Intricate role of mitochondrial lipid in mitophagy and mitochondrial apoptosis: its implication in cancer therapeutics.


Journal

Cellular and molecular life sciences : CMLS
ISSN: 1420-9071
Titre abrégé: Cell Mol Life Sci
Pays: Switzerland
ID NLM: 9705402

Informations de publication

Date de publication:
May 2019
Historique:
received: 19 09 2018
accepted: 06 12 2018
revised: 05 12 2018
pubmed: 13 12 2018
medline: 2 5 2019
entrez: 13 12 2018
Statut: ppublish

Résumé

The efficacy of chemotherapy is mostly restricted by the drug resistance developed during the course of cancer treatment. Mitophagy, as a pro-survival mechanism, crucially maintains mitochondrial homeostasis and it is one of the mechanisms that cancer cells adopt for their progression. On the other hand, mitochondrial apoptosis, a precisely regulated form of cell death, acts as a tumor-suppressive mechanism by targeting cancer cells. Mitochondrial lipids, such as cardiolipin, ceramide, and sphingosine-1-phosphate, act as a mitophageal signal for the clearance of damaged mitochondria by interacting with mitophagic machinery as well as activate mitochondrial apoptosis via the release of cytochrome c into the cytoplasm. In the recent time, the lipid-mediated lethal mitophagy has also been used as an alternative approach to abolish the survival role of lipid in cancer. Therefore, by targeting mitochondrial lipids in cancer cells, the detailed mechanism linked to drug resistance can be unraveled. In this review, we precisely discuss the current knowledge about the multifaceted role of mitochondrial lipid in regulating mitophagy and mitochondrial apoptosis and its application in effective cancer therapy.

Identifiants

pubmed: 30539200
doi: 10.1007/s00018-018-2990-x
pii: 10.1007/s00018-018-2990-x
doi:

Substances chimiques

Cardiolipins 0
Ceramides 0
Lysophospholipids 0
sphingosine 1-phosphate 26993-30-6
Cytochromes c 9007-43-6
Sphingosine NGZ37HRE42

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

1641-1652

Subventions

Organisme : DBT India Alliance
ID : BT/PR7791/BRB/10/1187/2013
Organisme : Board of Research in Nuclear Sciences
ID : 37(1)/14/38/2016-BRNS/37276
Organisme : Science and Engineering Research Board
ID : EMR/2016/001246

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Auteurs

Prakash P Praharaj (PP)

Department of Life Science, National Institute of Technology Rourkela, Rourkela, Odisha, 769008, India.

Prajna P Naik (PP)

Department of Life Science, National Institute of Technology Rourkela, Rourkela, Odisha, 769008, India.
PG Department of Zoology, Vikram Deb (Auto) College, Jeypore, Odisha, 764001, India.

Debasna P Panigrahi (DP)

Department of Life Science, National Institute of Technology Rourkela, Rourkela, Odisha, 769008, India.

Chandra S Bhol (CS)

Department of Life Science, National Institute of Technology Rourkela, Rourkela, Odisha, 769008, India.

Kewal K Mahapatra (KK)

Department of Life Science, National Institute of Technology Rourkela, Rourkela, Odisha, 769008, India.

Srimanta Patra (S)

Department of Life Science, National Institute of Technology Rourkela, Rourkela, Odisha, 769008, India.

Gautam Sethi (G)

Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, 117600, Singapore.

Sujit Kumar Bhutia (SK)

Department of Life Science, National Institute of Technology Rourkela, Rourkela, Odisha, 769008, India. sujitb@nitrkl.ac.in.

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