Inhibition of macroautophagy by bafilomycin A1 lowers proliferation and induces apoptosis in colon cancer cells

Wu, Yuzhong; Wu, William; Li, Youming; Yu, Li; Li, Zhi Jie; Wong, Clover Ching Man; Li, Hai Tao; Sung, Joseph J.Y.; Cho, Chi Hin

doi:10.1016/j.bbrc.2009.03.051

Cited by 100 publications

(72 citation statements)

References 30 publications

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“…There is also evidence for the stimulation of signaling pathways as MAPKs such as ERK, p38, and JNK were upregulated in response inhibition which might potentially provide a stimulus to apoptosis 78. This is in agreement with findings in breast cancer as ERK activation was shown to be increased as a pro‐survival mechanism in response to baf‐A1.…”

Section: V‐atpase As a Potential Cancer Therapeutic Targetsupporting

confidence: 87%

“…V‐ATPase inhibition has been shown to result in increased reactive oxygen species (ROS) in cancer cells75, 76, 77 and HIF1α upregulation 74. Furthermore, V‐ATPase inhibition induces caspase‐dependent apoptosis in invasive tumor cells via the mitochondrial pathways 74, 78. Archazolid was also shown to induce cell cycle arrest in MDA‐MB‐231 cells and double‐strand breaks in all cell lines investigated 79.…”

Section: V‐atpase As a Potential Cancer Therapeutic Targetmentioning

confidence: 98%

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Vacuolar ATPase as a potential therapeutic target and mediator of treatment resistance in cancer

et al. 2018

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Vacuolar ATPase (V‐ATPase) is an ATP‐dependent H+‐transporter that pumps protons across intracellular and plasma membranes. It consists of a large multi‐subunit protein complex and influences a wide range of cellular processes. This review focuses on emerging evidence for the roles for V‐ATPase in cancer. This includes how V‐ATPase dysregulation contributes to cancer growth, metastasis, invasion and proliferation, and the potential link between V‐ATPase and the development of drug resistance.

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Section: V‐atpase As a Potential Cancer Therapeutic Targetsupporting

confidence: 87%

Section: V‐atpase As a Potential Cancer Therapeutic Targetmentioning

confidence: 98%

Vacuolar ATPase as a potential therapeutic target and mediator of treatment resistance in cancer

et al. 2018

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“…There are reports showing that the long known V-ATPase inhibitors bafilomycin and concanamycin induce growth arrest and cell death in a variety of tumor cells (30), and more recently VATPase inhibitors like salicylihalamide (31) or NIK-12192 (32) have also been reported to possess antitumor activity. However, detailed information on the signaling pathways and molecular nodules used by these compounds is rather limited but crucial to understand the impact of pharmacological V-ATPase inhibition in cancer treatment.…”

Section: Discussionmentioning

confidence: 99%

Mode of Cell Death Induction by Pharmacological Vacuolar H+-ATPase (V-ATPase) Inhibition

Schwarzenberg

Wiedmann

Oak

et al. 2013

Journal of Biological Chemistry

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Background: V-ATPase is proposed as tumor target, but information on cell death-inducing mechanisms is rare. Results: Cell death induced by the V-ATPase inhibitor archazolid involves the cellular stress response. Conclusion: Archazolid is a chemical tool to decipher V-ATPase-related cell death signaling. Significance: Understanding the mechanism of V-ATPase inhibition-induced apoptosis is crucial to understand the impact of V-ATPase inhibition in cancer treatment.

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“…As early as 1998, bafilomycin A1 was reported to prevent maturation of autophagic vacuoles by inhibiting the fusion between autophagosomes and lysosomes in the rat hepatoma cell line H-4-II-E [90] . Inhibition of autophagy by bafilomycin A1 decreased proliferation and induced apoptosis in colon cancer cells [91] . However, Prof Daniel revealed an apparently contradictory result that bafilomycin A1 did not block the fusion of autophagosomes with lysosomes [92] .…”

Section: Vacuolar-type H (+)-Atpase Inhibitorsmentioning

confidence: 97%

Application and interpretation of current autophagy inhibitors and activators

et al. 2013

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Autophagy is the major intracellular degradation system, by which cytoplasmic materials are delivered to and degraded in the lysosome. As a quality control mechanism for cytoplasmic proteins and organelles, autophagy plays important roles in a variety of human diseases, including neurodegenerative diseases, cancer, cardiovascular disease, diabetes and infectious and inflammatory diseases. The discovery of ATG genes and the dissection of the signaling pathways involved in regulating autophagy have greatly enriched our knowledge on the occurrence and development of this lysosomal degradation pathway. In addition to its role in degradation, autophagy may also promote a type of programmed cell death that is different from apoptosis, termed type II programmed cell death. Owing to the dual roles of autophagy in cell death and the specificity of diseases, the exact mechanisms of autophagy in various diseases require more investigation. The application of autophagy inhibitors and activators will help us understand the regulation of autophagy in human diseases, and provide insight into the use of autophagy-targeted drugs. In this review, we summarize the latest research on autophagy inhibitors and activators and discuss the possibility of their application in human disease therapy.

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Inhibition of macroautophagy by bafilomycin A1 lowers proliferation and induces apoptosis in colon cancer cells

Cited by 100 publications

References 30 publications

Vacuolar ATPase as a potential therapeutic target and mediator of treatment resistance in cancer

Vacuolar ATPase as a potential therapeutic target and mediator of treatment resistance in cancer

Mode of Cell Death Induction by Pharmacological Vacuolar H+-ATPase (V-ATPase) Inhibition

Application and interpretation of current autophagy inhibitors and activators

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