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pmid:36003333

Identification of CXCL10 and CXCL11 as the candidate genes involving the development of colitis-associated colorectal cancer.

Can Lu · Xiaopeng Zhang · Yang Luo · Jingang Huang · Minhao Yu

Frontiers in genetics · 2022 doi:10.3389/fgene.2022.945414

Paper

complete

Experiment

complete

Data

partial

Analysis

partial

Execution

absent

Execution evidence has not yet been added to this .science file. Explore its methods, data and open questions to plan the next step.
Record details sci_version · id · kind · revision · content_hash · schema · created_at · updated_at · generator
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pmid:36003333
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title
Identification of CXCL10 and CXCL11 as the candidate genes involving the development of colitis-associated colorectal cancer.
doi
10.3389/fgene.2022.945414
pmid
36003333
authors array · 5 items
[0]
Can Lu
[1]
Xiaopeng Zhang
[2]
Yang Luo
[3]
Jingang Huang
[4]
Minhao Yu
journal
Frontiers in genetics
year
2022
abstract
Background: Ulcerative colitis (UC) is a well-known risk factor for developing colitis-associated colorectal cancer (CAC). However, the molecular mechanism of the pathogenesis of CAC remains unclear. This study aimed to explore candidate genes involved in the tumorigenesis of CAC. Methods: GSE75214 and the Cancer Genome Atlas Program (TCGA) dataset were used to analyze the differentially expressed genes (DEGs) in UC and colorectal cancer (CRC), respectively. Survival-hub genes were identified from these DEGs by sequentially constructing a protein-protein interaction network, selecting hub genes, and conducting survival analysis. Regulatory signatures were also predicted on these genes through the online database. Apc min/+ and UC mice models were used to validate the expression of the above-predicted molecules. Gene set enrichment analysis and CIBERSORT were performed to explore the enriched molecular pathways and associated tissue-infiltrating immune cells of genes. Results: Here, 376 common DEGs were identified from the GSE75214 and TCGA datasets. Through survival-hub gene selection and in vivo experiments, we confirmed that CXCL10 and CXCL11 were significantly upregulated in UC and CRC. We also proved that miR-34a-5p and miR-203a-5p were potential regulators of CXCL10 and CXCL11. Meanwhile, CXCL10 and CXCL11 may activate the JAK-STAT signaling pathway via the interaction with cytokine receptors in UC. Furthermore, CXCL10 and CXCL11 were positively associated with the tissue infiltration of proinflammatory M1 macrophages in UC and CRC. Conclusion: CXCL10 and CXCL11 may act as the candidate genes involved in the tumorigenesis of CAC and potential therapeutic targets to prevent the development of CAC from UC.
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Differential expression analysis in the GSE75214 and TCGA cohorts was conducted using the limma (RRID: SCR_010943) and DESeq2 (RRID: SCR_015687) R packages, respectively.
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CXCL10 and CXCL11 were significantly upregulated in UC and CRC and may act as candidate genes involved in the tumorigenesis of CAC and potential therapeutic targets to prevent the development of CAC from UC.
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Through survival-hub gene selection and in vivo experiments, we confirmed that CXCL10 and CXCL11 were significantly upregulated in UC and CRC.
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Conclusion: CXCL10 and CXCL11 may act as the candidate genes involved in the tumorigenesis of CAC and potential therapeutic targets to prevent the development of CAC from UC.
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CXCL10 and CXCL11 were significantly upregulated in UC and CRC and may act as candidate genes involved in the tumorigenesis of CAC and potential therapeutic targets to prevent the development of CAC from UC.
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ets. Through survival-hub gene selection and in vivo experiments, we confirmed that CXCL10 and CX
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Complete file
{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:36003333", "kind": "science-record", "revision": 5, "content_hash": "sha256:de56dd54f8ef9538f0f720c933f8f790a99dace177c6683ab60f5bcf90e1dc03", "created_at": "2026-11-01T18:15:10Z", "updated_at": "2026-11-01T22:49:52Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "Identification of CXCL10 and CXCL11 as the candidate genes involving the development of colitis-associated colorectal cancer.", "doi": "10.3389/fgene.2022.945414", "pmid": "36003333", "authors": ["Can Lu", "Xiaopeng Zhang", "Yang Luo", "Jingang Huang", "Minhao Yu"], "journal": "Frontiers in genetics", "year": 2022, "abstract": "Background: Ulcerative colitis (UC) is a well-known risk factor for developing colitis-associated colorectal cancer (CAC). However, the molecular mechanism of the pathogenesis of CAC remains unclear. This study aimed to explore candidate genes involved in the tumorigenesis of CAC. Methods: GSE75214 and the Cancer Genome Atlas Program (TCGA) dataset were used to analyze the differentially expressed genes (DEGs) in UC and colorectal cancer (CRC), respectively. Survival-hub genes were identified from these DEGs by sequentially constructing a protein-protein interaction network, selecting hub genes, and conducting survival analysis. Regulatory signatures were also predicted on these genes through the online database. Apc min/+ and UC mice models were used to validate the expression of the above-predicted molecules. Gene set enrichment analysis and CIBERSORT were performed to explore the enriched molecular pathways and associated tissue-infiltrating immune cells of genes. Results: Here, 376 common