Evidence map›Paper›PMID 25659585›Full record

ArticleOncogene2015

Targeting the hsp70 gene delays mammary tumor initiation and inhibits tumor cell metastasis.

J Gong, D Weng, T Eguchi, A Murshid, M Y Sherman, B Song, S K Calderwood

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 67 citations in OpenAlex.

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  15. Prevention of High Glucose-Mediated EMT by Inhibition of Hsp70 Chaperone.International journal of molecular sciences · 2021
    Article
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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

7 authors at 4 institutions in 1 country.

J GongDepartment of Medicine, Boston University Medical Center, Boston, MA, USA.
D WengDepartment of Medicine, Boston University Medical Center, Boston, MA, USA.
T EguchiMolecular and Cellular Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
A MurshidMolecular and Cellular Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
M Y ShermanDepartment of Biochemistry, Boston University Medical Center, Boston, MA, USA.
B SongDepartment of Medicine, Boston University Medical Center, Boston, MA, USA.
S K CalderwoodMolecular and Cellular Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Boston Medical Center · USHarvard University · USBeth Israel Deaconess Medical Center · USBoston University · US

Funding

TRANSMEMBRANE SIGNAL MODULATION BY HYPERTHERMIAR01CA047407 · NCI · DANA-FARBER CANCER INSTITUTE · PI CALDERWOOD, STUART KEITH · 1988 to 2014
$4.3M
Extracellular Hsp70 and hyperthermia in tumor therapyR01CA119045 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CALDERWOOD, STUART KEITH · 2007 to 2016
$3.1M
Complex Role of HSF1 in Breast CancerR01CA176326 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CALDERWOOD, STUART KEITH, SHERMAN, MICHAEL Y · 2014 to 2018
$1.8M
NCI NIH HHS R01 CA047407NCI NIH HHS R01 CA119045NCI NIH HHS R01CA119045NCI NIH HHS R01 CA176326NCI NIH HHS R01CA176326NCI NIH HHS R01CA47407
6 · The paper itself

Abstract

Elevated levels of the inducible heat-shock protein 70 (Hsp72) have been implicated in mammary tumorigenesis in histological investigations of human breast cancer. We therefore examined the role of Hsp72 in mice, using animals in which the hsp70 gene was inactivated. We used a spontaneous tumor system with mice expressing the polyomavirus middle T (PyMT) oncogene under control of the mouse mammary tumor virus (MMTV) long-terminal repeat (MMT mice). These mice developed spontaneous, metastatic mammary cancer. We then showed Hsp72 to be upregulated in a fraction of mammary cancer initiating cells (CIC) within the MMT tumor cell population. These cells were characterized by elevated surface levels of stem cell markers CD44 and Sca1 and by rapid metastasis. Inactivation of the hsp70 gene delayed the initiation of mammary tumors. This delay in tumor initiation imposed by loss of hsp70 was correlated with a decreased pool of CIC. Interestingly, hsp70 knockout significantly reduced invasion and metastasis by mammary tumor cells and implicated its product Hsp72 in cell migration and formation of secondary neoplasms. Impaired tumorigenesis and metastasis in hsp70-knockout MMT mice was associated with downregulation of the met gene and reduced activition of the oncogenic c-Met protein. These experiments therefore showed Hsp72 to be involved in the growth and progression of mammary carcinoma and highlighted this protein as a potential target for anticancer drug development.

Indexed as

AnimalsAntineoplastic AgentsCell MovementCell Transformation, NeoplasticDown-RegulationFemaleHSP72 Heat-Shock ProteinsMammary Neoplasms, ExperimentalMiceMice, Inbred C57BLMice, KnockoutNeoplasm MetastasisOncogenesProto-Oncogene Proteins c-metAntineoplastic AgentsHSP72 Heat-Shock ProteinsProto-Oncogene Proteins c-met

Identifiers

PMID25659585
PMCPMC7331470
OpenAlexW2034030812

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.