RETRACTED ARTICLE: Autophagy-independent induction of LC3B through oxidative stress reveals its non-canonical role in anoikis of ovarian cancer cells
Open accessAbstract
Cancer cells display abnormal redox metabolism. Autophagy, anoikis and reactive oxygen species (ROS) play a regulatory role during metastasis. LC3 is a well-known essential molecule for autophagy. Therefore, we wanted to explore the molecular interplay between autophagy, anoikis, and ROS in relation to LC3B. We observed enhanced LC3B level along with increased expression of p62 and modulation of other autophagy-related molecules (Atg 3, 5, 7, 12, 16L1 and Beclin1) by inducing oxidative-stress in ovarian cancer cells using a ROS-producing pro-oxidant molecule. Surprisingly, enhanced LC3B was unable to induce autophagosome formation rather promoted anoikis. ROS-induced inhibition of autophagosome-formation is possibly due to the instability of autophagy initiator, ULK1 complex. Moreover, such upregulation of LC3B via ROS enhanced several apoptotic molecules. Silencing LC3B reduced these apoptotic molecules and increased when overexpressed, suggesting its role in apoptosis. Furthermore, LC3B-dependent apoptosis was decreased by inhibiting ROS, indicating a possible link between ROS, LC3B, and apoptosis. Additionally, ROS-induced enhanced LC3B promoted detachment-induced cell death (anoikis). This was further reflected by reduced cell adhesion molecules (integrin-β3 and focal adhesion kinase) and mesenchymal markers (snail and slug). Our in vitro experimental data was further confirmed in primary tumors developed in syngeneic mice, which also showed ROS-mediated LC3B enhancement along with reduced autophagosomes, integrin-β3 and focal adhesion kinase ultimately leading to the decreased tumor mass. Additionally, primary cells from high-grade serous carcinoma patient’s ascites exhibited LC3B enhancement and autophagy inhibition through ROS which provided a clinical relevance of our study. Taken together, this is the first evidence for a non-canonical role of LC3B in promoting anoikis in contrast to autophagy and may, therefore, consider as a potential therapeutic target molecule in ovarian cancer. Taken together, autophagy-inhibition may be an alternative approach to induce apoptosis/anoikis in cancer.
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Multiple research results have shown that autophagy protects cells exposed to various forms of stress, including nutrient deprivation, growth factor regression, endoplasmic reticulum stress, and ischemia.
“In addition, multiple research results have shown that autophagy protects cells exposed to various forms of stress, including nutrient deprivation, growth factor regression, endoplasmic reticulum stress, and ischemia.[23–25]”
From Autophagy, not apoptosis, plays a role in lumen formation of eccrine gland organoids (2022) · cites this paper as [23]
The Introduction (page unavailable) describes autophagy as supplying energy needed for cell survival during stress. The Results section on autophagosomes (page unavailable) reports increased autophagy in serum-starved cells. Our copy does not establish a protective effect specifically under nutrient deprivation, growth-factor withdrawal, endoplasmic-reticulum stress, or ischemia. (LLM, conf=0.85)
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- Authors
- Satyavarapu, E. M., Das, R., Mandal, C., Mukhopadhyay, A., & Mandal, C.
- Affiliations
- Indian Institute of Chemical Biology (IN)
- Bose Institute (IN)
- Tata Medical Center (IN)
- Corresponding author
- Mandal, Chandan
- Mandal, Chitra
- Venue
- Cell Death & Disease
- Published
- 2018-09-17
- Volume
- 9
- Issue
- 10
- Pages
- 934-934
- ISSN
- 2041-4889 (ISSN-L)
- PMC
- PMC6141567
- OpenAlex
- W2890738628
- Cited by
- 69
- References
- 52
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 8 · 2023: 6 · 2022: 17 · 2021: 13 · 2020: 15 · 2019: 4 · 2018: 1
- FWCI
- 6.44
- Type
- journal article
- Language
- en
- Status
- Retracted
- Open access
- gold
- doi.org
- Locations
- Cell Death and Disease (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Funders
- Council of Scientific and Industrial Research (HCP0010, ESC0103)
- Department of Science and Technology, Ministry of Science and Technology (GAP 336, 339,J.C. Bose National Fellowship)
- Department of Biotechnology, Ministry of Science and Technology (GAP 346,Distinguished Biotechnology Research Professor)
- 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 › Redox biology and oxidative stress
- Keywords
- LC3B, autophagy, anoikis, reactive oxygen species, oxidative stress, ovarian cancer, apoptosis, autophagosome formation, ULK1 complex, CD61, focal adhesion kinase, epithelial-mesenchymal transition, high-grade serous carcinoma, autophagy inhibition, metastasis
- MeSH terms
- Animals, Autophagy, Cell Survival, Female, Humans, Microtubule-Associated Proteins, Ovarian Neoplasms, Reactive Oxygen Species, Oxidative Stress, Anoikis, Cell Line, Tumor, Cell Proliferation, Mice
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