Evidence map›Paper›PMID 30804683›Full record

ArticleCancer management and research2019

PTPN9 induces cell apoptosis by mitigating the activation of Stat3 and acts as a tumor suppressor in colorectal cancer.

Dawei Wang, Zhuoxin Cheng, Ming Zhao, Chengbin Jiao, Qinghui Meng, Huayang Pan, Yu Xie, Long Li, Yexing Zhu, Wei Wang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Cellular signaling meets bacterial infection: the integrative role of STAT3.Frontiers in cellular and infection microbiology · 2026
    Review
  2. PTPN9 dephosphorylates IGF1RJournal of experimental & clinical cancer research : CR · 2025
    Article
  3. Review
  4. Review
  5. Effect of L3MBTL3/PTPN9 polymorphisms on risk to alcohol-induced ONFH in Chinese Han population.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Article
  6. Article
  7. Review
  8. Frontiers in immunology · 2022
    Article
  9. Comprehensive analysis ofFrontiers in genetics · 2022
    Article
  10. Article
  11. Article
  12. Article
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

12 authors at 3 institutions in 1 country.

Dawei WangDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, People's Republic of China, deshengliang126@126.com.
Zhuoxin ChengDepartment of General Surgery, The First Affiliated Hospital of Jiamusi University, Jiamusi 154002, People's Republic of China.
Ming ZhaoDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, People's Republic of China, deshengliang126@126.com.
Chengbin JiaoDepartment of General Surgery, The First Affiliated Hospital of Jiamusi University, Jiamusi 154002, People's Republic of China.
Qinghui MengDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, People's Republic of China, deshengliang126@126.com.
Huayang PanDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, People's Republic of China, deshengliang126@126.com.
Yu XieDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, People's Republic of China, deshengliang126@126.com.
Long LiDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, People's Republic of China, deshengliang126@126.com.
Yexing ZhuDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, People's Republic of China, deshengliang126@126.com.
Wei WangDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, People's Republic of China, deshengliang126@126.com.
Chunlei QuDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, People's Republic of China, deshengliang126@126.com.
Deshen LiangDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, People's Republic of China, deshengliang126@126.com.
First Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CNJiamusi University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAccumulating evidence has shown that protein tyrosine phosphatases (PTPs) are involved in regulating the transduction of many signaling pathways and play important roles in modulating the progression of some cancers, but the functions of PTPs in cancers have not been well elucidated until now. Here, we aimed to identify the roles of protein tyrosine phosphatase nonreceptor type 9 (PTPN9), a cytoplasmic PTP, in the development of colorectal cancer and elucidate the regulatory mechanism involved. MATERIALS AND

methodsCell viability assessment, colony formation assay, caspase-3 and caspase-9 activity assay, real-time PCR, and Western blot analysis were applied.

resultsOur results showed that PTPN9 expression was frequently downregulated in colorectal cancer tissues compared with adjacent normal tissues. Overexpression of PTPN9 mitigated cell growth and colony formation and induced cell apoptosis in colorectal cancer. Conversely, PTPN9 knockdown promoted cell growth and survival. Moreover, PTPN9 negatively regulated the activation of Stat3 and depressed its nuclear translocation in colorectal cancer. The effects of PTPN9 knockdown on cell apoptosis were attenuated by inhibition of the Stat3 pathway.

conclusionThese results indicate that PTPN9 inhibits cell growth and survival by repressing the activation of Stat3 in colorectal cancer, which suggests an important underlying mechanism of regulating cell growth and provides a novel candidate therapeutic target for colorectal cancer.

Indexed as

apoptosiscell survivalcolorectal cancerPTPMeg2PTPN9Stat3

Identifiers

PMID30804683
PMCPMC6371942
OpenAlexW2996361701

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.