FOXA3 (Forkhead Box A3)

Our results from this genetic association study support that T2D, particularly the obesity and lipodystrophy mechanistic clusters, and MODY genomic susceptibility regions play a role in the etiology of PDAC.

We conclude that ALKBH5 is a critical oncogene in hepatocarcinogenesis. These results provide novel insights into the epigenetic regulation of hepatocarcinogenesis.

A strong additive association between CYP3A4 and CYP3A5 genotypes (informed as a CYP3A activity score [AS] variable) and lurbinectedin clearance (CL) and exposure was confirmed, for example, patients with an AS of 3, 2, or 1 showed a 2.3-, 1.6-, and 1.5-fold higher total lurbinectedin CL compared to those with an AS of 0 and 2.3-, 1.8-, and 1.6-fold higher unbound lurbinectedin CL. In conclusion, preemptive CYP3A genotyping may offer a valuable approach for personalizing treatment with lurbinectedin in cancer patients.

iHPCs reprogrammed from adult fibroblasts can repopulate hepatocytes and exert therapeutic effects in WD mice, representing a potential replacement therapy for clinical application.

These findings indicate that FOXA3 acts as a tumor suppressor in ESCC, and its low expression is linked to poor outcomes. FOXA3 may serve as a potential diagnostic and therapeutic target for ESCC.

We demonstrate that targeting this pathway with FGF inhibitors curtails tumor growth both in vitro and in xenograft models, unveiling a potential vulnerability and paving the way for targeted therapies. Overall, our work provides an important resource for studying LNETs to reveal regulatory networks, differentiation signals, and therapeutically relevant dependencies.

Additionally, we found that XMU-MP-1, a SPDEF inhibitor, suppressed the growth of IMA cells. These results revealed that IMA and SRCC contain heterogenous tumor cell types, some of which are targetable.

The involvement of FOXA1 in sex hormone-related tumors underscores its significance in cancer biology. This review provides an overview of multifaceted roles of FOXA1 in normal development and its implications in the pathogenesis of hormone-related cancers, particularly breast cancer and prostate cancer.

In addition, the potent FOXA3 inhibitor magnolol suppressed metastatic gene programs in lung adenocarcinoma patient-derived organoids (PDOs). Altogether, our findings shed light onto unique cholesterol metabolism and FOXA3 contribution to lung adenocarcinoma metastasis.

Moreover, we identified CpG-island methylator phenotypes and pinpointed chromatin state signatures and TF regulators for CIMP-High subtype. Our work systematically revealed the epigenetic basis of the well-known iCMS and CIMP classifications of CRCs.

HOXC10 was found to enhance the activation of the MAPK signaling pathway by regulating FOXA3 in ESCC cells. These results support a key role for HOXC10 in the tumorigenesis of ESCC by upregulating FOXA3 via the MAPK pathway and highlight its potential as a promising diagnostic and prognostic marker for ESCC.

Our findings demonstrate that reprogramming could be a promising method to produce hepatocytes and treat TNBC liver metastasis. And the LOC model could intimate the 3D liver microenvironment and assess the behavior of the reprogrammed TNBC cells.