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Anti-Neoplastic Activity of Estrogen Receptor Beta in Chemoresistant Triple-Negative Breast Cancer

ABSTRACT: Anti-Neoplastic Activity of Estrogen Receptor Beta in Chemoresistant Triple-Negative Breast Cancer

PROVIDER: PRJNA1280979 | ENA |

REPOSITORIES: ENA

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Anti-Neoplastic Activity of Estrogen Receptor Beta in Chemoresistant Triple-Negative Breast Cancer

Project description:The standard of care for triple-negative breast cancer is chemotherapy followed by surgical resection, and in most cases, additional rounds of chemotherapy treatment. While highly effective, approximately half of patients will experience disease recurrence that does not respond to additional rounds of treatment. Previous findings demonstrate that estrogen receptor beta (ERb) is expressed in upwards of 20% of triple-negative tumors, and that ERb functions as a tumor suppressor in triple-negative breast cancer models, it was of interest to determine if the tumor-suppressive effects of ERb persisted in chemo-therapy-resistant forms of the disease. Here, we demonstrate that the activation of ERb in chemotherapy-resistant triple-negative breast cancer cell lines elicits equivalent or superior inhibitory effects compared to chemotherapy-sensitive counterparts. These findings support the potential use of ERb-targeting agents in advanced forms of the disease.

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Project description:Targeting neddylation and sumoylation in chemoresistant triple negative breast cancer

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Project description:Triple negative breast cancer (TNBC) accounts for 15-20% of breast cancer cases in the United States. Systemic neoadjuvant chemotherapy (NACT), with or without immunotherapy, is the current standard of care for patients with early-stage TNBC. However, up to 70% of TNBC patients have significant residual disease once NACT is completed, which is associated with a high risk of developing recurrence within two to three years of surgical resection. To identify targetable vulnerabilities in chemoresistant TNBC, we generated longitudinal patient-derived xenograft (PDX) models from TNBC tumors before and after patients received NACT. We then compiled transcriptomes and drug response profiles for all models. Transcriptomic analysis identified the enrichment of aberrant protein homeostasis pathways in models from post-NACT tumors relative to pre-NACT tumors. This observation correlated with increased sensitivity in vitro to inhibitors targeting the proteasome, heat shock proteins, and neddylation pathways. Pevonedistat, a drug annotated as a NEDD8-activating enzyme (NAE) inhibitor, was prioritized for validation in vivo and demonstrated efficacy as a single agent in multiple PDX models of TNBC. Pharmacotranscriptomic analysis identified a pathway-level correlation between pevonedistat activity and post-translational modification (PTM) machinery, particularly involving neddylation and sumoylation targets. Elevated levels of both NEDD8 and SUMO1 were observed in models exhibiting a favorable response to pevonedistat compared to those with a less favorable response in vivo. Moreover, a correlation emerged between the expression of neddylation-regulated pathways and tumor response to pevonedistat, indicating that targeting these PTM pathways may prove effective in combating chemoresistant TNBC.

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