Evidence map›Paper›PMID 31745071›Full record

ArticleCell death & disease2019

Inhibition of PTP1B blocks pancreatic cancer progression by targeting the PKM2/AMPK/mTOC1 pathway.

Qi Xu, Ning Wu, Xiangqian Li, Chuanlong Guo, Chao Li, Bo Jiang, Huaizhi Wang, Dayong Shi

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
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  9. HarnessingInternational journal of molecular sciences · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 6 institutions in 1 country.

Qi XuKey Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, China.
Ning WuKey Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, China.
Xiangqian LiState Key Laboratory of Microbial Technology, Shandong University, Jinan, 250100, Shandong, China.
Chuanlong GuoKey Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, China.
Chao LiKey Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, China.
Bo JiangKey Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, China.
Huaizhi WangInstitute of Hepatopancreatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, 400038, China. whuaizhi@gmail.com.
Dayong ShiState Key Laboratory of Microbial Technology, Shandong University, Jinan, 250100, Shandong, China. shidayong@sdu.edu.cn.
Chinese Academy of Sciences · CNQingdao National Laboratory for Marine Science and Technology · CNInstitute of Oceanology · CNShandong University · CNSouthwest Hospital · CNUniversity of Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer is a highly malignant cancer and lacks effective therapeutic targets. Protein-tyrosine phosphatase 1B (PTP1B), a validated therapeutic target for diabetes and obesity, also plays a critical positive or negative role in tumorigenesis. However, the role of PTP1B in pancreatic cancer remains elusive. Here, we initially demonstrated that PTP1B was highly expressed in pancreatic tumors, and was positively correlated with distant metastasis and tumor staging, and indicated poor survival. Then, inhibition of PTP1B either by shRNA or by a specific small-molecule inhibitor significantly suppressed pancreatic cancer cell growth, migration and colony formation with cell cycle arrest in vitro and inhibited pancreatic cancer progression in vivo. Mechanism studies revealed that PTP1B targeted the PKM2/AMPK/mTOC1 signaling pathway to regulate cell growth. PTP1B inhibition directly increased PKM2 Tyr-105 phosphorylation to further result in significant activation of AMPK, which decreased mTOC1 activity and led to inhibition of p70S6K. Meanwhile, the decreased phosphorylation of PRAS40 caused by decreased PKM2 activity also helped to inhibit mTOC1. Collectively, these findings support the notion of PTP1B as an oncogene and a promising therapeutic target for PDAC.

Indexed as

AMP-Activated Protein KinasesAnimalsCarcinoma, Pancreatic DuctalCarrier ProteinsCell Line, TumorDisease ProgressionFemaleHumansMaleMechanistic Target of Rapamycin Complex 1Membrane ProteinsMiceMice, Inbred BALB CMice, NudePancreatic NeoplasmsProtein Tyrosine Phosphatase, Non-Receptor Type 1AMP-Activated Protein KinasesCarrier ProteinsMechanistic Target of Rapamycin Complex 1Membrane ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 1PTPN1 protein, humanRNA, Small InterferingSmall Molecule LibrariesThyroid Hormone-Binding ProteinsThyroid Hormones

Identifiers

PMID31745071
PMCPMC6864061
OpenAlexW2991378168

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.