ArticleMolecular cancer therapeutics2009
HYD1-induced increase in reactive oxygen species leads to autophagy and necrotic cell death in multiple myeloma cells.
Article in Molecular cancer therapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 46 citations in OpenAlex.
- Role of renin angiotensin system inhibitors and metformin in Glioblastoma Therapy: a review.Cancer chemotherapy and pharmacology · 2024Review
- Chelerythrine Chloride Inhibits Stemness of Melanoma Cancer Stem-Like Cells (CSCs) Potentially via Inducing Reactive Oxygen Species and Causing Mitochondria Dysfunction.Computational and mathematical methods in medicine · 2022Article
- Article
- Bioactivity improvement via display of the hydrophobic core of HYD1 in a cyclic β-hairpin-like scaffold, MTI-101.Peptide science (Hoboken, N.J.) · 2021Article
- Article
- Hypoxia-induced PIM kinase and laminin-activated integrin α6 mediate resistance to PI3K inhibitors in bone-metastatic CRPC.American journal of clinical and experimental urology · 2019Article
- Induction of reactive oxygen species-stimulated distinctive autophagy by chelerythrine in non-small cell lung cancer cells.Redox biology · 2017Article
- MTI-101 treatment inducing activation of Stim1 and TRPC1 expression is a determinant of response in multiple myeloma.Scientific reports · 2017Article
- Tumor-targeting peptides from combinatorial libraries.Advanced drug delivery reviews · 2017Review
- Targeting Intrinsic and Extrinsic Vulnerabilities for the Treatment of Multiple Myeloma.Journal of cellular biochemistry · 2017Review
- Dissecting the multiple myeloma-bone microenvironment reveals new therapeutic opportunities.Journal of molecular medicine (Berlin, Germany) · 2016Review
- Streptococcus pneumoniae induces autophagy through the inhibition of the PI3K-I/Akt/mTOR pathway and ROS hypergeneration in A549 cells.PloS one · 2015Article
- Combinatorial peptide libraries: mining for cell-binding peptides.Chemical reviews · 2014Review
- Proteomic analysis of gossypol induces necrosis in multiple myeloma cells.BioMed research international · 2014Article
- A preclinical assay for chemosensitivity in multiple myeloma.Cancer research · 2014Article
- REACTIVE OXYGEN SPECIES AND COLORECTAL CANCER.Current colorectal cancer reports · 2013Article
- MTI-101 (cyclized HYD1) binds a CD44 containing complex and induces necrotic cell death in multiple myeloma.Molecular cancer therapeutics · 2013Article
- Azacytidine induces necrosis of multiple myeloma cells through oxidative stress.Proteome science · 2013Article
- CRM1 Inhibition Sensitizes Drug Resistant Human Myeloma Cells to Topoisomerase II and Proteasome Inhibitors both In Vitro and Ex Vivo.Journal of Cancer · 2013Article
- DangER: protein ovERload. Targeting protein degradation to treat myeloma.Haematologica · 2012Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
HYD1 is a D-amino acid peptide that was previously shown to inhibit adhesion of prostate cancer cells to the extracellular matrix. In this study, we show that in addition to inhibiting adhesion of multiple myeloma (MM) cells to fibronectin, HYD1 induces cell death in MM cells as a single agent. HYD1-induced cell death was necrotic in nature as shown by: (a) decrease in mitochondrial membrane potential (Deltapsi(m)), (b) loss of total cellular ATP, and (c) increase in reactive oxygen species (ROS) production. Moreover, HYD1 treatment does not result in apoptotic cell death because it did not trigger the activation of caspases or the release of apoptosis-inducing factor and endonuclease G from the mitochondria, nor did it induce double-stranded DNA breaks. HYD1 did initiate autophagy in cells; however, autophagy was found to be an adaptive response contributing to cell survival rather than the cause of cell death. We were further able to show that N-acetyl-L-cysteine, a thiol-containing free radical scavenger, partially protects MM cells from HYD1-induced death. Additionally, N-acetyl-L-cysteine blocked HYD1-induced as well as basal levels of autophagy, suggesting that ROS can potentially trigger both cell death and cell survival pathways. Taken together, our data describe an important role of ROS in HYD1-induced necrotic cell death in MM cells.
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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.