Evidence map›Paper›PMID 21848913›Full record

ArticleCancer science2011

Downregulation of receptor for activated C-kinase 1 (RACK1) suppresses tumor growth by inhibiting tumor cell proliferation and tumor-associated angiogenesis.

Feng Wang, Tsuyoshi Osawa, Rika Tsuchida, Yasuhito Yuasa, Masabumi Shibuya

Open access · greenAbstract read
In one paragraph

Article in Cancer science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed, 33 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

5 authors at 1 institution in 1 country.

Feng WangDepartment of Molecular Oncology, Graduate School of Medicine and Dentistry, Tokyo Dental and Medical University, Tokyo, Japan.
Tsuyoshi Osawa
Rika Tsuchida
Yasuhito Yuasa
Masabumi Shibuya
Tokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

By behaving as molecular hubs, scaffold proteins can assemble a large number of signaling molecules and organize complicated intracellular signaling networks in time and space. Owing to their crucial role in mediating intracellular signaling related to tumor cell growth and migration, recent studies have highlighted the relevance of scaffold proteins in human cancers and indicated that interfering with their expression and/or their ability to bind effector proteins can inhibit cancer progression. Here, we show that receptor for activated C-kinase 1 (RACK1), a ubiquitously expressed scaffolding protein, plays a crucial regulatory role in tumor growth. Using an RNA silencing approach, we found that downregulation of RACK1 expression in HeLa and A673 tumor cells markedly suppressed the proliferation and invasion of these cells in vitro and tumor development in vivo. Consequently, we found that significant suppression of constitutive phosphorylation of Akt and MAPK by RACK1 silencing may contribute to the inhibition of tumor growth. Moreover, RACK1 silencing significantly attenuated tumor-associated angiogenesis by, at least in part, inhibiting the expression of two critical angiogenic factors, namely vascular endothelial growth factor-B and fibroblast growth factor 2. The results of the present study show that RACK1 is a potent enhancer of tumor growth and, thus, a potential anti-cancer therapeutic target.

Indexed as

RNA InterferenceAnimalsApoptosisCell DivisionCell Line, TumorDown-RegulationGTP-Binding ProteinsHeLa CellsHumansMiceMice, Inbred C57BLNeoplasm InvasivenessNeoplasm ProteinsNeovascularization, PathologicPhosphorylationProtein Processing, Post-TranslationalGTP-Binding ProteinsNeoplasm ProteinsRACK1 protein, humanReceptors, Cell SurfaceReceptors for Activated C KinaseRNA, Small InterferingVascular Endothelial Growth Factor BVEGFB protein, human

Identifiers

PMID21848913
PMCPMC11159629
OpenAlexW2049926565

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.