ArticleCancer cell international2026
MRPL13 sustains mitochondrial integrity and MAPK-associated aggressiveness in esophageal squamous cell carcinoma.
Article in Cancer cell international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMitochondrial ribosomal protein L13 (MRPL13) has been implicated in tumor progression, but its relevance to esophageal squamous cell carcinoma (ESCC) remains insufficiently defined. Because mitochondrial adaptation can influence tumor cell fitness under oncogenic and oxidative stress, we investigated whether MRPL13 is associated with aggressive ESCC biology and mitochondrial functional states.
methodsWe analyzed MRPL13 expression, clinical associations, survival relevance, mutation patterns, immune-related correlates, and pathway enrichment using TCGA and related public datasets, with an emphasis on ESCC-specific analyses. Experimental validation was performed using paired ESCC tissues and KYSE150 cells with shRNA-mediated MRPL13 knockdown. Western blotting, colony formation, transwell migration/invasion assays, mitochondrial membrane potential assessment, and ROS staining were used to evaluate protein expression, cellular behavior, and mitochondrial status.
resultsMRPL13 was up-regulated in ESCC and its expression was associated with tumor stage and unfavorable prognosis. MRPL13 expression correlated with a set of cancer-associated genes, including SIX2, SPP1, COL11A1, DSC3, and CCNA1, several of which were also increased at the protein level in paired ESCC tissues. ESCC tumors with higher MRPL13 expression showed distinct mutation and immune-related expression patterns; however, these immune associations were interpreted as correlates of tumor state rather than direct evidence of immune regulation. Pathway analyses indicated enrichment of MAPK-related signaling in MRPL13-high tumors. Consistently, MRPL13 knockdown in KYSE150 cells reduced phosphorylation of MEK1/2, ERK1/2, JNK1/2, and p38, impaired colony formation and in vitro migration/invasion, decreased mitochondrial membrane potential, and increased intracellular ROS levels.
conclusionThese findings suggest that MRPL13 identifies an aggressive ESCC state in which mitochondrial integrity, MAPK-associated signaling, and tumor cell fitness are functionally coupled. Rather than establishing MRPL13 as a fully defined upstream driver, our data support a more restrained interpretation: MRPL13 may help ESCC cells maintain mitochondrial stress tolerance, and its loss exposes a vulnerability characterized by reduced MAPK phosphorylation, impaired clonogenic and invasive capacity, mitochondrial depolarization, and ROS accumulation.
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