Cited by 542Autophagy in Disease and TherapyUbiquitin and proteasome pathwaysCalcium signaling and nucleotide metabolism

Dual role of autophagy in hallmarks of cancer

Singh, Shikha Satendra, Vats, Somya, Chia, Amelia Yi-Qian, Tan, Tuan Zea, Deng, Shuo, Ong, Mei Shan, Arfuso, Frank, Yap, Celestial T. +6 more·2018·Oncogene

Abstract

Evolutionarily conserved across eukaryotic cells, macroautophagy (herein autophagy) is an intracellular catabolic degradative process targeting damaged and superfluous cellular proteins, organelles, and other cytoplasmic components. Mechanistically, it involves formation of double-membrane vesicles called autophagosomes that capture cytosolic cargo and deliver it to lysosomes, wherein the breakdown products are eventually recycled back to the cytoplasm. Dysregulation of autophagy often results in various disease manifestations, including neurodegeneration, microbial infections, and cancer. In the case of cancer, extensive attention has been devoted to understanding the paradoxical roles of autophagy in tumor suppression and tumor promotion. In this review, while we summarize how this self-eating process is implicated at various stages of tumorigenesis, most importantly, we address the link between autophagy and hallmarks of cancer. This would eventually provide a better understanding of tumor dependence on autophagy. We also discuss how therapeutics targeting autophagy can counter various transformations involved in tumorigenesis. Finally, this review will provide a novel insight into the mutational landscapes of autophagy-related genes in several human cancers, using genetic information collected from an array of cancers.

Integrity signals

Registry

Crossref · 10.1038/s41388-017-0046-6

Cites

138 of 138 references verified0 citation errors · 0 not checkable

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  • Normally, autophagy plays a tumor suppressive role by preventing the accumulation of misfolded proteins, damaged organelles, and reactive oxygen species (ROS).

    “Normally, autophagy plays a tumor suppressive role by preventing the accumulation of misfolded proteins, damaged organelles, and reactive oxygen species (ROS) [54].”

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Authors
Singh, S. S., Vats, S., Chia, A. Y.-Q., Tan, T. Z., Deng, S., Ong, M. S., Arfuso, F., Yap, C. T., Goh, B. C., Sethi, G., Huang, R. Y.-J., Shen, H. M., Manjithaya, R., & Kumar, A. P.
Affiliations
  • National University of Singapore (SG)
  • Jawaharlal Nehru Centre for Advanced Scientific Research (IN)
  • Curtin University (AU)
Corresponding author
  • Manjithaya, Ravi
  • Kumar, Alan Prem
Venue
Oncogene
Published
2017-12-19
Volume
37
Issue
9
Pages
1142-1158
ISSN
  • 0950-9232 (ISSN-L)
  • 1476-5594
OpenAlex
W2772927056
Cited by
542
References
138
Citations by year
2026: 20 · 2025: 44 · 2024: 58 · 2023: 62 · 2022: 75 · 2021: 90 · 2020: 100 · 2019: 53 · 2018: 40
FWCI
6.99
Type
journal article
Language
en
Open access
closed
Locations
  • Oncogene (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Wellcome Trust
  • National Research Foundation Singapore
  • National Medical Research Council
  • Cancer Science Institute of Singapore, National University of Singapore
  • National Cancer Institute
Topics
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
Keywords
autophagy, cancer hallmarks, carcinogenesis, tumor suppression, tumor promotion, autophagy-related genes, autophagosomes, lysosomal degradation, cancer genomics
MeSH terms
Animals, Autophagy, Cell Transformation, Neoplastic, Humans, Neoplasms

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