CYP26A1 (Cytochrome P450 Family 26 Subfamily A Member 1)

Drug sensitivity analysis revealed that the high-risk group was more sensitive to fluorouracil and gemcitabine (P<0.001), whereas the low-risk group showed better responses to regorafenib (P=0.007). This study establishes a novel prognostic model for COAD based on cofactor and vitamin metabolism, enabling precise survival prediction and guiding personalized therapeutic strategies. The model underscores the interplay between metabolic-immune crosstalk and chemotherapy response heterogeneity, providing a framework for developing targeted metabolic therapies combined with immune modulation.

Overall, Psammaplysene D is a potent therapeutic agent for liver cancer, effective alone or combined with sorafenib, and overcomes resistance through direct targeting of FGFR4, initiating a cascade of CYP26A1 downregulation, RA accumulation, and ferroptosis induction-defining a novel FGFR4/CYP26A1/RA axis regulating ferroptosis in resistant liver cancer.

13cRA promoted RARβ/RXRβ receptor heterodimer formation, with pharmacological activation (Adapalene) potentiating LHR and PGR expression and receptor knockdown diminishing their expression...13cRA-mediated FoxA1 expression suppression occurred through CRABP2-dependent nuclear shuttling and RARβ/RXRβ receptor heterodimer activating, with combinatorial modulation of CRABP1/CYP26 system components (CYP26A1 and CYP26B1) significantly altering FoxA1 regulatory dynamics. Finally, we conclude that 13cRA can inhibit FoxA1 expression through RA signaling molecules (CRABP2, RARβ/RXRβ heterodimer, CRABP1, CYP26A1 and CYP26B1) and thus promote the differentiation of porcine ovarian granulosa cells.

This folate-based scoring system provides a novel tool for evaluating CRC prognosis, tumor microenvironment, and response to immunotherapy. We also propose CYP26A1 as a potential oncogene in CRC, offering new therapeutic insights.

Finally, the FRA/siCYP26A1 significantly suppressed neuroblastoma xenografts by 90.2 % and orthotopic hepatocellular carcinoma by 77.4 %. The present study, for the first time, showcased the potential of co-delivering ATRA and siRNA as a therapeutic approach to govern the concentration of ATRA in tumors and thus facilitate differentiation therapy for solid tumor treatment.

Among these agents are clotrimazole (inhibitor of CYP24A1, 3A4, 2A6, and 2C8), KD-35 (CYP24A1 inhibitor), liarozole (CYP26A1 inhibitor), letrozole (CYP19A1 inhibitor), lopinavir/ritonavir and quercetin (CYP3A4 inhibitors), α-naphthoflavone and furanfylline (CYP1A1 inhibitors), as well as phenylpyrrole (a CYP1A2 and CYP2A6 inhibitor). Thus, these metabolizing enzymes reveal a complex interaction with cancer therapeutics, opening the door to novel strategies that go beyond conventional treatment paradigms. Harnessing CYP modulators could transform the treatment of CRC, offering more targeted and flexible options.

Transcriptomic analysis revealed that in TAMRA + cells, the synthesis of mitochondrial genes, as well as caspases and some apoptosis inhibitors, is reduced. TAMRA + cells possess clonogenic properties, increased level of synthesis of mRNA for key genes associated with self-renewal and poorly differentiated state maintenance.ConclusionsInternalization of the TAMRA-DNA probe is the marker of B-lymphoma cancer stem cells and can be used to detect tumor stem cells and develop new approaches to targeted treatment of B-lymphoma.

We knocked out retinoic acid receptor beta (RAR-β) selectively in pancreatic cells by tamoxifen treatment after crossing these adult RAR-βfl/fl mice with Pdx1/CreER (PCer) and lox-stop-lox KRasG12D transgenic mice...Expression of SOX9, a key protein required for formation and maintenance of PDAC, was higher in PCer;RAR-βD/wt and PCer;RAR-βD pancreata compared to wild-type, indicating that deletion of RAR-β increases SOX9 levels even without the KRas activating mutation. In summary, lack of RAR-β in pancreatic acinar cells reduced cell proliferation and increased SOX9 protein levels in this transgenic model.

Independent of MYCN amplification, inhibitors of RA metabolism or HGF signaling might prevent the emergence of RA-resistant neuroblastoma cells when co-applied with RA.

Here, two LX-2 culture methods were applied as models of hepatic retinoid metabolism to demonstrate the effects of activation status and dose-dependent cytokine exposure on the expression of genes involved in retinoid metabolism. This study suggests that compared to quiescent cells, activated HSC are hypermetabolic, have reduced apparent formation of retinoic acid which may alter downstream retinoic acid signaling.

Angiogenesis- and ADME-related genes correlation was confirmed by cumulative genetic risk score and network and pathway enrichment analysis. Our findings provide a proof of concept that needs further validation in follow-up studies for HCC patient stratification for sorafenib prescription.

Notably, in wt-APC-CRCs, decreased CYP26A1 improved patient survival. These findings have strong potential for clinical translation.