What does this research mean for the field?

A seven-gene signature linked to mitochondrial quality control can stratify colorectal cancer patients by survival outcomes and correlates with tumor immune evasion, though it does not improve overall prognostic discrimination beyond standard clinical factors. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To identify and validate prognostic genes linked to mitochondrial quality control in colorectal cancer and characterize their immune and therapeutic associations.

August 24, 2026Scientific ReportsOpen Access

Identify and validate the genes linked to mitochondrial quality control in colorectal cancer

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Authors

HFHao Fu CCChanghua Chi WNWenhan Nie

Discussion

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Overview

Bioinformatic and experimental analysis reveals a seven-gene mitochondrial quality control signature in colorectal cancer, highlighting altered immune infiltration and therapeutic targets.

Key Points

To identify and validate prognostic genes linked to mitochondrial quality control in colorectal cancer and characterize their immune and therapeutic associations.
Calculated mitochondrial quality control scores in public colorectal cancer datasets using single-sample gene set enrichment analysis (ssGSEA) and identified co-expressed genes via WGCNA.
Constructed a prognostic risk signature using differential expression, univariate Cox regression, and LASSO regression, followed by immune profiling, drug sensitivity predictions, and RT-qPCR validation.
Identified a seven-gene prognostic signature (GIMAP1, SIGLEC1, FCGR2B, C1orf162, VSIG4, P2RY13, SLAMF1) that stratified patient survival, though adding it to clinical factors did not improve discrimination (C-index: 0.785 vs. 0.789; ΔC-index = −0.004).
High-risk tumors showed significant enrichment in focal adhesion pathways, marked differences across 20 immune cell types, positive correlation with regulatory T cells (p < 0.001), and heightened predicted sensitivity to Trk kinase and IGF1R inhibitors.
RT-qPCR analysis confirmed significant down-regulation of GIMAP1, FCGR2B, and VSIG4 in colorectal cancer tissue samples.

Cite This Study

Fu et al. (2026) studied this question.

synapsesocial.com/papers/6a8c005bbca056c88e6df086 https://doi.org/10.1038/s41598-026-67601-y

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August 24, 2026Scientific ReportsOpen Access

Identify and validate the genes linked to mitochondrial quality control in colorectal cancer

View Full Paper

Ask AI

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Authors

HFHao Fu CCChanghua Chi WNWenhan Nie

Discussion

Member takes

Overview

Bioinformatic and experimental analysis reveals a seven-gene mitochondrial quality control signature in colorectal cancer, highlighting altered immune infiltration and therapeutic targets.

Key Points

To identify and validate prognostic genes linked to mitochondrial quality control in colorectal cancer and characterize their immune and therapeutic associations.
Calculated mitochondrial quality control scores in public colorectal cancer datasets using single-sample gene set enrichment analysis (ssGSEA) and identified co-expressed genes via WGCNA.
Constructed a prognostic risk signature using differential expression, univariate Cox regression, and LASSO regression, followed by immune profiling, drug sensitivity predictions, and RT-qPCR validation.
Identified a seven-gene prognostic signature (GIMAP1, SIGLEC1, FCGR2B, C1orf162, VSIG4, P2RY13, SLAMF1) that stratified patient survival, though adding it to clinical factors did not improve discrimination (C-index: 0.785 vs. 0.789; ΔC-index = −0.004).
High-risk tumors showed significant enrichment in focal adhesion pathways, marked differences across 20 immune cell types, positive correlation with regulatory T cells (p < 0.001), and heightened predicted sensitivity to Trk kinase and IGF1R inhibitors.
RT-qPCR analysis confirmed significant down-regulation of GIMAP1, FCGR2B, and VSIG4 in colorectal cancer tissue samples.

Cite This Study

Fu et al. (2026) studied this question.

synapsesocial.com/papers/6a8c005bbca056c88e6df086 https://doi.org/10.1038/s41598-026-67601-y

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