SREBF2 (Sterol Regulatory Element Binding Transcription Factor 2)

The present study underscores the pivotal function of ACAT2 in CC progression and delineates its potential as a therapeutic latent strategy. This approach involves the strategic obstruction of the metabolic pathway associated with ACAT2.

Although the R-CHOP regimen effectively cures 60-70% of patients, 30-40% of patients relapse or develop resistance, highlighting the need for new biomarkers to improve prognosis and therapeutic strategies...Our findings suggest that the SREBF2-ACOT7 axis plays a critical role in DLBCL by promoting tumor cell growth, invasion, and survival. ACOT7 could serve as a potential prognostic biomarker and therapeutic target for DLBCL, providing new insights into the molecular mechanisms of this aggressive lymphoma.

Here, we describe a novel DHODH inhibitor, JNJ-74856665, that showed strong efficacy in a subset of AML samples. The transcriptional regulator SREBF2, known to control cholesterol and lipid metabolism, was upregulated in DHODHi sensitive AMLs, and a strong synergy was observed between combination of both DHODHi and the SREBP inhibitor dipyridamole. Our data indicate that combined DHODH and SREBP inhibition is of interest to explore further as a therapeutic target option in AML.

Reduced cholesterol content inhibited tumor growth and sensitized tumor cells to statins, drugs lowering cholesterol. Overall, our study reveals that IFN-γ-mediated inhibition of cholesterol biosynthesis in tumor cells is an important antitumor mechanism of immunotherapy.

Our study identified SREBF2 as a novel prognostic biomarker in CN-AML. Through gene enrichment and microRNA network analysis, SREBF2 interactions with genomic/transcriptomic elements were found to drive CN-AML pathogenesis, providing clinical insights for treatment strategies.

Altered histone acetylation was associated with differential expression of CDKN1A, HSPA1, SREBF2 and TGFB. The evidence demonstrates that nanotherapeutics can alter histone acetylation patterns by modulating EP300/CBP, GCN5 and HDAC, preventing cancer progression and invasion.

Consequently, this reduces the transcription of sterol regulatory element binding transcription factor 2 (SREBF2) and suppresses cholesterol biosynthesis, thereby remodeling HCC microenvironment and impeding HCC development. In summary, this study highlights the unconventional role of CXCL2 in regulating neutrophil polarization and immune responses in HCC, positioning it as a potential therapeutic target for HCC.

Finally, we provide an open, interactive web resource to make these data broadly accessible. This work provides a generalizable blueprint for linking spatial regulation to therapeutic hypotheses across diverse human diseases.

Cholesterol homeostasis signature serves as a potential biomarker for prognosis, immune microenvironment status, and clinicopathological characteristics in ccRCC. Genes related to cholesterol homeostasis, such as SREBF2, may offer new therapeutic targets for immunomodulation in ccRCC.

This research highlights that HBx upregulates SREBP2 and increases autophagic flux, accompanied by changes in cholesterol metabolism, which offers an additional theoretical foundation to elucidate that chronic HBV infection causes abnormal lipid metabolism and induces tumorigenesis.

In contrast, BSO-treated cells exhibited increased sphingomyelin content, upregulated Srebf2 and Cyp46a1 gene expression, and decreased membrane packing. Both treatments induced an insulin-resistant state, which we attribute to alterations in the membrane environment.

This study highlights the influence of gut bacteria on host cholesterol synthesis. Targeted modulation of gut microbiota to reduce cholesterol may represent a promising preventive strategy for CRC.