Lysosomes as Oxidative Targets for Cancer Therapy
Open accessAbstract
Lysosomes are membrane‐bound vesicles that contain hydrolases for the degradation and recycling of essential nutrients to maintain homeostasis within cells. Cancer cells have increased lysosomal function to proliferate, metabolize, and adapt to stressful environments. This has made cancer cells susceptible to lysosomal membrane permeabilization (LMP). There are many factors that mediate LMP such as Bcl‐2 family member, p53; sphingosine; and oxidative stress which are often altered in cancer. Upon lysosomal disruption, reactive oxygen species (ROS) levels increase leading to lipid peroxidation, mitochondrial dysfunction, autophagy, and reactive iron. Cathepsins are also released causing degradation of macromolecules and cellular structures. This ultimately kills the cancer cell through different types of cell death (apoptosis, autosis, or ferroptosis). In this review, we will explore the contributions lysosomes play in inducing cell death, how this is regulated by ROS in cancer, and how lysosomotropic agents might be utilized to treat cancers.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The critical dependency of ferroptosis on iron can be ascribed to the ability of iron to promote non-enzymatic lipid oxidation via lysosomal Fenton reactions.
“Alternatively, the critical dependency of ferroptosis on iron can also be ascribed to the ability of this heavy metal to promote non-enzymatic lipid oxidation via lysosomal Fenton reactions [538, 572, 576, 577].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [577]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 62 · Cited by 123
Research works printed but not linked: 1
- P. Boya and G. Kroemer, "Lysosomal membrane perme- abilization in cell death," Oncogene, vol. 27, no. 50, pp. 6434- 6451, 2008.
- Authors
- Dielschneider, R. F., Henson, E. S., & Gibson, S. B.
- Affiliations
- Providence University College and Theological Seminary (CA)
- CancerCare Manitoba (CA)
- University of Manitoba (CA)
- Corresponding author
- Gibson, Spencer B.
- ORCID
- Gibson, Spencer B.
- Venue
- Oxidative Medicine and Cellular Longevity
- Publisher
- Wiley
- Published
- 2017-01
- Volume
- 2017
- Issue
- 1
- Pages
- 3749157-3749157
- ISSN
- 1942-0994 (ISSN-L)
- 1942-0900
- PMC
- PMC5516749
- OpenAlex
- W2731353557
- Cited by
- 123
- References
- 62
- Citations by year
- 2026: 8 · 2025: 5 · 2024: 13 · 2023: 11 · 2022: 15 · 2021: 20 · 2020: 17 · 2019: 23 · 2018: 8 · 2017: 3
- FWCI
- 1.85
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Oxidative Medicine and Cellular Longevity (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- lysosomes, lysosomal membrane permeabilization, reactive oxygen species, oxidative stress, cancer therapy, lysosomotropic agents, cathepsins, ferroptosis, autophagy, apoptosis, lipid peroxidation, mitochondrial dysfunction, Bcl-2 family proteins, p53, sphingosine, cancer metabolism
- MeSH terms
- Animals, Humans, Lysosomes, Neoplasm Proteins, Neoplasms, Cell Death, Reactive Oxygen Species
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
