ArticleOncology letters2016
V8 induces apoptosis and the endoplasmic reticulum stress response in human multiple myeloma RPMI 8226 cells via the PERK-eIF2α-ATF4 signaling pathway.
Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Targeting VCP with V8 suppresses glioblastoma development via formation of aggregates and disruption of mitophagy flux.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Inhibition of acyl-CoA synthetase long-chain isozymes decreases multiple myeloma cell proliferation and causes mitochondrial dysfunction.Molecular oncology · 2025Article
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- Role of the unfolded protein response in determining the fate of tumor cells and the promise of multi-targeted therapies.Cell stress & chaperones · 2018Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple myeloma (MM) is a fatal hematological cancer characterized by clonal plasma cell proliferation in the bone marrow. MM has an increasing global incidence and a poor prognosis. There are limited treatment options available for MM, and this is further compounded by the development of drug resistance. The present study demonstrated that 7-{4-[Bis-(2-hydroxyethyl)-amino]-butoxy}-5-hydroxy-8-methoxy-2-phenylchromen-4-one (V8), a novel synthetic flavonoid, induced apoptosis in human MM RPMI 8226 cells in a dose- and time-dependent manner, using cell viability assays and flow cytometry. Subsequently, V8-induced apoptosis in RPMI 8226 cells was revealed to occur via mitochondria-mediated pathways. The activity of caspase-3, -8 and -9, and the mRNA level of B-cell lymphoma 2 (Bcl-2) and B-cell lymphoma-extra large were greatly increased, while the expression of Bcl-2-like protein 4 and BH3 interacting domain death agonist was significantly decreased in RPMI 8226 cells following V8 treatment, as observed using quantitative polymerase chain reaction (qPCR). In addition, western blotting revealed that the release of mitochondrial cytochrome
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Registered trials
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