ER-mitochondria interactions: Both strength and weakness within cancer cells
Mabrouka Doghman-Bouguerra1, Enzo Lalli1
1Université Côte d'Azur, Valbonne 06560, France; CNRS UMR 7275, Sophia Antipolis, Valbonne 06560, France; EXPOGEN-CANCER CNRS International Associated Laboratory, Valbonne 06560, France; Institut de Pharmacologie Moléculaire et Cellulaire, Valbonne 06560, France.
Biochimica Et Biophysica Acta. Molecular Cell Research
|January 23, 2019
Summary
Mitochondria and endoplasmic reticulum (ER) contact sites are crucial in cancer development and progression. Targeting these communication points offers new therapeutic strategies for cancer treatment.
Area of Science:
- Cell Biology
- Cancer Biology
- Mitochondrial Biology
Background:
- Endoplasmic reticulum (ER)-mitochondria contact sites are key signaling hubs regulating cellular survival, metabolism, and cell death.
- Dysfunctional ER-mitochondria contacts disrupt calcium (Ca2+) homeostasis, phospholipid metabolism, and mitochondrial dynamics, contributing to cancer onset and progression.
- These contact sites, known as Mitochondria-Associated Membranes (MAM), are implicated in tumorigenesis and represent a potential therapeutic vulnerability.
Purpose of the Study:
- To review the central role of ER-mitochondria contact sites in tumorigenesis.
- To explore how cancer-related proteins at MAM regulate cell signaling and apoptosis.
- To discuss current and potential therapeutic strategies targeting MAM properties in cancer.
Main Methods:
- Literature review focusing on ER-mitochondria communication in cancer.
- Analysis of proteins localized at MAM, including oncogenes and tumor suppressors.
- Examination of signaling pathways involving Ca2+ transfer between ER and mitochondria.
Main Results:
- ER-mitochondria contact sites are critical for cancer cell survival, metastasis, and drug resistance.
- Aberrant Ca2+ signaling and metabolic alterations at MAM promote cancer development.
- Numerous cancer-associated proteins modulate MAM functions, influencing apoptosis and cell fate.
Conclusions:
- ER-mitochondria contact sites are integral to cancer biology, influencing multiple hallmarks of cancer.
- Targeting MAM offers promising avenues for novel cancer chemotherapeutics.
- Understanding MAM-mediated signaling is essential for developing effective cancer treatment strategies.
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