Autophagy in breast cancer metastatic dormancy: Tumor suppressing or tumor promoting functions?
Identifieur interne : 000A35 ( Main/Exploration ); précédent : 000A34; suivant : 000A36Autophagy 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
Affiliations:
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Schiemann</name><affiliation wicri:level="1"><nlm:aff id="A2">Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH, 44106, USA.</nlm:aff><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH, 44106</wicri:regionArea><wicri:noRegion>44106</wicri:noRegion></affiliation></author></analytic><series><title level="j">Journal of cancer metastasis and treatment</title><idno type="ISSN">2394-4722</idno><idno type="eISSN">2454-2857</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><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></div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Flynn, Alyssa La Belle" sort="Flynn, Alyssa La Belle" uniqKey="Flynn A" first="Alyssa La Belle" last="Flynn">Alyssa La Belle Flynn</name></noRegion><name sortKey="Schiemann, William P" sort="Schiemann, William P" uniqKey="Schiemann W" first="William P." last="Schiemann">William P. Schiemann</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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