ArticleLeukemia & lymphoma2013
Identification of endoplasmic reticulum stress-inducing agents by antagonizing autophagy: a new potential strategy for identification of anti-cancer therapeutics in B-cell malignancies.
Article in Leukemia & lymphoma, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Identification of 4 autophagy-related genetic variants as risk factors for chronic lymphocytic leukemia.Blood advances · 2025Pooled it
- Integrative Analysis of Multi-Omics Data to Identify Deregulated Molecular Pathways and Druggable Targets in Chronic Lymphocytic Leukemia.Journal of personalized medicine · 2024Article
- Antiretroviral Drugs Impact Autophagy: Opportunities for Drug Repurposing.Frontiers in bioscience (Landmark edition) · 2024Review
- Article
- Review
- ER Stress and Unfolded Protein Response in Leukemia: Friend, Foe, or Both?Biomolecules · 2021Review
- Review
- Regulation of autophagy by canonical and non-canonical ER stress responses.Seminars in cancer biology · 2020Review
- New drugs are not enough‑drug repositioning in oncology: An update.International journal of oncology · 2020Review
- Endoplasmic reticulum stress and cell death in mTORC1-overactive cells is induced by nelfinavir and enhanced by chloroquine.Molecular oncology · 2015Article
- Nelfinavir and other protease inhibitors in cancer: mechanisms involved in anticancer activity.F1000Research · 2015Review
- Nelfinavir impairs glycosylation of herpes simplex virus 1 envelope proteins and blocks virus maturation.Advances in virology · 2015Article
- Know the enemy as well as the weapons in hand: the aberrant death pathways and therapeutic agents in chronic lymphocytic leukemia.American journal of cancer research · 2015Review
- Inhibitory effect of chloroquine derivatives on presenilin 1 and ubiquilin 1 expression in Alzheimer's disease.International journal of clinical and experimental pathology · 2015Article
- Article
- ER stress, autophagy, and RNA viruses.Frontiers in microbiology · 2014Review
- Endoplasmic reticulum stress in hepatic steatosis and inflammatory bowel diseases.Frontiers in genetics · 2014Review
- Insights into the broad cellular effects of nelfinavir and the HIV protease inhibitors supporting their role in cancer treatment and prevention.Current opinion in oncology · 2013Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The endoplasmic reticulum (ER) plays a vital function in multiple cellular processes. There is a growing interest in developing therapeutic agents that can target the ER in cancer cells, inducing a stress response that leads to cell death. However, ER stress-inducing agents can also induce autophagy, a survival strategy of cancer cells. Therefore, by inhibiting autophagy we can increase the efficacy of the ER stress-inducing agents. Nelfinavir, a human immunodeficiency virus (HIV) protease inhibitor with anti-cancer properties, can induce ER stress. Nelfinavir's effects on chronic lymphocytic leukemia (CLL) are yet to be elucidated. Herein we demonstrate that nelfinavir induces ER morphological changes and stress response, along with an autophagic protective strategy. Our data reveal that chloroquine, an autophagy inhibitor, significantly increases nelfinavir cytotoxicity. These results identify a novel strategy potentially effective in CLL treatment, by repositioning two well-known drugs as a combinatorial therapy with anti-cancer properties.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.