International immunopharmacologyOct 17, 2025

NDUFAB1 may help liver cancer grow by disturbing mitochondrial balance and the removal of damaged mitochondria

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Jan 19, 2026

Abstract

NDUFAB1 expression is significantly elevated in hepatocellular carcinoma tissues and is associated with poor patient prognosis (P < 0.05).

Elevated NDUFAB1 levels may serve as an independent risk factor for HCC.
Knockdown of NDUFAB1 reduced HCC cell proliferation, metastatic potential, and invasive capacity, while promoting cell death.
Loss of NDUFAB1 function resulted in mitochondrial depolarization, decreased ATP production, and increased reactive oxygen species.
Changes in protein expression were observed, including downregulation of fusion proteins and upregulation of fission proteins.
Mitochondrial fragmentation and increased autolysosome formation were identified through transmission electron microscopy.
NDUFAB1 may disrupt mitochondrial quality control and influence HCC pathogenesis by modulating the mitophagy pathway.

Simplified

NADH: ubiquinone oxidoreductase subunit AB1 (NDUFAB1), a critical factor of mitochondrial complex I in electron transport chain, is essential for cellular energy metabolism; however, its specific functions and mechanisms in hepatocellular carcinoma (HCC) remain elusive. We found significantly elevated NDUFAB1 expression in HCC tissues, which is correlated significantly with poor patient prognosis and may serve as an independent risk factor (P < 0.05). Loss-of-function experiments revealed that NDUFAB1 knockdown reduced HCC cell proliferation, metastatic potential, and invasive capacity while promoting apoptosis. Furthermore, NDUFAB1 knockdown led to mitochondrial depolarization, impaired ATP production, and ROS accumulation, concomitant with downregulation of fusion proteins (OPA1, MFN1, MFN2) and upregulation of fission proteins (DRP1, MFF). Transmission electron microscopy revealed mitochondrial fragmentation and increased autolysosomes formation. Transcriptome sequencing data further indicated that NDUFAB1 may contribute to HCC pathogenesis by disrupting mitochondrial quality control, particularly through modulation of the mitophagy pathway. Collectively, NDUFAB1 likely promotes HCC progression by disrupting mitochondrial homeostasis, potentially through activation of the mitophagy pathway. These findings demonstrate that NDUFAB1 may be used as an independent prognostic risk factor in HCC patients.

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Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

PubMed

NDUFAB1 may help liver cancer grow by disturbing mitochondrial balance and the removal of damaged mitochondria

Abstract

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Competing interests

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Abstract

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