TRAP1 regulates autophagy in lung cancer cells

TRAP1 regulates autophagy in lung cancer cells INTRODUCTIONTumour Necrosis Factor Receptor‐Associated Protein 1 (TRAP1) is a member of the HSP90 family with predominantly mitochondrial localization, whose cytoprotective role has been widely documented. Several studies suggest that TRAP1 preserves cellular function by protecting mitochondrial function, limiting the effects of oxidative stress either by decreasing reactive oxygen species (ROS)‐mediated oxidation or by attenuating ROS production and through preservation of the mitochondrial membrane potential by limiting mitochondrial permeability transition pore (mPTP) opening through its interaction with HSP90 and cyclophilin D (CypD). Recent studies identify additional cytoprotective roles for TRAP1 in cellular stress responses including the unfolded protein response to ER stress and autophagy. Together, these effects seem to contribute for TRAP1 protective effect against apoptosis. These anti‐apoptotic functions contribute to human oncogenesis. TRAP1 expression is increased in numerous human malignancies. Functionally, inhibition of mitochondrial TRAP1 and related chaperones is cytotoxic to tumour cells, but not normal cells. Anti‐apoptotic functions of TRAP1 confer tumour cells resistance against different chemotherapeutic agents. For these reasons, TRAP1 has been proposed as a potential biomarker and target for anticancer therapies. In this context, mitochondrial‐targeted agents have been developed to selectively inhibit HSP90‐like mitochondrial chaperones inducing cell death and reverting tumour cell multi‐drug‐resistant phenotype.It has http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Clinical Investigation Wiley

Loading next page...
 
/lp/wiley/trap1-regulates-autophagy-in-lung-cancer-cells-ttlwD0jkn7
Publisher
Wiley
Copyright
Copyright © 2018 Stichting European Society for Clinical Investigation Journal Foundation. Published by John Wiley & Sons Ltd
ISSN
0014-2972
eISSN
1365-2362
D.O.I.
10.1111/eci.12900
Publisher site
See Article on Publisher Site

Abstract

INTRODUCTIONTumour Necrosis Factor Receptor‐Associated Protein 1 (TRAP1) is a member of the HSP90 family with predominantly mitochondrial localization, whose cytoprotective role has been widely documented. Several studies suggest that TRAP1 preserves cellular function by protecting mitochondrial function, limiting the effects of oxidative stress either by decreasing reactive oxygen species (ROS)‐mediated oxidation or by attenuating ROS production and through preservation of the mitochondrial membrane potential by limiting mitochondrial permeability transition pore (mPTP) opening through its interaction with HSP90 and cyclophilin D (CypD). Recent studies identify additional cytoprotective roles for TRAP1 in cellular stress responses including the unfolded protein response to ER stress and autophagy. Together, these effects seem to contribute for TRAP1 protective effect against apoptosis. These anti‐apoptotic functions contribute to human oncogenesis. TRAP1 expression is increased in numerous human malignancies. Functionally, inhibition of mitochondrial TRAP1 and related chaperones is cytotoxic to tumour cells, but not normal cells. Anti‐apoptotic functions of TRAP1 confer tumour cells resistance against different chemotherapeutic agents. For these reasons, TRAP1 has been proposed as a potential biomarker and target for anticancer therapies. In this context, mitochondrial‐targeted agents have been developed to selectively inhibit HSP90‐like mitochondrial chaperones inducing cell death and reverting tumour cell multi‐drug‐resistant phenotype.It has

Journal

European Journal of Clinical InvestigationWiley

Published: Jan 1, 2018

Keywords: ; ; ; ; ;

References

You’re reading a free preview. Subscribe to read the entire article.


DeepDyve is your
personal research library

It’s your single place to instantly
discover and read the research
that matters to you.

Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.

All for just $49/month

Explore the DeepDyve Library

Search

Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly

Organize

Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.

Access

Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.

Your journals are on DeepDyve

Read from thousands of the leading scholarly journals from SpringerNature, Elsevier, Wiley-Blackwell, Oxford University Press and more.

All the latest content is available, no embargo periods.

See the journals in your area

DeepDyve

Freelancer

DeepDyve

Pro

Price

FREE

$49/month
$360/year

Save searches from
Google Scholar,
PubMed

Create lists to
organize your research

Export lists, citations

Read DeepDyve articles

Abstract access only

Unlimited access to over
18 million full-text articles

Print

20 pages / month

PDF Discount

20% off