Autophagy in breast cancer metastatic dormancy: Tumor suppressing or tumor promoting functions?
Identifieur interne : 000386 ( Pmc/Curation ); précédent : 000385; suivant : 000387Autophagy in breast cancer metastatic dormancy: Tumor suppressing or tumor promoting functions?
Auteurs : Alyssa La Belle Flynn [États-Unis] ; William P. Schiemann [États-Unis]Source :
- Journal of cancer metastasis and treatment [ 2394-4722 ] ; 2019.
Abstract
Breast cancer is the second leading cause of cancer-associated death in women in the United States, with more than 90% of those deaths attributed to metastasis. Breast cancer metastasis is incurable and possesses few treatment options and a poor overall prognosis due in part to confounding metastatic attributes, particularly the acquisition of dormancy-associated phenotypes. Dormant disseminated tumor cells (DTCs) can persist for years-to-decades before recurring as highly aggressive, secondary lesions. Dormancy-associated phenotypes are exhibited by breast cancer stem cells (BCSCs), which undergo tumor initiation and unlimited self-renewal. In addition to their specialized abilities to circumvent chemotherapeutic insults, BCSCs also upregulate autophagy during metastatic dormancy as a means to survive in nutrient poor conditions and environmental stress. As such, therapeutic targeting of autophagy is actively being pursued as an attractive strategy to alleviate metastatic disease and the recurrence of dormant BCSCs. Here we review the molecular and cellular features of autophagy, as well as its paradoxical role in both suppressing and promoting mammary tumor development and metastatic progression. Finally, we highlight the clinical challenges associated with therapeutic targeting of autophagy in metastatic breast cancers.
Url:
DOI: 10.20517/2394-4722.2019.13
PubMed: 31431926
PubMed Central: 6701850
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<front><div type="abstract" xml:lang="en"><p id="P4">Breast cancer is the second leading cause of cancer-associated death in women in the United States, with more than 90% of those deaths attributed to metastasis. Breast cancer metastasis is incurable and possesses few treatment options and a poor overall prognosis due in part to confounding metastatic attributes, particularly the acquisition of dormancy-associated phenotypes. Dormant disseminated tumor cells (DTCs) can persist for years-to-decades before recurring as highly aggressive, secondary lesions. Dormancy-associated phenotypes are exhibited by breast cancer stem cells (BCSCs), which undergo tumor initiation and unlimited self-renewal. In addition to their specialized abilities to circumvent chemotherapeutic insults, BCSCs also upregulate autophagy during metastatic dormancy as a means to survive in nutrient poor conditions and environmental stress. As such, therapeutic targeting of autophagy is actively being pursued as an attractive strategy to alleviate metastatic disease and the recurrence of dormant BCSCs. Here we review the molecular and cellular features of autophagy, as well as its paradoxical role in both suppressing and promoting mammary tumor development and metastatic progression. Finally, we highlight the clinical challenges associated with therapeutic targeting of autophagy in metastatic breast cancers.</p>
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<contrib-group><contrib contrib-type="author"><name><surname>Flynn</surname>
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<aff id="A1"><label>1</label>
Department of Pharmacology, Case Western Reserve University, Cleveland, OH, 44106, USA.</aff>
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Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH, 44106, USA.</aff>
<author-notes><fn fn-type="con" id="FN1"><p id="P1">Author’s Contributions</p>
<p id="P2">Conception and study design: Flynn AL, Schiemann WP</p>
<p id="P3">Drafted and revised the manuscript: Flynn AL, Schiemann WP</p>
</fn>
<corresp id="CR1"><label>*</label>
<bold>Address Correspondence to:</bold>
William P. Schiemann, Case Comprehensive Cancer Center, Case Western Reserve University, Wolstein Research Building, Room 2131, 2103 Cornell Road Cleveland, OH 44106. Phone: 216-368-5763. Fax: 216-368-1166. <email>william.schiemann@case.edu</email>
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<fn fn-type="COI-statement" id="FN3"><p id="P23">Conflict of Interest</p>
<p id="P24">All authors declare that there are no conflicts of interest.</p>
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<abstract id="ABS1"><p id="P4">Breast cancer is the second leading cause of cancer-associated death in women in the United States, with more than 90% of those deaths attributed to metastasis. Breast cancer metastasis is incurable and possesses few treatment options and a poor overall prognosis due in part to confounding metastatic attributes, particularly the acquisition of dormancy-associated phenotypes. Dormant disseminated tumor cells (DTCs) can persist for years-to-decades before recurring as highly aggressive, secondary lesions. Dormancy-associated phenotypes are exhibited by breast cancer stem cells (BCSCs), which undergo tumor initiation and unlimited self-renewal. In addition to their specialized abilities to circumvent chemotherapeutic insults, BCSCs also upregulate autophagy during metastatic dormancy as a means to survive in nutrient poor conditions and environmental stress. As such, therapeutic targeting of autophagy is actively being pursued as an attractive strategy to alleviate metastatic disease and the recurrence of dormant BCSCs. Here we review the molecular and cellular features of autophagy, as well as its paradoxical role in both suppressing and promoting mammary tumor development and metastatic progression. Finally, we highlight the clinical challenges associated with therapeutic targeting of autophagy in metastatic breast cancers.</p>
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<kwd-group><kwd>autophagy</kwd>
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