SSR4 Promote Gastric Cancer Progression by Regulating Mitochondrial Oxidative Phosphorylation via NDUFB11 and ATP6AP1

Gastric cancer (GC) is one of the most common cancers worldwide. Cancer cell metastasis is a major factor leading to poor prognosis. Previous proteomic data suggested that SSR4 might be closely associated with the occurrence and development of GC. However, the role and molecular mechanism of SSR4 in GC is not yet clear. The present study found that the expression level of SSR4 was increased in GC tissue and serum from GC patients. In addition, SSR4 could promote the malignant biological behavior of GC cells in vitro and in vivo. The mechanism may be that SSR4 regulates the expression of NDUFB11 and ATP6AP1, and then enhanced the function of mitochondrial respiratory chain complex I (CI) and mitochondrial respiratory chain complex V (CV), which promoted the mitochondrial oxidative phosphorylation and thus promoted GC progression. These findings expand the understanding of the role of SSR4 and provide a new target for the treatment of GC.

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Publication Details

Journal
Molecular Carcinogenesis
Published
2025-09-25
DOI
https://doi.org/10.1002/mc.70047
Citations
1
Primary Topic
RNA modifications and cancer
Type
article
Field-Weighted Citation Impact
0.81
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article

SSR4 Promote Gastric Cancer Progression by Regulating Mitochondrial Oxidative Phosphorylation via NDUFB11 and ATP6AP1

Baixue Liao, Ruiling Fan, Lei Liu, Xiaobin Sun et al.
1 citations
Molecular Carcinogenesis
RNA modifications and cancer
0.81
article

SSR4 Promote Gastric Cancer Progression by Regulating Mitochondrial Oxidative Phosphorylation via NDUFB11 and ATP6AP1

Baixue Liao, Ruiling Fan, Lei Liu, Xiaobin Sun, Kaiwen Wu, Aoshuang Li, Binjun Zhu
article en
1 citations

Abstract

Gastric cancer (GC) is one of the most common cancers worldwide. Cancer cell metastasis is a major factor leading to poor prognosis. Previous proteomic data suggested that SSR4 might be closely associated with the occurrence and development of GC. However, the role and molecular mechanism of SSR4 in GC is not yet clear. The present study found that the expression level of SSR4 was increased in GC tissue and serum from GC patients. In addition, SSR4 could promote the malignant biological behavior of GC cells in vitro and in vivo. The mechanism may be that SSR4 regulates the expression of NDUFB11 and ATP6AP1, and then enhanced the function of mitochondrial respiratory chain complex I (CI) and mitochondrial respiratory chain complex V (CV), which promoted the mitochondrial oxidative phosphorylation and thus promoted GC progression. These findings expand the understanding of the role of SSR4 and provide a new target for the treatment of GC.

Molecular CarcinogenesisVol. 64(12)
North Sichuan Medical University (CN), Tongji University (CN), Third People's Hospital of Chengdu (CN), Affiliated Hospital of North Sichuan Medical College (CN), Shanghai Pulmonary Hospital (CN), Southwest Jiaotong University (CN)
Openalex Percentile: Top 23%
RNA modifications and cancer
0.81
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