Evidence map›Paper›PMID 19609950›Full record

ArticleInternational journal of cancer2010

Increased expression of the heterogeneous nuclear ribonucleoprotein K in pancreatic cancer and its association with the mutant p53.

Renyuan Zhou, Reneé Shanas, Mark A Nelson, Achyut Bhattacharyya, Jiaqi Shi

Open access · greenAbstract read
In one paragraph

Article in International journal of cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. The emerging role of mFrontiers in immunology · 2026
    Review
  3. Article
  4. hnRNP K induces HPV16 oncogene expression and promotes cervical cancerization.Journal of cancer research and clinical oncology · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Splicing-factor alterations in cancers.RNA (New York, N.Y.) · 2016
    Review
  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

5 authors at 1 institution in 1 country.

Renyuan ZhouDepartment of Urology, Fifth People's Hospital of Shanghai, P.R. China.
Reneé Shanas
Mark A Nelson
Achyut Bhattacharyya
Jiaqi Shi
University of Arizona · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
SPORE in Gastrointestinal CancerP50CA095060 · NCI · UNIVERSITY OF ARIZONA · PI GERNER, EUGENE W · 2002 to 2012
$25.3M
Role of eIF3f in Pancreatic CancerR03CA133449 · NCI · UNIVERSITY OF ARIZONA · PI SHI, JIAQI · 2008 to 2009
$151k
NCI NIH HHS CA023074NCI NIH HHS CA133449NCI NIH HHS P30 CA023074NCI NIH HHS P50 CA095060NCI NIH HHS R03 CA133449
6 · The paper itself

Abstract

The heterogeneous nuclear ribonucleoprotein (hnRNP) K is an essential RNA and DNA binding protein involved in gene expression and signal transduction including DNA transcription, RNA splicing, RNA stability and translation. The role of hnRNP K in cancer is relatively understudied. However, several cellular functions strongly indicate that hnRNP K is involved in tumorigenesis. In this study, we investigated the altered protein expression and the subcellular distribution of the hnRNP K protein using tissue microarrays in pancreatic cancer. We showed an increased cytoplasmic hnRNP K in pancreatic cancer. This increase in hnRNP K protein occurs at the posttranscriptional level. We postulate that the cytoplasmic accumulation of hnRNP K will lead to silenced mRNA translation of tumor suppressor genes and thus contributes to pancreatic cancer development. We also demonstrated that knocking down of hnRNP K expression by siRNA inhibited pancreatic cancer cell growth and colony formation. hnRNP K was identified as a member of the p53/HDM2 pathway. Whether hnRNP K interacts with the mutant p53 is not known. Using two different pancreatic cancer cell lines, we can demonstrate that hnRNP K interacts with the mutant p53. The subcellular distribution and function of the mutant p53 and the interaction of hnRNP K/mutant p53 were affected by the Ras/MEK/ERK pathway, growth factors and the specific p53 mutations in pancreatic cancer cells. Since Kras is activated and p53 is mutated in most pancreatic cancers, these data unveiled an important new signaling pathway that linked by hnRNP K and mutant p53 in pancreatic cancer tumorigenesis.

Indexed as

Blotting, WesternCell Line, TumorCell ProliferationHeterogeneous-Nuclear Ribonucleoprotein KHumansImmunohistochemistryImmunoprecipitationMitogen-Activated Protein KinasesMutant ProteinsMutationNeoplastic Stem CellsPancreatic NeoplasmsProtein Bindingras ProteinsRNA InterferenceSignal TransductionHeterogeneous-Nuclear Ribonucleoprotein KMitogen-Activated Protein KinasesMutant Proteinsras ProteinsTumor Suppressor Protein p53

Identifiers

PMID19609950
PMCPMC2795109
OpenAlexW1969539383

What OpenQuestion holds

Textmetadata
LicenceTDM
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.