Evidence map›Paper›PMID 16965600›Full record

ArticleCancer science2006

High expression of insulin-like growth factor binding protein-3 is correlated with lower portal invasion and better prognosis in human hepatocellular carcinoma.

Shinichi Aishima, Yuji Basaki, Yoshinao Oda, Yousuke Kuroda, Yunosuke Nishihara, Kenichi Taguchi, Akinobu Taketomi, Yoshihiko Maehara, Fumihito Hosoi, Yuichiro Maruyama and 9 more

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In one paragraph

Article in Cancer science, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 26% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

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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

19 authors at 3 institutions in 2 countries.

Shinichi AishimaDepartment of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Yuji Basaki
Yoshinao Oda
Yousuke Kuroda
Yunosuke Nishihara
Kenichi Taguchi
Akinobu Taketomi
Yoshihiko Maehara
Fumihito Hosoi
Yuichiro Maruyama
Abbas Fotovati
Shinji Oie
Mayumi Ono
Takato Ueno
Michio Sata
Hirohisa Yano
Masamichi Kojiro
Michihiko Kuwano
Masazumi Tsuneyoshi
Kurume University · JPKyushu University · JPNational Hospital Organization Kyushu Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin-like growth factor binding protein-3 (IGFBP-3) modulates cell proliferation of various cancer cell types. However, it remains unclear how IGF-IGFBP-3-signaling is involved in growth and progression of hepatocellular carcinoma (HCC). The aim of the present study was to evaluate the role of IGFBP-3 in HCC. Type 1 receptor for IGF (IGF-1R) was expressed at various levels in the seven lines examined, but IGF-2R was not expressed. Of the seven lines, the growth of HAK-1B, KIM-1, KYN-2 and HepG2 cells was stimulated in a dose-dependent manner by the exogenous addition of IGF-I or IGF-II, but the HAK-1A, KYN-1 and KYN-3 cell lines showed no growth. Exogenous addition of IGFBP-3 markedly blocked IGF-I and IGF-II-stimulated cell growth of KYN-2 and HepG2 cells, and moderately stimulated that of KIM-1 and HAK-1B cells, but no growth of the KYN-1, KYN-3 and HAK-1A cell lines was observed. IGF-I enhanced the phosphorylation of IGF-1R, Akt and Erk1/2 in KYN-2 cells, and coadministration of IGFBP-3 blocked all types of activation by IGF-I investigated here. In contrast, no such activation by IGF-I was detected in KYN-3 cells. IGFBP-3 also suppressed IGF-I-induced cell invasion by KYN-2 cells. Moreover, we were able to observe the apparent expression of IGFBP-3 in KYN-3 cells, but not in the other six cell lines. Furthermore reduced expression of IGFBP-3, but not that of IGF-1R, was significantly correlated with tumor size, histological differentiation, capsular invasion and portal venous invasion. Low expression of IGFBP-3 was independently associated with poor survival. IGFBP-3 could be a molecular target of intrinsic importance for further development of novel therapeutic strategy against HCC.

Indexed as

AgedAged, 80 and overCarcinoma, HepatocellularFemaleHumansImmunoenzyme TechniquesInsulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor ILiver NeoplasmsMaleMiddle AgedNeoplasm InvasivenessPortal VeinPrognosisProto-Oncogene Proteins c-aktReceptor, Fibroblast Growth Factor, Type 1Insulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor IProto-Oncogene Proteins c-aktReceptor, Fibroblast Growth Factor, Type 1RNA, Small Interfering

Identifiers

PMID16965600
PMCPMC11158442
OpenAlexW1968490444

What OpenQuestion holds

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Registered trials

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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.