The Cancer Stem Cell Marker Aldehyde Dehydrogenase Is Required to Maintain a Drug-Tolerant Tumor Cell Subpopulation
Selective kinase inhibitors have emerged as an important class of cancer therapeutics, and several such drugs are now routinely used to treat advanced-stage disease. However, their clinical benefit is typically short-lived because of the relatively rapid acquisition of drug resistance following trea...
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Published in | Cancer research (Chicago, Ill.) Vol. 74; no. 13; pp. 3579 - 3590 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Philadelphia, PA
American Association for Cancer Research
01.07.2014
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Subjects | |
Online Access | Get full text |
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Abstract | Selective kinase inhibitors have emerged as an important class of cancer therapeutics, and several such drugs are now routinely used to treat advanced-stage disease. However, their clinical benefit is typically short-lived because of the relatively rapid acquisition of drug resistance following treatment response. Accumulating preclinical and clinical data point to a role for a heterogeneous response to treatment within a subpopulation of tumor cells that are intrinsically drug-resistant, such as cancer stem cells. We have previously described an epigenetically determined reversibly drug-tolerant subpopulation of cancer cells that share some properties with cancer stem cells. Here, we define a requirement for the previously established cancer stem cell marker ALDH (aldehyde dehydrogenase) in the maintenance of this drug-tolerant subpopulation. We find that ALDH protects the drug-tolerant subpopulation from the potentially toxic effects of elevated levels of reactive oxygen species (ROS) in these cells, and pharmacologic disruption of ALDH activity leads to accumulation of ROS to toxic levels, consequent DNA damage, and apoptosis specifically within the drug-tolerant subpopulation. Combining ALDH inhibition with other kinase-directed treatments delayed treatment relapse in vitro and in vivo, revealing a novel combination treatment strategy for cancers that might otherwise rapidly relapse following single-agent therapy. |
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AbstractList | Selective kinase inhibitors have emerged as an important class of cancer therapeutics, and several such drugs are now routinely used to treat advanced-stage disease. However, their clinical benefit is typically short-lived because of the relatively rapid acquisition of drug resistance following treatment response. Accumulating preclinical and clinical data point to a role for a heterogeneous response to treatment within a subpopulation of tumor cells that are intrinsically drug-resistant, such as cancer stem cells. We have previously described an epigenetically determined reversibly drug-tolerant subpopulation of cancer cells that share some properties with cancer stem cells. Here, we define a requirement for the previously established cancer stem cell marker ALDH (aldehyde dehydrogenase) in the maintenance of this drug-tolerant subpopulation. We find that ALDH protects the drug-tolerant subpopulation from the potentially toxic effects of elevated levels of reactive oxygen species (ROS) in these cells, and pharmacologic disruption of ALDH activity leads to accumulation of ROS to toxic levels, consequent DNA damage, and apoptosis specifically within the drug-tolerant subpopulation. Combining ALDH inhibition with other kinase-directed treatments delayed treatment relapse in vitro and in vivo, revealing a novel combination treatment strategy for cancers that might otherwise rapidly relapse following single-agent therapy. Abstract Selective kinase inhibitors have emerged as an important class of cancer therapeutics, and several such drugs are now routinely used to treat advanced-stage disease. However, their clinical benefit is typically short-lived because of the relatively rapid acquisition of drug resistance following treatment response. Accumulating preclinical and clinical data point to a role for a heterogeneous response to treatment within a subpopulation of tumor cells that are intrinsically drug-resistant, such as cancer stem cells. We have previously described an epigenetically determined reversibly drug-tolerant subpopulation of cancer cells that share some properties with cancer stem cells. Here, we define a requirement for the previously established cancer stem cell marker ALDH (aldehyde dehydrogenase) in the maintenance of this drug-tolerant subpopulation. We find that ALDH protects the drug-tolerant subpopulation from the potentially toxic effects of elevated levels of reactive oxygen species (ROS) in these cells, and pharmacologic disruption of ALDH activity leads to accumulation of ROS to toxic levels, consequent DNA damage, and apoptosis specifically within the drug-tolerant subpopulation. Combining ALDH inhibition with other kinase-directed treatments delayed treatment relapse in vitro and in vivo, revealing a novel combination treatment strategy for cancers that might otherwise rapidly relapse following single-agent therapy. Cancer Res; 74(13); 3579–90. ©2014 AACR. |
Author | WILSON, Catherine JING PENG RAHA, Debasish PETERSON, David SETTLEMAN, Jeff PENG YUE EVANGELISTA, Marie MERCHANT, Mark WILSON, Timothy R |
Author_xml | – sequence: 1 givenname: Debasish surname: RAHA fullname: RAHA, Debasish organization: Department of Discovery Oncology, Genentech, Inc., South San Francisco, California, United States – sequence: 2 givenname: Timothy R surname: WILSON fullname: WILSON, Timothy R organization: Department of Discovery Oncology, Genentech, Inc., South San Francisco, California, United States – sequence: 3 surname: JING PENG fullname: JING PENG organization: Department of Translational Oncology, Genentech, Inc., South San Francisco, California, United States – sequence: 4 givenname: David surname: PETERSON fullname: PETERSON, David organization: Department of Translational Oncology, Genentech, Inc., South San Francisco, California, United States – sequence: 5 surname: PENG YUE fullname: PENG YUE organization: Department of Bioinformatics, Genentech, Inc., South San Francisco, California, United States – sequence: 6 givenname: Marie surname: EVANGELISTA fullname: EVANGELISTA, Marie organization: Department of Discovery Oncology, Genentech, Inc., South San Francisco, California, United States – sequence: 7 givenname: Catherine surname: WILSON fullname: WILSON, Catherine organization: Department of Discovery Oncology, Genentech, Inc., South San Francisco, California, United States – sequence: 8 givenname: Mark surname: MERCHANT fullname: MERCHANT, Mark organization: Department of Translational Oncology, Genentech, Inc., South San Francisco, California, United States – sequence: 9 givenname: Jeff surname: SETTLEMAN fullname: SETTLEMAN, Jeff organization: Department of Discovery Oncology, Genentech, Inc., South San Francisco, California, United States |
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Keywords | Drug Enzyme Aldehyde dehydrogenase (NAD Stem cell Biological marker ) Oxidoreductases Cell subpopulation Tumor cell |
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SubjectTerms | Aldehyde Dehydrogenase - antagonists & inhibitors Aldehyde Dehydrogenase - metabolism Animals Antineoplastic agents Apoptosis - drug effects Biological and medical sciences Cell Line, Tumor Cell Survival Disulfiram - pharmacology DNA Damage Drug Resistance, Neoplasm Erlotinib Hydrochloride Humans Medical sciences Mice Mice, Nude Neoplastic Stem Cells - drug effects Neoplastic Stem Cells - enzymology Oxidative Stress Pharmacology. Drug treatments Protein Kinase Inhibitors - pharmacology Pyrazoles - pharmacology Pyridines - pharmacology Quinazolines - pharmacology Reactive Oxygen Species - metabolism Receptor, Epidermal Growth Factor - antagonists & inhibitors RNA Interference RNA, Small Interfering Tumors Xenograft Model Antitumor Assays |
Title | The Cancer Stem Cell Marker Aldehyde Dehydrogenase Is Required to Maintain a Drug-Tolerant Tumor Cell Subpopulation |
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