Targeting autophagy as a therapeutic strategy against pancreatic cancer
Open accessAbstract
Macroautophagy (hereafter autophagy) is a catabolic process through which cytosolic components are captured in the autophagosome and degraded in the lysosome. Autophagy plays two major roles: nutrient recycling under starvation or stress conditions and maintenance of cellular homeostasis by removing the damaged organelles or protein aggregates. In established cancer cells, autophagy-mediated nutrient recycling promotes tumor progression, whereas in normal/premalignant cells, autophagy suppresses tumor initiation by eliminating the oncogenic/harmful molecules. Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease that is refractory to most currently available treatment modalities, including immune checkpoint blockade and molecular-targeted therapy. One prominent feature of PDAC is its constitutively active and elevated autophagy-lysosome function, which enables PDAC to thrive in its nutrient-scarce tumor microenvironment. In addition to metabolic support, autophagy promotes PDAC progression in a metabolism-independent manner by conferring resistance to therapeutic treatment or facilitating immune evasion. Besides to cell-autonomous autophagy in cancer cells, host autophagy (autophagy in non-cancer cells) supports PDAC progression, further highlighting autophagy as a promising therapeutic target in PDAC. Based on a growing list of compelling preclinical evidence, there are numerous ongoing clinical trials targeting the autophagy-lysosome pathway in PDAC. Given the multifaceted and context-dependent roles of autophagy in both cancer cells and normal host cells, a deeper understanding of the mechanisms underlying the tumor-promoting roles of autophagy as well as of the consequences of autophagy inhibition is necessary for the development of autophagy inhibition-based therapies against PDAC.
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Autophagy is elevated in the late stages of PDAC, where it fuels tumour metabolism to promote tumour growth and drug resistance.
“autophagy is elevated in the late stages of PDAC, where it fuels tumour metabolism to promote tumour growth and drug resistance [47]”
From Pyrvinium Pamoate Alone and With Gemcitabine Exhibits Anti‐Pancreatic Cancer Activity in <scp>2D</scp> and <scp>3D</scp> Cell Culture Models (2024) · cites this paper as [47]
The Background describes elevated autophagy in PDAC as supporting growth through nutrient recycling and promoting treatment resistance. It distinguishes established cancer from premalignant cells, but does not establish that autophagy becomes elevated specifically in the late stages of PDAC. (LLM, conf=0.84)
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Targeting PIKfyve-driven lipid metabolism in pancreatic cancer
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- Authors
- Yamamoto, K., Iwadate, D., Kato, H., Nakai, Y., Tateishi, K., & Fujishiro, M.
- Affiliations
- The University of Tokyo (JP)
- Corresponding author
- Yamamoto, Keisuke
- ORCID
- Venue
- Journal of Gastroenterology
- Published
- 2022-06-21
- Volume
- 57
- Issue
- 9
- Pages
- 603-618
- ISSN
- 0944-1174 (ISSN-L)
- 1435-5922
- PMC
- PMC9392712
- OpenAlex
- W4283211173
- Cited by
- 29
- References
- 151
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 8 · 2023: 7 · 2022: 2
- FWCI
- 4.15
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Journal of Gastroenterology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Yasuda Memorial Medical Foundation
- The Tokyo Society of Medical Sciences
- MSD Life Science Foundation
- Astellas Foundation for Research on Metabolic Disorders
- Uehara Memorial Foundation
- Princess Takamatsu Cancer Research Fund
- Life Science Foundation of Japan
- Japan Society for the Promotion of Science (21K20828, 22H02898, 22H03053)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- autophagy, pancreatic ductal adenocarcinoma, autophagy inhibition, autophagy-lysosome pathway, host autophagy, tumor microenvironment, immune evasion, drug resistance, metabolic reprogramming, autophagy-targeted therapy
- MeSH terms
- Autophagy, Humans, Pancreatic Neoplasms, Carcinoma, Pancreatic Ductal, Cell Line, Tumor, Tumor Microenvironment
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