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pmid:32063710

Downregulation of the Helicase Lymphoid-Specific (HELLS) Gene Impairs Cell Proliferation and Induces Cell Cycle Arrest in Colorectal Cancer Cells.

Xi Liu · Xuyang Hou · Yan Zhou · Qinglong Li · Fanhua Kong · Shichao Yan · Sanlin Lei · Li Xiong · Jun He

OncoTargets and therapy · 2019 doi:10.2147/OTT.S223668

Paper

complete

Experiment

complete

Data

partial

Analysis

partial

Execution

absent

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pmid:32063710
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title
Downregulation of the Helicase Lymphoid-Specific (HELLS) Gene Impairs Cell Proliferation and Induces Cell Cycle Arrest in Colorectal Cancer Cells.
doi
10.2147/OTT.S223668
pmid
32063710
authors array · 9 items
[0]
Xi Liu
[1]
Xuyang Hou
[2]
Yan Zhou
[3]
Qinglong Li
[4]
Fanhua Kong
[5]
Shichao Yan
[6]
Sanlin Lei
[7]
Li Xiong
[8]
Jun He
journal
OncoTargets and therapy
year
2019
abstract
AIM: Colorectal cancer (CRC) is the fourth most frequently diagnosed cancer worldwide. Despite the decrease in mortality of CRC patients, further investigation of the molecular pathogenesis of CRC could unveil new therapeutic targets and offer better prognosis predictions, which might direct attention to epigenetic regulators. METHODS: Publicly available data from the Gene Expression Omnibus (GEO) database and clinical samples were collected. Bioinformatics methods were used to screen hub genes expressed in CRC. qRT-PCR and Western blotting were used to experimentally determine the expression of one gene of interest, the helicase lymphoid-specific (HELLS) gene, at the RNA and protein levels. Immunohistochemical (IHC) assays were used to correlate the stained HELLS proteins to survival data. Cell proliferation levels were assayed by a CCK-8 kit, a colony formation assay was performed, and flow cytometry was used to quantify the cells at each stage of the cell cycle. RESULTS: A total of 225 overlapping genes were screened, including 14 hub genes. Analysis through a protein-protein interaction (PPI) network and the Gene Ontology database was performed by using the Cytoscape and DAVID online tools, respectively. HELLS RNA and protein expression levels in tumor tissues were 2.09-fold higher and 1.46-fold higher, respectively, than in the peritumoral tissues (p < 0.001, p<0.001). HELLS expression was significantly associated with the T stage (p=0.0027), M stage (p=0.0119), and TNM clinical stage (p = 0.0312) and a higher pathological grade (p=0.049). Highly expressed HELLS was reversibly associated with overall survival (log-rank p = 0.027). HELLS siRNA impaired cell proliferation and colony generation in vitro. HELLS siRNA induced significant G2+M arrest in HT29 and HCT116 cells compared with the respective negative controls (82.29% vs 25.85% and 35.41% vs 15.26%, respectively). CONCLUSION: Our data revealed that HELLS was significantly upregulated in CRC and correlated with clinicopathological parameters. High expression of HELLS indicated poor prognosis for CRC patients. HELLS knockdown led to impaired cell proliferation, colony generation, and G2+M cell cycle arrest.
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The differentially expressed genes (DEGs) of tumor and peritumoral tissues were identified by GEO2R.
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Hsa_circ_101555 functions as a competing endogenous RNA of miR-597-5p to promote colorectal cancer progression [lncRNA/mRNAs]
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Screening for Epigenetically Masked Genes in Colorectal Cancer using 5-aza-2’-deoxycytidine treatment, Microarray and Gene Expression Profile
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HELLS Was Correlated with the Clinical Significance and Prognosis of Colorectal Cancer
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Correlation of Other Clinicopathological Variables with HELLS Expression
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[2]
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22
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68
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The differentially expressed genes (DEGs) of tumor and peritumoral tissues were identified by GEO2R.
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method.reader_named_unmapped
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gwas
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Automated Assays Laravel application and simulated adapters
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basis
The paper names the method it used and the corpus's method extractor maps it onto the DSL catalogue: anova.
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GSE8671
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GSE8671
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GSE126092
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Four GEO data sets (GSE8671, GSE24514, GSE32323, and GSE126092) were selected and downloaded for analysis. The differentially expressed genes (DEGs) of tumor and peritumoral tissues were identified by GEO2R.
basis
The paper names GSE8671, GSE24514, GSE32323, GSE126092 in Gene Expression Omnibus (GEO) and the accession resolves in the repository. No dataset was downloaded and no licence was read.
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minimax
