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Chloroquine in cancer therapy: a double-edged sword of autophagy.

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TLDR
The functions of autophagy in cancer and kidney injury are summarized, especially focusing on the use of chloroquine to treat cancer, and the possible side effects are addressed in the combined use ofchloroquine and anticancer drugs.
Abstract
Autophagy is a homeostatic cellular recycling system that is responsible for degrading damaged or unnecessary cellular organelles and proteins. Cancer cells are thought to use autophagy as a source of energy in the unfavorable metastatic environment, and a number of clinical trials are now revealing the promising role of chloroquine, an autophagy inhibitor, as a novel antitumor drug. On the other hand, however, the kidneys are highly vulnerable to chemotherapeutic agents. Recent studies have shown that autophagy plays a protective role against acute kidney injury, including cisplatin-induced kidney injury, and thus, we suspect that the use of chloroquine in combination with anticancer drugs may exacerbate kidney damage. Moreover, organs in which autophagy also plays a homeostatic role, such as the neurons, liver, hematopoietic stem cells, and heart, may be sensitive to the combined use of chloroquine and anticancer drugs. Here, we summarize the functions of autophagy in cancer and kidney injury, especially focusing on the use of chloroquine to treat cancer, and address the possible side effects in the combined use of chloroquine and anticancer drugs.

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The novel mTOR inhibitor Torin-2 induces autophagy and downregulates the expression of UHRF1 to suppress hepatocarcinoma cell growth

TL;DR: It is found that Torin-2 effectively suppressed the growth and survival of HCC cell lines, demonstrated by reduced proliferation and a high rate of apoptosis, and sheds light on a novel therapeutic approach for HCC.
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Autophagy inhibitors chloroquine and LY294002 enhance temozolomide cytotoxicity on cutaneous melanoma cell lines in vitro.

TL;DR: It is shown that autophagy inhibition could enhance melanoma cell death combined with TMZ therapy, making this combination applicable as a potent antitumor treatment for metastatic melanoma.
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Sesamin induces ER stress-mediated apoptosis and activates autophagy in cervical cancer cells.

TL;DR: Sesamin inhibits proliferation/migration of HeLa cells and induces ER stress‐mediated apoptosis through IRE1&agr;/JNK pathway, and that it activates autophagy and autophagic death in these cells, further validate the anticancer effect of sesamin.
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Essential role for acid sphingomyelinase-inhibited autophagy in melanoma response to cisplatin

TL;DR: The fact that A-SMase in melanomas affects mTOR-regulated autophagy and plays a central role in cisplatin efficacy encourages pre-clinical testing on the modulation of A- SMase levels/activity as possible novel anti-neoplastic strategy.
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Glimpse into the future: harnessing autophagy to promote anti-tumor immunity with the DRibbles vaccine

TL;DR: The rationale and preclinical development ofDRibbles, translational evidence in support of DRibbles as a therapeutic strategy in humans, as well as recent developments and expected future directions of the DRibble vaccine in the clinic are summarized.
References
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Journal ArticleDOI

Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation

TL;DR: It is proposed that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass needed to produce a new cell.
Journal ArticleDOI

Acute Kidney Injury Network: Report of an Initiative to Improve Outcomes in Acute Kidney Injury

TL;DR: The Acute Kidney Injury Network (AKI Network) as discussed by the authors is a multidisciplinary collaborative network focused on AKI, which was established to improve care for patients with or at risk for AKI.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Autophagy: Renovation of Cells and Tissues

TL;DR: It is explored how recent mouse models in combination with advances in human genetics are providing key insights into how the impairment or activation of autophagy contributes to pathogenesis of diverse diseases, from neurodegenerative diseases such as Parkinson disease to inflammatory disorders such as Crohn disease.
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