Vinblastine-induced autophagocytosis: The effect of disorganization of microfilaments by cytochalasin B

Hirsimäki, Y.; Hirsimäki, Pirkko

doi:10.1016/0014-4800(84)90066-2

Cited by 10 publications

(2 citation statements)

References 18 publications

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“…From the initial observations of basal autophagy in cancer cells, the important discovery that standard chemotherapeutic agents induced autophagy was made. In the 1980s, the popular cytotoxic therapies vincristine and vinblastine were shown to cause autophagosome accumulation [ 35 , 36 ]. Around the same time, radiation was found to do the same across multiple malignancies [ 37 ].…”

Section: Hydroxychloroquine In Cancer Clinical Trialsmentioning

confidence: 99%

Leaving the Lysosome Behind: Novel Developments in Autophagy Inhibition

Solitro

MacKeigan

2015

Future Med. Chem.

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The search for a single silver bullet for the treatment of cancer has now been overshadowed by the identification of multiple therapeutic targets unique to each malignancy and even to each patient. In recent years, autophagy has emerged as one such therapeutic target. In response to both therapeutic and oncogenic stress, cancer cells upregulate and demonstrate an increased dependence upon this intracellular recycling process. Particularly in malignancies that currently lack targeted therapeutic options, autophagy inhibitors are the next hopeful prospects for the treatment of this disease. In this review, we discuss the rapid evolution of autophagy inhibitors from early lysosomotropic agents to next-generation lysosome-targeted drugs and beyond.

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Section: Hydroxychloroquine In Cancer Clinical Trialsmentioning

confidence: 99%

Leaving the Lysosome Behind: Novel Developments in Autophagy Inhibition

Solitro

MacKeigan

2015

Future Med. Chem.

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“…In one study, phalloidin, which stabilizes actin filaments, inhibited the formation of autophagic vacuoles (Ueno et al, 1990). In a second report, vacuole formation was apparently unaffected when F-actin was destabilized by cytochalasin B treatment (Hirsimaki and Hirsimaki, 1984). Drugs that cause a depolymerization of microtubules (e.g., vinblastine and colchicine) have been shown to inhibit protein degradation in cultured cells and perfused liver concommitant with an accumulation of autophagic vacuoles Grinde and Seglen, 1981;Kovacs et al, 1985).…”

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confidence: 99%

Cytoskeletal elements are required for the formation and maturation of autophagic vacuoles

Aplin

Jasionowski

Tuttle

et al. 1992

Journal Cellular Physiology

173

128

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We evaluated the role of cytoskeletal elements in the degradation of endogenous proteins via autophagy using biochemical and morphological techniques. In the absence of exogenous amino acids, degradation of endogenous proteins was enhanced in cultured normal rat kidney cells. This enhanced degradative state was accompanied by a 4-fold increase in the occurrence of autophagic vacuoles. In the presence of drugs that induce the depolymerization of microfilaments (cytochalasins B and D) or microtubules (nocodazole), protein degradation was not enhanced in nutrient-deprived cells. Although these drugs had similar inhibitory effects on the protein degradation, their effect on autophagy differed. Cytochalasins B and D interfered with the formation of the autophagosome. In cells treated with these drugs, the fractional volume represented by autophagic vacuoles was not substantially increased despite nutrient depletion. On the contrary, nocodazole appeared to have no effect on the formation of autophagosomes. Instead, this drug suppressed the delivery of hydrolytic enzymes, thereby resulting in an accumulation of acidic autophagic vacuoles containing undegraded cellular components.

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Regulation of Protein Metabolism in Liver

Mortimore

Kadowaki

2001

Comprehensive Physiology

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The sections in this article are: Turnover of Cellular Protein and RNA Determination of General Protein Turnover Classes of General Protein Turnover Cytoplasmic RNA Turnover Autophagy Macroautophagy Microautophagy A Unified Mechanism of Macro‐ and Microautophagic Proteolysis Regulation of Autophagy Control of Macroautophagy by Amino Acids Hormonal Control of Cellular Protein Turnover Control of Macro‐ and Microautophagy during Starvation and Refeeding Overview

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Vinblastine-induced autophagocytosis: The effect of disorganization of microfilaments by cytochalasin B

Cited by 10 publications

References 18 publications

Leaving the Lysosome Behind: Novel Developments in Autophagy Inhibition

Leaving the Lysosome Behind: Novel Developments in Autophagy Inhibition

Cytoskeletal elements are required for the formation and maturation of autophagic vacuoles

Regulation of Protein Metabolism in Liver

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