Evidence map›Paper›PMID 23085757›Full record

ArticleOncogene2013

miR-30d, miR-181a and miR-199a-5p cooperatively suppress the endoplasmic reticulum chaperone and signaling regulator GRP78 in cancer.

S-F Su, Y-W Chang, C Andreu-Vieyra, J Y Fang, Z Yang, B Han, A S Lee, G Liang

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 3 pooled it
5.5field-weighted citation impact, top 3% 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

80 citing papers in PubMed, 3 syntheses or guidelines pooled it, 135 citations in OpenAlex.

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20 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

8 authors at 2 institutions in 1 country.

S-F Su1] Department of Urology, Los Angeles, CA, USA [2] Program in Genetic, Molecular, and Cellular Biology, Los Angeles, CA, USA.
Y-W Chang
C Andreu-Vieyra
J Y Fang
Z Yang
B Han
A S Lee
G Liang
University of Southern California · USUniversity of California, Los Angeles · US

Funding

STRESS INDUCTION OF THE GLUCOSE REGULATED PROTEINSR01CA027607 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LEE, AMY S · 1985 to 2021
$11.1M
Determining the mechanistic and therapeutic roles of microRNAs in bladder cancerR01CA138794 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LIANG, GANGNING · 2010 to 2013
$1.0M
NCI NIH HHS R01 CA027607NCI NIH HHS R01 CA138794
6 · The paper itself

Abstract

GRP78, a major endoplasmic reticulum chaperone and signaling regulator, is commonly overexpressed in cancer. Moreover, induction of GRP78 by a variety of anti-cancer drugs, including histone deacetylase inhibitors, confers chemoresistance to cancer, thereby contributing to tumorigenesis. Thus, therapies aimed at decreasing GRP78 levels, which results in the inhibition of tumor cell proliferation and resensitization of tumor cells to chemotherapeutic drugs may hold promise for cancer treatment. Despite advances in our understanding of GRP78 actions, little is known about endogenous inhibitors controlling its expression. As endogenous regulators, microRNAs (miRNAs) play important roles in modulating gene expression; therefore, we sought to identify miRNA(s) that target GRP78, under the hypothesis that these miRNAs may serve as therapeutic agents. Here, we report that three miRNAs (miR-30d, miR-181a, miR-199a-5p) predicted to target GRP78 are down-regulated in prostate, colon and bladder tumors, and human cancer cell lines. We show that in C42B prostate cancer cells, these miRNAs down-regulate GRP78 and induce apoptosis by directly targeting its 3' untranslated region. Importantly, we demonstrate that the three miRNAs act cooperatively to decrease GRP78 levels, suggesting that multiple miRNAs may be required to efficiently control the expression of some genes. In addition, delivery of multiple miRNAs by either transient transfection or lentivirus transduction increased the sensitivity of cancer cells to the histone deacetylase inhibitor, trichostatin A, in C42B, HCT116 and HL-60 cells. Together, our results indicate that the delivery of co-transcribed miRNAs can efficiently suppress GRP78 levels and GRP78-mediated chemoresistance, and suggest that this strategy holds therapeutic potential.

Indexed as

Gene Expression Regulation, Neoplastic3' Untranslated RegionsAdenocarcinomaAnimalsApoptosisCell Line, TumorColonic NeoplasmsDrug Resistance, NeoplasmEndoplasmic Reticulum Chaperone BiPGenes, ReporterGenetic VectorsHeat-Shock ProteinsHistone Deacetylase InhibitorsHL-60 CellsHumansHydroxamic Acids3' Untranslated RegionsEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsHistone Deacetylase InhibitorsHSPA5 protein, humanHspa5 protein, mouseHydroxamic AcidsMicroRNAsMIrn181 microRNA, humanmirn199 microRNA, humanMIRN30b microRNA, humanRNARNA, MessengerRNA, recombinantThapsigargintrichostatin A

Identifiers

PMID23085757
PMCPMC3787795
OpenAlexW2060917827

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.