more cell death of high shear force initiation. The present study finds a possible auto-protective role of SCD-1 upregulation in high shear force-damaged human MG63 osteosarcoma cells. However, its detailed regulation in the cancer fate decision of high shear force should be further examined.
Insights
High shear force increases Stearoyl-CoA desaturase (SCD)-1 expression in osteosarcoma cells, potentially protecting them. This suggests SCD-1 plays a role in cancer cell response to mechanical stress.
Area of Science:
- Biomedical Engineering
- Cancer Biology
- Mechanobiology
Background:
- Mechanical forces, particularly high shear stress, significantly influence cancer progression and malignancy.
- Stearoyl-CoA desaturase (SCD)-1, a key lipogenic enzyme, is a potential therapeutic target in cancer treatment.
Purpose of the Study:
- To investigate if shear force-induced cell fate in cancer is mediated by regulating Stearoyl-CoA desaturase (SCD)-1 expression.
- To explore the signaling pathways involved in shear force-induced SCD-1 regulation.
Main Methods:
- Human MG63 osteosarcoma cells were exposed to low (2 dynes/cm²) and high (20 dynes/cm²) shear forces.
- Gene knockdown of peroxisome proliferator-activated receptor delta (PPARδ) and SCD-1 was performed.
- Cell cycle progression, cell death, and differentiation inhibition were analyzed.
Main Results:
- High shear force (20 dynes/cm²) significantly upregulated SCD-1 expression in MG63 cells, a response mediated by Smad1/5 and peroxisome proliferator-activated receptor delta (PPARδ) signaling.
- Knockdown of PPARδ and SCD-1 attenuated differentiation inhibition and increased cell death under high shear force.
- SCD-1 upregulation appears to play a protective role in high shear force-damaged osteosarcoma cells.
Conclusions:
- The study identifies a novel mechanism where high shear force induces SCD-1 expression in osteosarcoma cells, potentially as an auto-protective response.
- PPARδ and Smad1/5 signaling pathways are crucial regulators of this shear force-induced SCD-1 upregulation.
- Further research is needed to fully elucidate the role of SCD-1 in cancer cell fate decisions under mechanical stress.
