SCD (Stearoyl-CoA Desaturase)

Furthermore, transcriptomic and Western blot analysis manifested that Nar upregulated the expression levels of peroxisome proliferator-activated receptor γ, stearoyl CoA desaturase 1, and phosphoenolpyruvate carboxykinase 1, which manifested its action mechanism related to the activation of the PPAR signaling pathway. These findings demonstrated the multipathway-mediated anti-IM effects of Nar, which indicate its promising potential as an adjunctive treatment strategy for chemotherapy-induced intestinal toxicity in cancer patients.

Furthermore, PS reduced hepatic pro-inflammatory cytokine mRNA levels: tumor necrosis factor α(tnf-α), cyclooxygenase 2 (cox-2), and interleukins (il-6, il-1β). In conclusion, dietary inclusion of 0.006%-0.018% PS effectively enhanced growth and antioxidant capacity, altered lipid handling, and affected transcriptional inflammatory responses.

Elevated SCD1 levels correlate with increased MYLK4 levels, and their concurrent expression forecasts regorafenib resistance and poor prognosis in colorectal cancer...Patients with colorectal cancer exhibiting elevated MYLK4 activity and wild-type p53 may derive clinical benefits from this combination therapy. These results suggest that MYLK4 may serve as a promising therapeutic target for the treatment of colorectal cancer.

These findings suggest SCD plays a role in redox regulation and DNA repair sensitivity, with therapeutic potential for targeting DNA repair pathways in combination with SCD inhibition. Impact statement This study reveals that stearoyl-CoA desaturase (SCD) supports prostate cancer growth in adipocyte-rich bone by regulating redox balance and DNA repair responses, uncovering a metabolic mechanism linking lipid metabolism to genomic stability and suggesting therapeutic potential for combining SCD and DNA repair pathway inhibition.

We demonstrate that SCD1 contributes to Th9 differentiation and their antitumoral activity via the regulation of Smad2/3 signaling.

This article systematically reviews the regulatory effects of curcumin on these critical metabolic processes and pathways in tumor metabolic reprogramming, revealing its molecular mechanisms in disrupting tumor growth and progression by targeting energy and biosynthetic metabolism. These findings provide a significant theoretical foundation and a preclinical research perspective for the development of natural antitumor drugs based on metabolic regulation, as well as for optimizing combination therapy strategies.

SCD activity is a critical regulator of SFA to MUFA ratio and, therefore, of overall cell function, growth, and survival. In this review, we will provide the latest updates on the expected as well as unanticipated roles of SCD in development, metabolism and disease with a focus on cancer and the central nervous system.

Our findings reveal a novel regulatory YTHDF2-SREBF1 axis that links m6A-dependent post-transcriptional regulation to ferroptosis modulation through lipid metabolic remodeling. Therapeutically targeting the YTHDF2-SREBF1 pathway may represent a promising strategy to overcome radiotherapy resistance in ATC through metabolic intervention.

Notably, SLC38A5 depletion sensitizes CRC cells to RSL3-induced ferroptosis...Our findings reveal a novel mechanism wherein SLC38A5 confers ferroptosis resistance in CRC via YAP nuclear translocation within the Hippo signaling pathway. Collectively, this study highlights SLC38A5 as a potential therapeutic target to enhance ferroptosis-based cancer therapy, offering new strategies to improve CRC treatment outcomes.

Oncofetal reprogramming-based prognostic signature robustly stratifies HCC patient survival across independent cohorts. DUSP9 is identified as a core oncofetal regulator that drives stem-like traits in HCC. Mechanistically, DUSP9 suppresses ERK1/2-phosphorylation, stabilizes PPARG, and transcriptionally activates SCD. The DUSP9-ERK1/2-PPARG-SCD axis remodels lipid metabolism to support proliferation, cell mobility, and sorafenib resistance.

This disruption ultimately suppressed CYP24A1 transcription. Our findings revealed that pharmacological blockade of the LSH/CYP24A1/SCD axis triggers calcium-driven ferroptosis, positioning ATT as a potent, mechanism-based therapeutic for CRC.