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2026-10-31T18:18:13Z
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PMID 32063710 full text
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data:geo:GSE126092
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data:geo:GSE126092
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GEO GSE126092
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lineage object · 4 fields
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reen hub genes expressed in CRC. qRT-PCR and Western blotting were used to experimentally determine the ex
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paper_text_order:632
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assay:1
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(HELLS) gene, at the RNA and protein levels. Immunohistochemical (IHC) assays were used to correlate the stai
[1]
RNA and protein levels. Immunohistochemical (IHC) assays were used to correlate the stained H
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Cell proliferation levels were assayed by a CCK-8 kit, a colony formation assay was performed,
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a colony formation assay was performed, and flow cytometry was used to quantify the cells at each stage
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cated poor prognosis for CRC patients. HELLS knockdown led to impaired cell proliferation, colony g
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overall survival (log-rank p = 0.027). HELLS siRNA impaired cell proliferation and colony gener
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ration and colony generation in vitro. HELLS siRNA induced significant G2+M arrest in HT29 and
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paper_text_order:1772
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Complete file
{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:32063710", "kind": "science-record", "revision": 8, "content_hash": "sha256:ea0e7e511ac4be23c2d38bc0b1150bfa3b63ae7bad33b1f286c1fe89f76df5eb", "created_at": "2026-11-01T15:40:56Z", "updated_at": "2026-11-01T22:01:17Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "Downregulation of the Helicase Lymphoid-Specific (HELLS) Gene Impairs Cell Proliferation and Induces Cell Cycle Arrest in Colorectal Cancer Cells.", "doi": "10.2147/OTT.S223668", "pmid": "32063710", "authors": ["Xi Liu", "Xuyang Hou", "Yan Zhou", "Qinglong Li", "Fanhua Kong", "Shichao Yan", "Sanlin Lei", "Li Xiong", "Jun He"], "journal": "OncoTargets and therapy", "year": 2019, "abstract": "AIM: Colorectal cancer (CRC) is the fourth most frequently diagnosed cancer worldwide. Despite the decrease in mortality of CRC patients, further investigation of the molecular pathogenesis of CRC could unveil new therapeutic targets and offer better prognosis predictions, which might direct attention to epigenetic regulators.\nMETHODS: Publicly available data from the Gene Expression Omnibus (GEO) database and clinical samples were collected. Bioinformatics methods were used to screen hub genes expressed in CRC. qRT-PCR and Western blotting were used to experimentally determine the expression of one gene of interest, the helicase lymphoid-specific (HELLS) gene, at the RNA and protein levels. Immunohistochemical (IHC) assays were used to correlate the stained HELLS proteins to survival data. Cell proliferation levels were assayed by a CCK-8 kit, a colony formation assay was performed, and flow cytometry was used to quantify the cells at each stage of the cell cycle.\nRESULTS: A total of 225 overlapping genes were screened, including 14 hub genes. Analysis through a protein-protein interaction (PPI) network and the Gene Ontology database was performed by using the Cytoscape and DAVID online tools, respectively. HELLS RNA and protein expression levels in tumor tissues were 2.09-fold higher and 1.46-fold higher, respectively, than in the peritumoral tissues (p < 0.001, p<0.001). HELLS expression was significantly associated with the T stage (p=0.0027), M stage (p=0.0119), and TNM clinical stage (p = 0.0312) and a higher pathological grade (p=0.049). Highly expressed HELLS was reversibly associated with overall survival (log-rank p = 0.027). HELLS siRNA impaired cell proliferation and colony generation in vitro. HELLS siRNA induced significant G2+M arrest in HT29 and HCT116 cells compared with the respective negative controls (82.29% vs 25.85% and 35.41% vs 15.26%, respectively).\nCONCLUSION: Our data revealed that HELLS was significantly upregulated in CRC and correlated with clinicopathological parameters. High expression of HELLS indicated poor prognosis for CRC patients. HELLS knockdown led to impaired cell proliferation, colony generation, and G2+M cell cycle arrest.", "claims": [{"id": "claim-method", "statement": "The differentially expressed genes (DEGs) of tumor and peritumoral tissues were identified by GEO2R.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:32063710", "locator": "sections[3] \"Identification of the Hub Genes\" paragraph 2", "quote": "The differentially expressed genes (DEGs) of tumor and peritumoral tissues were identified by GEO2R."}], "state": "complete"}, {"id": "claim-data-access", "statement": "Four GEO data sets (GSE8671, GSE24514, GSE32323, and GSE126092) were selected and downloaded for analysis. 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