Evidence map›Paper›PMID 19302291›Full record

ArticleCancer science2009

Down-regulation of cIAP2 enhances 5-FU sensitivity through the apoptotic pathway in human colon cancer cells.

Hideaki Karasawa, Koh Miura, Wataru Fujibuchi, Kazuyuki Ishida, Naoyuki Kaneko, Makoto Kinouchi, Mitsunori Okabe, Toshinori Ando, Yukio Murata, Hiroyuki Sasaki and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

40 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  11. Genetic variants ofAmerican journal of cancer research · 2020
    Article
  12. Intestinal Microbiota: A Novel Target to Improve Anti-Tumor Treatment?International journal of molecular sciences · 2019
    Review
  13. Article
  14. Article
  15. Global Investigations ofFrontiers in oncology · 2019
    Review
  16. Article
  17. The emerging role of long non-coding RNAs in the drug resistance of colorectal cancer.International journal of clinical and experimental pathology · 2018
    Review
  18. Article
  19. Article
  20. Review
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

14 authors at 3 institutions in 1 country.

Hideaki KarasawaDivision of Biological-Regulation and Oncology, Department of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, Miyagi, Japan 980-8574.
Koh Miura
Wataru Fujibuchi
Kazuyuki Ishida
Naoyuki Kaneko
Makoto Kinouchi
Mitsunori Okabe
Toshinori Ando
Yukio Murata
Hiroyuki Sasaki
Kazuhiro Takami
Akihiro Yamamura
Chikashi Shibata
Iwao Sasaki
Tohoku University · JPNational Institute of Advanced Industrial Science and Technology · JPTohoku University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Currently 5-fluorouracil (5-FU) plays a central role in the chemotherapeutic regimens for colorectal cancers and thus it is important to understand the mechanisms that determine 5-FU sensitivity. The expression profiles of human colon cancer cell line DLD-1, its 5-FU-resistant subclone DLD-1/FU and a further 21 types of colon cancer cell lines were compared to identify the novel genes defining the sensitivity to 5-FU and to estimate which population of genes is responsible for 5-FU sensitivity. In the hierarchical clustering, DLD-1 and DLD-1/FU were most closely clustered despite over 100 times difference in their 50% inhibitory concentration of 5-FU. In DLD-1/FU, the population of genes differentially expressed compared to DLD-1 was limited to 3.3%, although it ranged from 4.8% to 24.0% in the other 21 cell lines, thus indicating that the difference of 5-FU sensitivity was defined by a limited number of genes. Next, the role of the cellular inhibitor of apoptosis 2 (cIAP2) gene, which was up-regulated in DLD-1/FU, was investigated for 5-FU resistance using RNA interference. The down-regulation of cIAP2 efficiently enhanced 5-FU sensitivity, the activation of caspase 3/7 and apoptosis under exposure to 5-FU. The immunohistochemistry of cIAP2 in cancer and corresponding normal tissues from colorectal cancer patients in stage III revealed that cIAP2 was more frequently expressed in cancer tissues than in normal tissues, and cIAP2-positive patients had a trend toward early recurrence after fluorouracil-based chemotherapy. Although the association between drug sensitivity and the IAP family in colorectal cancer has not yet been discussed, cIAP2 may therefore play an important role as a target therapy in colorectal cancer.

Indexed as

ApoptosisDown-RegulationBaculoviral IAP Repeat-Containing 3 ProteinCaspase 3Caspase 7Cell Line, TumorColonic NeoplasmsDrug Resistance, NeoplasmEnzyme ActivationFluorouracilGene Expression Regulation, NeoplasticHumansInhibitor of Apoptosis ProteinsOligonucleotide Array Sequence AnalysisPrognosisRNA, Small InterferingBaculoviral IAP Repeat-Containing 3 ProteinBIRC3 protein, humanCaspase 3Caspase 7FluorouracilInhibitor of Apoptosis ProteinsRNA, Small InterferingUbiquitin-Protein Ligases

Identifiers

PMID19302291
PMCPMC11159709
OpenAlexW2004826992

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.