Evidence map›Paper›PMID 22252525›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2012

PAK1-dependent MAPK pathway activation is required for colorectal cancer cell proliferation.

Haitao Qing, Wei Gong, Yufang Che, Xinying Wang, Liang Peng, Yan Liang, Weifei Wang, Qiliang Deng, Hongquan Zhang, Bo Jiang

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Fragile GeneFrontiers in oncology · 2021
    Article
  7. Review
  8. Two-Faced: Roles of JNK Signalling During Tumourigenesis in theFrontiers in cell and developmental biology · 2020
    Review
  9. Article
  10. Article
  11. Relationships amongWorld journal of gastroenterology · 2019
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

10 authors at 4 institutions in 1 country.

Haitao QingGuangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, People's Republic of China.
Wei Gong
Yufang Che
Xinying Wang
Liang Peng
Yan Liang
Weifei Wang
Qiliang Deng
Hongquan Zhang
Bo Jiang
Nanfang Hospital · CNSouthern Medical University · CNPeking University · CNThird Affiliated Hospital of Southern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

P21-activated protein kinase1 (PAK1), a main downstream effector of small Rho GTPases, Rac1, and Cdc42, plays an important role in the regulation of cell morphogenesis, motility, mitosis, and angiogenesis. Despite its importance, the molecular mechanisms of PAK1 that contributed to colorectal carcinogenesis remain unclear. Our immunohistochemistry showed that PAK1 expression was increased with colorectal cancer (CRC) progression through the adenoma to carcinoma sequence. Furthermore, our results suggested a relationship between PAK1 nuclear localization and the Dukes staging. In the present study, we showed that PAK1 knockdown decreased proliferation and delayed the G1/S cell-cycle transition, and increased apoptosis in vivo and in vitro. In addition, PAK1 knock-down downregulated c-Jun amino terminal kinases (JNK) activity and the levels of cyclinD1, CDK4/6. Inhibition of the JNK activity by chemical inhibitor (SP600125) significantly reduced the effects of PAK1 on CRC proliferation via accumulation of phosphatase and tensin homolog deleted on chromosome 10 (PTEN). In conclusion, our results demonstrate that knockdown of PAK1 could enhance the chemosensitivity of CRCs to 5-fluorouracil through G1 arrest. The mechanism by which PAK1 induced cancer growth might involve activation of JNK as well as downregulation of PTEN. Targeting PAK1 may represent a novel treatment strategy for developing novel chemotherapeutic agents.

Indexed as

Cell ProliferationMAP Kinase Signaling SystemAnimalsAnthracenesAntimetabolites, AntineoplasticApoptosisCell Cycle CheckpointsCell Line, TumorCell NucleusColorectal NeoplasmsCyclin D1Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6FluorouracilG1 PhaseHumansAnthracenesAntimetabolites, AntineoplasticCyclin D1Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6FluorouracilJNK Mitogen-Activated Protein Kinasesp21-Activated KinasesPAK1 protein, humanPTEN PhosphohydrolasePTEN protein, humanpyrazolanthrone

Identifiers

PMID22252525
OpenAlexW2050563501

What OpenQuestion holds

Textmetadata
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.