DEGs were identified from the GSE75214 and TCGA datasets. Through survival-hub gene selection and in vivo experiments, we confirmed that CXCL10 and CXCL11 were significantly upregulated in UC and CRC. We also proved that miR-34a-5p and miR-203a-5p were potential regulators of CXCL10 and CXCL11. Meanwhile, CXCL10 and CXCL11 may activate the JAK-STAT signaling pathway via the interaction with cytokine receptors in UC. Furthermore, CXCL10 and CXCL11 were positively associated with the tissue infiltration of proinflammatory M1 macrophages in UC and CRC. Conclusion: CXCL10 and CXCL11 may act as the candidate genes involved in the tumorigenesis of CAC and potential therapeutic targets to prevent the development of CAC from UC.", "claims": [{"id": "claim-method", "statement": "Differential expression analysis in the GSE75214 and TCGA cohorts was conducted using the limma (RRID: SCR_010943) and DESeq2 (RRID: SCR_015687) R packages, respectively.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:36003333", "locator": "sections[4] \"Differential expression analysis\" paragraph 2", "quote": "Differential expression analysis in the GSE75214 and TCGA cohorts was conducted using the limma (RRID: SCR_010943) and DESeq2 (RRID: SCR_015687) R packages, respectively."}], "state": "complete"}, {"id": "claim-data-access", "statement": "The original contributions presented in the study are included in the article/Supplementary Material. Further inquiries can be directed to the corresponding author.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:36003333", "locator": "sections[26] \"Data availability statement\" paragraph 2", "quote": "The original contributions presented in the study are included in the article/Supplementary Material. Further inquiries can be directed to the corresponding author."}], "state": "complete"}, {"id": "claim-target-result", "statement": "CXCL10 and CXCL11 were significantly upregulated in UC and CRC and may act as candidate genes involved in the tumorigenesis of CAC and potential therapeutic targets to prevent the development of CAC from UC.", "kind": "qualitative", "target": null, "evidence": [{"asset": "source:pmid:36003333", "locator": "sections[0] \"Abstract\" paragraph 3", "quote": "Through survival-hub gene selection and in vivo experiments, we confirmed that CXCL10 and CXCL11 were significantly upregulated in UC and CRC."}, {"asset": "source:pmid:36003333", "locator": "sections[0] \"Abstract\" paragraph 4", "quote": "Conclusion: CXCL10 and CXCL11 may act as the candidate genes involved in the tumorigenesis of CAC and potential therapeutic targets to prevent the development of CAC from UC."}], "state": "complete"}], "gaps": []}, "experiment": {"state": "complete", "objective": "CXCL10 and CXCL11 were significantly upregulated in UC and CRC and may act as candidate genes involved in the tumorigenesis of CAC and potential therapeutic targets to prevent the development of CAC from UC.", "steps": [{"id": "read_published_estimate", "order": 1, "name": "Read the published estimate from the source", "kind": "other", "state": "complete", "blocked_on": null, "description": "The claim, method and evidence span published with the source article.", "duration_hours": null, "parameters": {}, "inputs": ["source:pmid:36003333"], "outputs": ["the published estimate and its evidence"], "instruments": [], "reagents": []}, {"id": "obtain_source_data", "order": 2, "name": "Obtain the source data from the named repository", "kind": "data-preparation", "state": "complete", "blocked_on": null, "description": "The GEO series accession resolves and its sample accessions are listed. This lane did not download the dataset or read its licence.", "duration_hours": null, "parameters": {}, "inputs": ["data:geo:GSE75214"], "outputs": ["the source data with its repository provenance"], "instruments": [], "reagents": []}, {"id": "run_analysis", "order": 3, "name": "Run the published analysis", "kind": "analysis", "state": "complete", "blocked_on": null, "description": "Apply the paper's statistical method to the resolved series and compare the result with the published target.", "duration_hours": null, "parameters": {}, "inputs": ["data:geo:GSE75214"], "outputs": ["the replicated result and its comparison"], "instruments": [], "reagents": []}], "materials": [], "instruments": [], "reagents": [], "conditions": {}, "gaps": []}, "data": {"state": "partial", "assets": [{"id": "source:pmid:36003333", "role": "manuscript", "format": "xml", "media_type": "application/xml", "uri": "https://doi.org/10.3389/fgene.2022.945414", "sha256": "sha256:788cee7a90e92f7d8e3a12bca5decbdeeddd189a812f2c8a7037521377819bac", "bytes": 45126, "access": "open", "state": "resolved", "reader": null, "reader_status": "reader_required", "identifier": "10.3389/fgene.2022.945414", "version": null, "note": "Full article fetched from PMC; the checksum covers the rendered section body, not the original XML bytes.", "structure": {"pmcid": "PMC9393335", "source": "europe_pmc_fulltext", "coverage": "whole_body", "text_hash_scope": "rendered_section_body"}}, {"id": "data:geo:GSE75214", "role": "raw", "format": "geo-series", "media_type": "application/vnd.ncbi.geo-series+json", "uri": "https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE75214", "sha256": null, "bytes": null, "access": "open", "state": "resolved", "reader": null, "reader_status": "reader_required", "identifier": "GSE75214", "version": null, "note": "The original contributions presented in the study are included in the article/Supplementary Material. Further inquiries can be directed to the corresponding author.", "structure": {"repository": "GEO", "access_route": "GEO accession URL", "access_statement_verbatim": "The original contributions presented in the study are included in the article/Supplementary Material. 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