ER-mitochondria interactions: Both strength and weakness within cancer cells
Open accessAbstract
ER-mitochondria contact sites represent hubs for signaling that control mitochondrial biology related to several aspects of cellular survival, metabolism, cell death sensitivity and metastasis, which all contribute to tumorigenesis. Altered ER-mitochondria contacts can deregulate Ca 2+ homeostasis, phospholipid metabolism, mitochondrial morphology and dynamics. MAM represent both a hot spot in cancer onset and progression and an Achilles' heel of cancer cells that can be exploited for therapeutic perspectives. Over the past years, an increasing number of cancer-related proteins, including oncogenes and tumor suppressors, have been localized in MAM and exert their pro- or antiapoptotic functions through the regulation of Ca 2+ transfer and signaling between the two organelles. In this review, we highlight the central role of ER-mitochondria contact sites in tumorigenesis and focus on chemotherapeutic drugs or potential targets that act on MAM properties for new therapeutic approaches in cancer.
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Mitochondria shared greater location similarity with the ER (SEC61β and SERCA) than any other structures.
“Mitochondria shared greater location similarity with the ER (SEC61β and SERCA) than any other structures, consistent with the functional interactions between these cellular structures22,23.”
From Integrated intracellular organization and its variations in human iPS cells (2023) · cites this paper as [23]
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Integrated intracellular organization and its variations in human iPS cells
Viana, M. P., Chen, J., Knijnenburg, T. A., Vasan, R., Yan, C., Arakaki, J. E., Bailey, M., Berry, B., Borensztejn, A., Brown, E. M., et al. (2023) · Nature · doi:10.1038/s41586-022-05563-7 · Cited by 132 · see citing works
“Mitochondria shared greater location similarity with the ER (SEC61β and SERCA) than any other structures, consistent with the functional interactions between these cellular structures 22,23 .”
- Authors
- Doghman-Bouguerra, M., & Lalli, E.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Lalli, Enzo
- ORCID
- Lalli, Enzo
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
- Publisher
- Elsevier BV
- Published
- 2019-04
- Volume
- 1866
- Issue
- 4
- Pages
- 650-662
- ISSN
- 0167-4889 (ISSN-L)
- OpenAlex
- W2909858565
- Cited by
- 94
- References
- 5
- Citations by year
- 2026: 7 · 2025: 11 · 2024: 11 · 2023: 14 · 2022: 11 · 2021: 14 · 2020: 19 · 2019: 7
- FWCI
- 1.14
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by-nc)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- ER-mitochondria contact sites, mitochondria-associated membranes, carcinogenesis, calcium homeostasis, calcium transfer, apoptosis, mitochondrial dynamics, phospholipid metabolism, oncogenes, tumor suppressor, cancer therapy targets, metastasis
- MeSH terms
- Autophagy, Endoplasmic Reticulum, Humans, Intracellular Membranes, Mitochondria, Neoplasms, Drug Resistance, Neoplasm, Calcium Signaling, Mitochondrial Membranes, Mitochondrial Dynamics, Carcinogenesis
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