Evidence map›Paper›PMID 20141613›Full record

ArticleJournal of cellular and molecular medicine2009

Stimulation of protein kinase C-alpha suppresses colon cancer cell proliferation by down-regulation of beta-catenin.

Jungsug Gwak, Soo-Jin Jung, Dong-Ii Kang, Eun-Young Kim, Dong-Eun Kim, Young-Hwa Chung, Jae-Gook Shin, Sangtaek Oh

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

  1. PKCActa pharmaceutica Sinica. B · 2024
    Article
  2. Review
  3. Review
  4. Root Bark ofJournal of microbiology and biotechnology · 2021
    Article
  5. The complexities of PKCα signaling in cancer.Advances in biological regulation · 2021
    Review
  6. Article
  7. Article
  8. Hyperglycemia promotes microvillus membrane expression of DMT1 in intestinal epithelial cells in a PKCα-dependent manner.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  9. Tumor promoter TPA activates Wnt/β-catenin signaling in a casein kinase 1-dependent manner.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. 2-Hydroxyoleate, a nontoxic membrane binding anticancer drug, induces glioma cell differentiation and autophagy.Proceedings of the National Academy of Sciences of the United States of America · 2012
    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

8 authors at 4 institutions in 1 country.

Jungsug GwakPharmcoGenomics Research Center, Inje University, Busan, Korea.
Soo-Jin Jung
Dong-Ii Kang
Eun-Young Kim
Dong-Eun Kim
Young-Hwa Chung
Jae-Gook Shin
Sangtaek Oh
Inje University · KRInje University Busan Paik Hospital · KRKonkuk University · KRPusan National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We reported previously that protein kinase C-alpha (PKC-alpha) negatively regulates Wnt/beta-catenin signalling pathway. The current study explores the role of PKC-alpha in the regulation of proliferation of colon cancer cells, which contain aberrant up-regulation of intracellular beta-catenin. In colon tissue and cells, an inverse correlation was observed between the expression levels of PKC-alpha and intracellular beta-catenin. Activation of PKC-alpha inhibited beta-catenin response transcription by down-regulation of intracellular beta-catenin and induced phosphorylation of the N-terminal serine and threonine residues (Ser33/Ser37/Thr41) of beta-catenin, marking it for proteasomal degradation, in colon cancer cells. Pharmacological inhibition or depletion of PKC-alpha-abrogated PKC-alpha-mediated beta-catenin down-regulation and phosphorylation in colon cancer cells. Notably, the Ser45 residue of beta-catenin was essential for PKC-alpha-induced beta-catenin down-regulation in colon cancer cells. Moreover, PKC-alpha activation repressed the expression of cyclin D1 and c-myc, which are known beta-catenin target genes, and thus inhibited the growth of colon cancer cells. These findings suggest that PKC-alpha negatively regulates colon cancer cell proliferation viabeta-catenin phosphorylation/down-regulation and may facilitate the development of new strategies to treatment of colon cancer.

Indexed as

Cell ProliferationDown-RegulationBase Sequencebeta CateninColonic NeoplasmsDNA PrimersEnzyme ActivationHumansImmunohistochemistryProtein Kinase C-alphaReverse Transcriptase Polymerase Chain Reactionbeta CateninDNA PrimersProtein Kinase C-alpha

Identifiers

PMID20141613
PMCPMC9181363
OpenAlexW2010808726

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.