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RPL27 Promotes Gastric Cancer Progression by Enhancing Oxidative Phosphorylation Via FMC1.

Yan Zheng^1,2, Yuhui Ye^1,2, Yang Cheng³

¹Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, China.

Cell Biology International

|June 15, 2026

Summary

This summary is machine-generated.

Ribosomal protein L27 (RPL27) drives gastric cancer progression by disrupting mitochondrial function via FMC1. Targeting this RPL27-FMC1 axis offers a potential new therapy for gastric cancer.

Keywords:

RPL27 gastric cancer ribosomal protein tumor progression

Related Experiment Videos

Area of Science:

Oncology
Molecular Biology
Biochemistry

Background:

Gastric cancer is a major global health concern requiring new biomarkers and treatments.
Ribosomal proteins are increasingly recognized for roles in cancer beyond protein synthesis.

Purpose of the Study:

To investigate the role of ribosomal protein L27 (RPL27) in gastric cancer.
To elucidate the mechanism by which RPL27 influences tumor progression.

Main Methods:

Western blotting and immunohistochemistry to assess RPL27 expression.
Cell proliferation, migration, and invasion assays.
Transcriptomic analysis to identify downstream targets.
Mitochondrial function assays and xenograft mouse models.

Main Results:

RPL27 is upregulated in gastric cancer and linked to poor survival.
RPL27 knockdown inhibits cancer cell proliferation, migration, and invasion.
RPL27 regulates mitochondrial function through FMC1, impacting ATP5A expression and oxidative phosphorylation.
RPL27 inhibition suppressed tumor growth in vivo.

Conclusions:

RPL27 acts as an oncogenic driver in gastric cancer.
The RPL27-FMC1 pathway regulates mitochondrial oxidative phosphorylation and promotes tumor progression.
The RPL27-FMC1-mitochondrial axis presents a potential therapeutic target for gastric cancer.