NGDC - GSA for Human

HRA012300

HRA012300.xlsx

Title:

FAD Synthase Confers Ferroptosis Resistance and Restrains CD8+ T Cell Recruitment in Hepatocellular Carcinoma

Release date:

2025-08-27

Description:

VB2 metabolism regulates numerous cellular processes, but its role in HCC progression remains unclear. We found that HCC tumors showed upregulation of VB2 metabolism signature, and VB2 metabolism promoted HCC progression. Among VB2 metabolic enzymes, FADS was the only one widely overexpressed in human HCC. Elevated FADS expression correlated with resistance to anti-PD-1 therapy and poor prognosis. In vivo, FADS facilitated HCC cell growth and suppressed T cell-mediated antitumor immunity. Single-cell transcriptomic analysis revealed that FADS affected both tumor cells and CD8+ T cells. FADS knockdown induced HCC cell death and increased CD8+ T cell infiltration. Mechanistically, FADS confers ferroptosis resistance on HCC cells via enzymatic function to produce FAD and non-enzymatic function to stabilize PCBP2. Moreover, FADS impaired CD8+ T cell recruitment by disrupting the cGAS-STING pathway.

Data Accessibility:

Controlled access Request Data

BioProject:

PRJCA013484

Study type:

Disease Study

Disease name:

liver cancer

Data Access Committee

For each controlled access study, there is a corresponding Data Access Committee(DAC) to determine the access permissions. Access to actual data files is not managed by NGDC.

DAC NO.:

HDAC002018

DAC name:

HDAC006374

Contact person:

Zhao Haitao

Email:

zhaoht@pumch.cn

Description:

scPLC_Zhao

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