FTCD (Formimidoyltransferase Cyclodeaminase)

This model provides a new tool for CRC prognosis, deepens the understanding of PNI pathogenesis, and helps identify therapeutic targets like Claudin 18, whose expression was confirmed as a potential biomarker. This tool can enhance personalized treatment strategies for this high-risk patient population.

We identified novel loci influencing arsenic metabolites measured in both urine and blood. FMOs are involved in the oxidation of xenobiotics but have no known direct role in arsenic metabolism, while GSTO1 has a well-established role in catalyzing the reduction of arsenic species. The novel associations we report appear specific to blood or urine, with no detectable impact on skin toxicity risk, pointing to complexities in arsenic metabolism and its genetic contributors that require further study.

Hub genes were enriched in various cell types. Trametinib, selumetinib, RDEA119, and teniposide were identified as potential drugs for LIHC treatment.ConclusionCDC20, TOP2A, CDK1, CAT, TAT, and FTCD may contribute to LIHC development and serve as novel prognostic biomarkers.

Silencing CCT5 inhibited the viability, migration, and invasion of HCC cells. The present work developed a novel LRG gene signature that could be considered a promising therapeutic target and biomarker for HCC.

Overexpression of FTCD-AS1 and PXR alleviated cell damage in exposure to 5μM AFB1 for 48h. In summary, inactivation of the FTCD-AS1-PXR-MASP1 axis was pinpointed as the key event in AFB1-enhanced HBV infection, metabolic dysregulation and carcinogenic injury.

This study offers a prognostic prediction model for HCC patient risk stratification, identifying the FTCD gene as a crucial prognostic marker and therapeutic target. This highlights FTCD's potential impact on HCC clinical diagnosis and treatment strategies.

The risk model associated with pyproptosis is crucial for the tumor immunity of LC and may serve as a prognostic indicator for patients suffering from LC. Our findings will offer new perspectives for immunotherapies targeting LC.

FTCD expression was weakened along with acquisition of lenvatinib-resistance, and was restored by cabozantinib administration. FTCD may be a novel therapeutic target of cabozantinib in case of lenvatinib treatment failure.

We generated and characterised the first Ftcd liver-specific knockout murine model. We found loss of FTCD expression upregulated peroxisome proliferator-activated receptor (PPAR)γ and sterol regulatory element-binding protein 2 (SREBP2) by regulating the PTEN/Akt/mTOR signalling axis, leading to lipid accumulation and hepatocarcinogenesis, and provided a rationale for therapeutic targeting of HCC driven by downregulation of FTCD.