Stearoyl‐CoA Desaturase 1 Activity Index and Expression in Breast Cancer Subclasses

Cancer cells in the tumor microenvironment face difficulties in obtaining nutrients. SCD1, an important enzyme that converts saturated fatty acids to MUFAs, exhibits increased activity index in cancers, including breast cancer, indicating the role of SCD1 in tumor growth. BC cell lines were cultured in standard conditions for 72 h. The tissue samples were also immersed in the RNA‐later solution, and after harvesting the cells and tissue samples, the expression and activity index of SCD1 was analyzed using quantitative PCR and gas liquid chromatography, respectively. MCF7 cell line showed higher SCD1 expression compared to MDA‐MB‐231 (250‐fold, p < 0.0001) and SK‐BR3 (83‐fold, p < 0.0001) cell lines. SCD1 expression was also significantly elevated in luminal tissue samples compared with HER2‐positive (4.9‐fold, p < 0.0001) and triple‐negative (2‐fold, p = 0.01) BC subtypes. SCD1 activity index in both MCF7 and MDA‐MB‐231 cell lines was 2.10 and 2.09, respectively, and was significantly higher compared to the SK‐BR3 cell line (1.27, p = 0.04 for both). Triple negative tissue samples (9.93 ± 4.93) also showed the highest SCD1 activity index compared to luminal samples (3.93 ± 2.4, p = 0.0002) and HER2 positive samples (5.43 ± 3.44, p > 0.05). Data showed a higher capacity of the luminal subgroup to convert SFAs into MUFAs through the activity of the SCD1 enzyme. It seems that the high activity index in the triple negative subgroup is the result of the high entry of lipids from the extracellular environment. These data demonstrate the potential for SCD1 to be a metabolic vulnerability and a treatment target in certain BC subtypes. Practical applications : This research highlights SCD1 as a potential therapeutic target in breast cancer, specifically luminal and triple‐negative breast cancer. Increased SCD1 activity is a substantial contributor to tumor growth in breast cancer by either converting saturated to monounsaturated fatty acids or by using extracellular lipids. If SCD1 can be targeted, it will likely inhibit cancer cell metabolism while leaving normal cells alone, providing a more selective therapeutic modality of treatment. Inhibitors, in particular, are needed for triple‐negative breast cancer patients, where effective therapies are extremely limited. We also suggest measuring SCD1 expression levels in patients to inform personalized treatment plans, potentially leading to improved patient outcomes by matching metabolic vulnerabilities with specific targeted treatment plans.