Evidence map›Paper›PMID 22158033›Full record

ArticleOncogene2012

Involvement of the SKP2-p27(KIP1) pathway in suppression of cancer cell proliferation by RECK.

Y Yoshida, K Ninomiya, H Hamada, M Noda

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.3field-weighted citation impact, top 19% 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, 31 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

4 authors at 3 institutions in 2 countries.

Y YoshidaDepartment of Molecular Oncology and Global COE Program, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto, Japan.
K Ninomiya
H Hamada
M Noda
Kyoto University · JPKyoto University of Education · JPTokyo University of Pharmacy and Life Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The membrane-anchored matrix metalloproteinase-regulator RECK is often downregulated in cancers; in some cases, a significant correlation between the level of residual RECK in resected tumors and patient survival has been noted. Furthermore, restoration of RECK expression in certain cancer-derived cell lines results in reduced tumorigenicity. Here we report that acute RECK expression in colon carcinoma cells results in cell cycle-arrest accompanied by downregulation of a ubiquitin ligase component, S-phase kinase-associated protein 2 (SKP2), and upregulation of its substrate, p27(KIP1). Our data indicate that RECK-induced growth suppression is at least partially dependent on p27, and that RECK and type I collagen share similar effects on the SKP2-p27 pathway. Importantly, in patients with lung, colorectal and bladder cancers, the RECK/SKP2 ratio is high in normal tissues and lower in the cancer tissues. These findings reveal a novel molecular pathway linking cell-cycle progression to RECK downregulation, extracellular matrix degradation and SKP2 upregulation, and suggest that treatment regimens that induce RECK expression could be promising cancer therapies.

Indexed as

AnimalsCell Cycle CheckpointsCell Line, TumorCell ProliferationColonic NeoplasmsCyclin-Dependent Kinase Inhibitor p27Down-RegulationGPI-Linked ProteinsHumansMiceNIH 3T3 CellsPhosphorylationRNA InterferenceRNA, Small InterferingS-Phase Kinase-Associated ProteinsUp-RegulationCyclin-Dependent Kinase Inhibitor p27GPI-Linked ProteinsRECK protein, humanRNA, Small InterferingS-Phase Kinase-Associated Proteins

Identifiers

PMID22158033
OpenAlexW2095539567

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.