Cited by 305Autophagy in Disease and TherapyCell death mechanisms and regulationUbiquitin and proteasome pathways

Autophagy and Cancer Therapy

Open access
Kondo, Yasuko, Kondo, Seiji·2006·Autophagy

Abstract

Autophagy is a dynamic process of protein degradation, which is typically observed during nutrient deprivation. Recently, interest in autophagy has been renewed among oncologists, because different types of cancer cells undergo autophagy after various anticancer therapies. This type of nonapoptotic cell death has been documented mainly by observing morphological changes, e.g., numerous autophagic vacuoles in the cytoplasm of dying cells. Thus, autophagic cell death is considered programmed cell death type II, whereas apoptosis is programmed cell death type I. These two types of cell death are predominantly distinctive, but many studies demonstrate cross-talk between them. Whether autophagy in cancer cells causes death or protects cells is controversial. In multiple studies, autophagy has been inhibited pharmacologically or genetically, resulting in contrasting outcomes--survival or death--depending on the specific context. Interestingly, the regulatory pathways of autophagy share several molecules with the oncogenic pathways activated by tyrosine kinase receptors. Tumor suppressors such as Beclin 1, PTEN and p53 also play an important role in autophagy induction. Taken together, these accumulating data may lead to development of new cancer therapies that manipulate autophagy.

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  • Oncogenes can inhibit autophagy and tumour suppressors can stimulate it.

    “Indeed, although the available evidence indicates that oncogenes can inhibit autophagy and tumour suppressors can stimulate it, the exact mechanistic link between cancer and autophagy remains obscure (Fig. 3).”

    From The common biology of cancer and ageing (2007) · cites this paper as [78]

  • In human malignancies, the BECN1 locus is commonly deleted, and tumour suppressors including Pten and p53 stimulate autophagy.

    “This notion is also supported by observations that in human malignancies the BECN1 locus is commonly deleted and by experimental evidence that several tumour suppressors, including the phosphatase and tensin homologue Pten and p53, stimulate autophagy 78 .”

    From The common biology of cancer and ageing (2007) · cites this paper as [78]

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Cited by

Sorted by citations

Authors
Kondo, Y., & Kondo, S.
Affiliations
The University of Texas MD Anderson Cancer Center (US)
Venue
Autophagy
Published
2006-01-26
Volume
2
Issue
2
Pages
85-90
ISSN
  • 1554-8627 (ISSN-L)
  • 1554-8635
OpenAlex
W2041033535
Cited by
305
References
0
Citations by year
2026: 1 · 2025: 5 · 2024: 7 · 2023: 8 · 2022: 17 · 2021: 13 · 2020: 22 · 2019: 10 · 2018: 13 · 2017: 19 · 2016: 22 · 2015: 14 · 2014: 21 · 2013: 22 · 2012: 33
FWCI
1.76
Type
journal article
Language
en
Open access
Locations
  • Autophagy (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (1r01ca108558-01)
  • U.S. Public Health Service
  • National Cancer Institute (CA 108558, R01CA088936, CA-088936)
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 › Molecular Biology › Ubiquitin and proteasome pathways
Keywords
autophagic cell death, cancer therapy, apoptosis, non-apoptotic cell death, autophagy inhibition, Beclin-1, PTEN, p53, receptor tyrosine kinase, oncogenic signaling, tumor suppressor, nutrient deprivation, autophagy regulation
MeSH terms
Antineoplastic Agents, Autophagy, Neoplasms, Signal Transduction, Genes, Tumor Suppressor, Cell Death

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