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pmid:29374493

Over-expression of oncigenic pesudogene DUXAP10 promotes cell proliferation and invasion by regulating LATS1 and β-catenin in gastric cancer.

Yongcan Xu · Xiang Yu · Chenchen Wei · Fengqi Nie · Mingde Huang · Ming Sun

Journal of experimental & clinical cancer research : CR · 2018 doi:10.1186/s13046-018-0684-8

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title
Over-expression of oncigenic pesudogene DUXAP10 promotes cell proliferation and invasion by regulating LATS1 and β-catenin in gastric cancer.
doi
10.1186/s13046-018-0684-8
pmid
29374493
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Yongcan Xu
[1]
Xiang Yu
[2]
Chenchen Wei
[3]
Fengqi Nie
[4]
Mingde Huang
[5]
Ming Sun
journal
Journal of experimental & clinical cancer research : CR
year
2018
abstract
BACKGROUND: Recently, the pesudogenes have emerged as critical regulators in human cancers tumorigenesis and progression, and been identified as a key revelation in post-genomic biology. However, the expression pattern, biological function and mechanisms responsible for these molecules in human gastric cancer (GC) are not fully understood. METHODS: In this study, we globally assessed the transcriptomic differences of pesudogenes in gastric cancer using publicly available microarray data. DUXAP10 expression levels in GC tissues and cells was detected using quantitative real-time PCR (qPCR). DUXAP10 siRNAs and over-expression vector were transfected into GC cells to down-regulate or up-regulate DUXAP10 expression. Loss- and gain-of function assays were performed to investigate the role of DUXAP10 in GC cells cell proliferation, and invasion. RIP, RNA pulldown, and ChIP assays were used to determine the mechanism of DUXAP10's regulation of underlying targets. RESULTS: The pesudogene DUXAP10 is the only pseudogene that significantly over-expressed in all four GEO datasets, and frequently over-expressed in many other cancers including Liver Hepatocellular carcinoma, Bladder cancer, and Esophageal Cancer. High DUXAP10 expression is associated with GC patients poor prognosis, and knockdown of DUXAP10 significantly inhibits cells proliferation, migration and invasion in GC. Mechanistic investigation shows that DUXAP10 can interact with PRC2 and LSD1 to repress LATS1 expression at transcriptional level, and bind with HuR to maintain the stability of β-catenin mRNA and increase its protein levels at post-transcriptional level. CONCLUSIONS: Overall, our findings illuminate how increased DUXAP10 confers an oncogenic function in GC development and progression that may serve as a candidate prognostic biomarker and target for clinical management of GC.
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s detected using quantitative real-time PCR (qPCR). DUXAP10 siRNAs and over-expression vector
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es and cells was detected using quantitative real-time PCR (qPCR). DUXAP10 siRNAs and over-expression v
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ransfection with DUXAP10 siRNAs or shRNAs by qPCR. (c) Analysis of DUXAP10 expression levels i
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m sh-DUXAP10 group and control group mice by qPCR. (b) Statistical analysis of E-cadherin, N-c
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ociated with GC patients poor prognosis, and knockdown of DUXAP10 significantly inhibits cells prol
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s in BGC823, SGC7901, and MGC803 cells after transfection with DUXAP10 siRNAs or shRNAs by qPCR. (c) A
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DUXAP10 expression levels in AGS cells after transfection with DUXAP10 over-expression vector. (d, e)
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Complete file
{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:29374493", "kind": "science-record", "revision": 8, "content_hash": "sha256:8b88ae251dfb9af9191b8b3402a9a2c66a542aa9f53bf9c621abaccfb9be708b", "created_at": "2026-11-01T15:40:31Z", "updated_at": "2026-11-01T22:43:15Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "Over-expression of oncigenic pesudogene DUXAP10 promotes cell proliferation and invasion by regulating LATS1 and β-catenin in gastric cancer.", "doi": "10.1186/s13046-018-0684-8", "pmid": "29374493", "authors": ["Yongcan Xu", "Xiang Yu", "Chenchen Wei", "Fengqi Nie", "Mingde Huang", "Ming Sun"], "journal": "Journal of experimental & clinical cancer research : CR", "year": 2018, "abstract": "BACKGROUND: Recently, the pesudogenes have emerged as critical regulators in human cancers tumorigenesis and progression, and been identified as a key revelation in post-genomic biology. However, the expression pattern, biological function and mechanisms responsible for these molecules in human gastric cancer (GC) are not fully understood.\nMETHODS: In this study, we globally assessed the transcriptomic differences of pesudogenes in gastric cancer using publicly available microarray data. DUXAP10 expression levels in GC tissues and cells was detected using quantitative real-time PCR (qPCR). DUXAP10 siRNAs and over-expression vector were transfected into GC cells to down-regulate or up-regulate DUXAP10 expression. Loss- and gain-of function assays were performed to investigate the role of DUXAP10 in GC cells cell proliferation, and invasion. RIP, RNA pulldown, and ChIP assays were used to determine the mechanism of DUXAP10's regulation of underlying targets.\nRESULTS: The pesudogene DUXAP10 is the only pseudogene that significantly over-expressed in all four GEO datasets, and frequently over-expressed in many other cancers including Liver Hepatocellular carcinoma, Bladder cancer, and Esophageal Cancer. High DUXAP10 expression is associated with GC patients poor prognosis, and knockdown of DUXAP10 significantly inhibits cells proliferation, migration and invasion in GC. Mechanistic investigation shows that DUXAP10 can interact with PRC2 and LSD1 to repress LATS1 expression at transcriptional level, and bind with HuR to maintain the stability of β-catenin mRNA and increase its protein levels at post-transcriptional level.\nCONCLUSIONS: Overall, our findings illuminate how increased DUXAP10 confers an oncogenic function in GC development and progression that may serve as a candidate prognostic biomarker and target for clinical management of GC.", "claims": [{"id": "claim-method", "statement": "The Students t test (2 tailed), one-way ANOVA, and Mann-Whitney U test were conducted to analyze the in vitro and in vivo data by SPSS 17.0 software. 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