Evidence map›Paper›PMID 21721029›Full record

ArticleHepatology (Baltimore, Md.)2011

Intercellular nanovesicle-mediated microRNA transfer: a mechanism of environmental modulation of hepatocellular cancer cell growth.

Takayuki Kogure, Wen-Lang Lin, Irene K Yan, Chiara Braconi, Tushar Patel

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Hepatology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 333 papers.

0numbers the graph read from it
0cells of the map it votes in
333citing papers in PubMed
16.8field-weighted citation impact, top 1% 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

333 citing papers in PubMed, 530 citations in OpenAlex.

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  6. Diagnostic and prognostic significance of circulating extracellular vesicles in gastrointestinal cancers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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273 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

5 authors at 3 institutions in 1 country.

Takayuki KogureMayo Clinic, Jacksonville, FL 32224, USA.
Wen-Lang Lin
Irene K Yan
Chiara Braconi
Tushar Patel
Jacksonville College · USThe Ohio State University · USMayo Clinic in Florida · US

Funding

Mechanisms of Survival Signaling in Biliary EpitheliaR01DK069370 · NIDDK · SCOTT AND WHITE MEMORIAL HOSPITAL · PI PATEL, TUSHAR · 2005 to 2014
$2.4M
NIDDK NIH HHS R01 DK069370
6 · The paper itself

Abstract

unlabelledHepatocellular carcinoma (HCC) is characterized by a propensity for multifocality, growth by local spread, and dysregulation of multiple signaling pathways. These features may be determined by the tumoral microenvironment. The potential of tumor cells to modulate HCC growth and behavior by secreted proteins has been extensively studied. In contrast, the potential for genetic modulation is poorly understood. We investigated the role and involvement of tumor-derived nanovesicles capable of altering gene expression and characterized their ability to modulate cell signaling and biological effects in other cells. We show that HCC cells can produce nanovesicles and exosomes that differ in both RNA and protein content from their cells of origin. These can be taken up and internalized by other cells and can transmit a functional transgene. The microRNA (miRNA) content of these exosomes was examined, and a subset highly enriched within exosomes was identified. A combinatorial approach to identify potential targets identified transforming growth factor β activated kinase-1 (TAK1) as the most likely candidate pathway that could be modulated by these miRNAs. Loss of TAK1 has been implicated in hepatocarcinogenesis and is a biologically plausible target for intercellular modulation. We show that HCC cell-derived exosomes can modulate TAK1 expression and associated signaling and enhance transformed cell growth in recipient cells.

conclusionExosome-mediated miRNA transfer is an important mechanism of intercellular communication in HCC cells. These observations identify a unique intercellular mechanism that could potentially contribute to local spread, intrahepatic metastases, or multifocal growth in HCC.

Indexed as

Cell ProliferationCarcinoma, HepatocellularCell CommunicationExosomesFemaleHumansLiver NeoplasmsMaleMicroRNAsNeoplasm InvasivenessReal-Time Polymerase Chain ReactionSampling StudiesSignal TransductionTumor Cells, CulturedTumor MicroenvironmentMicroRNAs

Identifiers

PMID21721029
PMCPMC3310362
OpenAlexW1982255083

What OpenQuestion holds

Textmetadata
LicenceTDM
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.