Evidence map›Paper›PMID 19686745›Full record

ArticleGastroenterology2010

RNA-binding protein quaking, a critical regulator of colon epithelial differentiation and a suppressor of colon cancer.

Guodong Yang, Haiyan Fu, Jie Zhang, Xiaozhao Lu, Fang Yu, Liang Jin, Liyuan Bai, Bo Huang, Lan Shen, Yue Feng and 2 more

Abstract read
In one paragraph

Article in Gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

84 citing papers in PubMed, 127 citations in OpenAlex.

  1. RNA-Binding Proteins: Modulators of Canonical Wnt Signaling Pathway.International journal of molecular sciences · 2025
    Review
  2. Review
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  5. miR-574-5p in epigenetic regulation and Toll-like receptor signaling.Cell communication and signaling : CCS · 2024
    Review
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  16. Promoter Methylation ofFrontiers in genetics · 2022
    Article
  17. Tumor-Progressive Mechanisms Mediating miRNA-Protein Interaction.International journal of molecular sciences · 2021
    Review
  18. Article
  19. Review
  20. Article

24 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Guodong YangThe State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, the Fourth Military Medical University, Xi'an, China.
Haiyan Fu
Jie Zhang
Xiaozhao Lu
Fang Yu
Liang Jin
Liyuan Bai
Bo Huang
Lan Shen
Yue Feng
Libo Yao
Zifan Lu
Air Force Medical University · CNEmory University · US

Funding

Function of QKI RNA-binding Protein in CNS MyelinationR01NS039551 · NINDS · EMORY UNIVERSITY · PI FENG, YUE · 2001 to 2006
$1.5M
NINDS NIH HHS R01 NS039551
6 · The paper itself

Abstract

BACKGROUND &

aimsColon cancer is one of the best understood neoplasms from a genetic perspective, yet it remains the second most common cause of cancer-related death. Post-transcriptional regulation mediated by RNA-binding proteins or microRNAs coordinately targets multiple genes, holding promise involved in colon cancer initiation and development. Here we studied the role of RNA-binding protein quaking (QKI) in colon cancer.

methodsWe observed the expression pattern of QKI in normal colon and colon cancers through reverse-transcription polymerase chain reaction and Western blot. Bisulfite sequencing and methylation-specific PCR were applied for QKI promoter methylation analysis. We used enterocyte differentiation markers and soft agar assay to test the role of QKI in colon differentiation and colon cancer development. 3' Untranslated region (UTR) reporter assay and RNA-immunoprecipitation were used to confirm the interaction between QKI and beta-catenin or p27.

resultsQKI is significantly down-regulated and even absent in some colon cancers, which is at least partially because of the promoter hypermethylation. Forced expression of QKI in the colon cancer cells increased the expression of enterocyte differentiation marker intestinal alkaline phosphatase and lactase, together with the enhancement of p27Kip1 protein level, and membrane localized beta-catenin. Finally, QKI overexpression reduced the proliferation and tumorigenesis ability.

conclusionsOur study establishes that QKI functions as a principal regulator in the differentiation of colon epithelium and a suppressor of carcinogenesis through coordinately targeting multiple genes associated with cell growth and differentiation, whose deregulation by methylation is involved in colon cancer onset and progress.

Indexed as

AdultAgedCell DifferentiationCell DivisionColonic NeoplasmsDNA MethylationEnterocytesFemaleGene Expression Regulation, NeoplasticHT29 CellsHumansIntestinal MucosaMaleMicroRNAsMiddle AgedProliferating Cell Nuclear AntigenMicroRNAsp27 antigenProliferating Cell Nuclear AntigenQKI protein, humanRNA-Binding Proteins

Identifiers

PMID19686745
PMCPMC2847771
OpenAlexW2029349263

What OpenQuestion holds

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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.