Therapeutic Potential for Targeting Autophagy in ER+ Breast Cancer

Ryan M. Finnegan, Ahmed M. Elshazly, Patricia V. Schoenlein, David A. Gewirtz

Research output: Contribution to journalReview articlepeer-review

4 Scopus citations


While endocrine therapy remains the mainstay of treatment for ER-positive, HER2-negative breast cancer, tumor progression and disease recurrence limit the utility of current standards of care. While existing therapies may allow for a prolonged progression-free survival, however, the growth-arrested (essentially dormant) state of residual tumor cells is not permanent and is frequently a precursor to disease relapse. Tumor cells that escape dormancy and regain proliferative capacity also tend to acquire resistance to further therapies. The cellular process of autophagy has been implicated in the adaptation, survival, and reactivation of dormant cells. Autophagy is a cellular stress mechanism induced to maintain cellular homeostasis. Tumor cells often undergo therapy-induced autophagy which, in most contexts, is cytoprotective in function; however, depending on how the autophagy is regulated, it can also be non-protective, cytostatic, or cytotoxic. In this review, we explore the literature on the relationship(s) between endocrine therapies and autophagy. Moreover, we address the different functional roles of autophagy in response to these treatments, exploring the possibility of targeting autophagy as an adjuvant therapeutic modality together with endocrine therapies.

Original languageEnglish (US)
Article number4289
Issue number17
StatePublished - Sep 2022
Externally publishedYes


  • autophagy
  • breast cancer
  • cytoprotective
  • endocrine
  • estrogen
  • resistance

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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