Evidence map›Paper›PMID 27752061›Full record

ArticleScientific reports2016

Protein tyrosine phosphatase 1B targets PITX1/p120RasGAP thus showing therapeutic potential in colorectal carcinoma.

Hao-Wei Teng, Man-Hsin Hung, Li-Ju Chen, Mao-Ju Chang, Feng-Shu Hsieh, Ming-Hsien Tsai, Jui-Wen Huang, Chih-Lung Lin, Hsiang-Wen Tseng, Zong-Keng Kuo and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 31% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. PITX1 plays essential functions in cancer.Frontiers in oncology · 2023
    Review
  4. Article
  5. Article
  6. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 1 country.

Hao-Wei TengDivision of Medical Oncology, Department of Oncology, Taipei Veterans General Hospital, Taipei, Taiwan.
Man-Hsin HungDivision of Medical Oncology, Department of Oncology, Taipei Veterans General Hospital, Taipei, Taiwan.
Li-Ju ChenDepartment of Medical Research, National Taiwan University Hospital, Taipei, Taiwan.
Mao-Ju ChangDepartment of Medical Research, National Taiwan University Hospital, Taipei, Taiwan.
Feng-Shu HsiehDepartment of Medical Research, National Taiwan University Hospital, Taipei, Taiwan.
Ming-Hsien TsaiDepartment of Medical Research, National Taiwan University Hospital, Taipei, Taiwan.
Jui-Wen HuangIndustrial Technology Research Institute, Hsin-Chu, Taiwan.
Chih-Lung LinIndustrial Technology Research Institute, Hsin-Chu, Taiwan.
Hsiang-Wen TsengIndustrial Technology Research Institute, Hsin-Chu, Taiwan.
Zong-Keng KuoIndustrial Technology Research Institute, Hsin-Chu, Taiwan.
Jeng-Kai JiangSchool of Medicine, National Yang-Ming University, Taipei, Taiwan.
Shung-Haur YangSchool of Medicine, National Yang-Ming University, Taipei, Taiwan.
Chung-Wai ShiauInstitute of Biopharmaceutical Sciences, National Yang-Ming University, Taipei, Taiwan.
Kuen-Feng ChenDepartment of Medical Research, National Taiwan University Hospital, Taipei, Taiwan.
National Taiwan University Hospital · TWIndustrial Technology Research Institute · TWNational Yang Ming Chiao Tung University · TWTaipei Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein tyrosine phosphatase 1B (PTP1B) is known to promote the pathogenesis of diabetes and obesity by negatively regulating insulin and leptin pathways, but its role associated with colon carcinogenesis is still under debate. In this study, we demonstrated the oncogenic role of PTP1B in promoting colon carcinogenesis and predicting worse clinical outcomes in CRC patients. By co-immunoprecipitation, we showed that PITX1 was a novel substrate of PTP1B. Through direct dephosphorylation at Y160, Y175 and Y179, PTP1B destabilized PITX1, which resulted in downregulation of the PITX1/p120RasGAP axis. Interestingly, we found that regorafenib, the approved target agent for advanced CRC patients, exerted a novel property against PTP1B. By inhibiting PTP1B activity, regorafenib treatment augmented the stability of PITX1 protein and upregulated the expression of p120RasGAP in CRC. Importantly, we found that this PTP1B-dependant PITX1/p120RasGAP axis determines the in vitro anti-CRC effects of regorafenib. The above-mentioned effects of regorafenib were confirmed by the HT-29 xenograft tumor model. In conclusion, we demonstrated a novel oncogenic mechanism of PTP1B on affecting PITX1/p120RasGAP in CRC. Regorafenib inhibited CRC survival through reserving PTP1B-dependant PITX1/p120RasGAP downregulation. PTP1B may be a potential biomarker predicting regorafenib effectiveness, and a potential solution for CRC.

Indexed as

AgedAnimalsCarcinogenesisColorectal NeoplasmsFemaleGene Expression Regulation, NeoplasticHT29 CellsHumansMaleMiceMiddle Agedp120 GTPase Activating ProteinPaired Box Transcription FactorsPhenylurea CompoundsProtein Tyrosine Phosphatase, Non-Receptor Type 1Pyridineshomeobox protein PITX1p120 GTPase Activating ProteinPaired Box Transcription FactorsPhenylurea CompoundsProtein Tyrosine Phosphatase, Non-Receptor Type 1PTPN1 protein, humanPyridinesregorafenib

Identifiers

PMID27752061
PMCPMC5082755
OpenAlexW2532210174

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.