DECR1 (2,4-Dienoyl-CoA Reductase 1)

Our findings highlight the potential of lactylation-associated genes, particularly XRCC4, in BC progression and clinical treatment strategies. The development of an XRCC4 inhibitor may be eligible for patent protection and could potentially serve as a novel therapeutic option for BC.

This study established a risk score model based on six DFRGs, which demonstrated favorable prognostic value. DECR1 promotes the progression of LUAD and holds promise as an effective biomarker.

DECR1 is associated with breast cancer progression and may serve as a potential therapeutic indicator, and AC plays an antitumor role by modulating DECR1 expression and promoting ACSL4-mediated ferroptosis. Therefore, AC may be considered a potential candidate drug for treating breast cancer.

Further, by computer aided virtual screening, we identified various compounds with DECR1 targeting properties, and verified-Erigoster B, exerts antitumor effects by promoting ferroptosis. In conclusion, DECR1 could be a candidate target for breast cancer, and the DECR1 inhibitor Erigoster B can be a potential drug to exert therapeutic effect on breast cancer.

Quercetin inhibits the expression of CPT1B via the STAT3 signaling pathway, affecting lipid metabolism and exerting antitumor effects. Furthermore, the combined administration of quercetin and gemcitabine exhibits enhanced therapeutic efficacy.

Ferroptosis can serve as a potential therapeutic target for CRPC, and could be a new strategy for combination therapy. Moreover, ferroptosis-related genes may be great indicators of PCa prognosis. Further research on ferroptosis in CRPC therapy can benefit from the frameworks provided by this review.

Consequently, decreased HNF4A-AS1 levels caused DECR1 overexpression, leading to decreased intracellular PUFA content and promoting resistance to sorafenib-induced ferroptosis in HCC. Our results indicated the pivotal role of lipid metabolism-related and liver-specific HNF4A-AS1 in inhibiting sorafenib resistance by promoting ferroptosis and suggesting that HNF4A-AS1 might be a potential target for HCC.

Subsequently, we discovered that SLC7A11 interacts with DECR1, inhibition of SLC7A11 led to decreased expression levels of DECR1 along with an accumulation of MDA and Fe2+, effects that were similarly reversed by DECR1 overexpression. Collectively, our findings suggest that targeted therapy against DECR1 combined with further inhibition of its downstream pathway involving SLC7A11/GPX4 may represent a promising strategy for treating breast cancer.

This study revealed that PD may regulate multiple signaling pathways by targeting genes such as EGFR, TNF, and LMRGS to inhibit NSCLC proliferation and metastasis.

DECR1 may be a potential cancer suppressor in CC and may be involved in apoptotic pathways and associated with immune infiltration.