Data from Attenuating Adaptive VEGF-A and IL8 Signaling Restores Durable Tumor Control in AR Antagonist–Treated Prostate Cancers Article Swipe
Pamela Maxwell
,
Melanie McKechnie
,
Christopher W. Armstrong
,
Judith M. Manley
,
Chee Wee Ong
,
Jenny Worthington
,
Ian G. Mills
,
Daniel B. Longley
,
James P. Quigley
,
Amina Zoubeidi
,
Johann S. de Bono
,
Elena I. Deryugina
,
Melissa J. LaBonte
,
David Waugh
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/1541-7786.c.6545405
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/1541-7786.c.6545405
Inhibiting androgen signaling using androgen signaling inhibitors (ASI) remains the primary treatment for castrate-resistant prostate cancer. Acquired resistance to androgen receptor (AR)-targeted therapy represents a major impediment to durable clinical response. Understanding resistance mechanisms, including the role of AR expressed in other cell types within the tumor microenvironment, will extend the clinical benefit of AR-targeted therapy. Here, we show the ASI enzalutamide induces vascular catastrophe and promotes hypoxia and microenvironment adaptation. We characterize treatment-induced hypoxia, and subsequent induction of angiogenesis, as novel mechanisms of relapse to enzalutamide, highlighting the importance of two hypoxia-regulated cytokines in underpinning relapse. We confirmed AR expression in CD34+ vascular endothelium of biopsy tissue and human vascular endothelial cells (HVEC). Enzalutamide attenuated angiogenic tubule formation and induced cytotoxicity in HVECs in vitro, and rapidly induced sustained hypoxia in LNCaP xenografts. Subsequent reoxygenation, following prolonged enzalutamide treatment, was associated with increased tumor vessel density and accelerated tumor growth. Hypoxia increased AR expression and transcriptional activity in prostate cells in vitro. Coinhibition of IL8 and VEGF-A restored tumor response in the presence of enzalutamide, confirming the functional importance of their elevated expression in enzalutamide-resistant models. Moreover, coinhibition of IL8 and VEGF-A resulted in a durable, effective resolution of enzalutamide-sensitive prostate tumors. We conclude that concurrent inhibition of two hypoxia-induced factors, IL8 and VEGF-A, prolongs tumor sensitivity to enzalutamide in preclinical models and may delay the onset of enzalutamide resistance.Implications:Targeting hypoxia-induced signaling may extend the therapeutic benefit of enzalutamide, providing an improved treatment strategy for patients with resistant disease.
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Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1158/1541-7786.c.6545405
- OA Status
- gold
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4392686199
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4392686199Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1158/1541-7786.c.6545405Digital Object Identifier
- Title
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Data from Attenuating Adaptive VEGF-A and IL8 Signaling Restores Durable Tumor Control in AR Antagonist–Treated Prostate CancersWork title
- Type
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preprintOpenAlex work type
- Language
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enPrimary language
- Publication year
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2023Year of publication
- Publication date
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2023-04-03Full publication date if available
- Authors
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Pamela Maxwell, Melanie McKechnie, Christopher W. Armstrong, Judith M. Manley, Chee Wee Ong, Jenny Worthington, Ian G. Mills, Daniel B. Longley, James P. Quigley, Amina Zoubeidi, Johann S. de Bono, Elena I. Deryugina, Melissa J. LaBonte, David WaughList of authors in order
- Landing page
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https://doi.org/10.1158/1541-7786.c.6545405Publisher landing page
- Open access
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YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://doi.org/10.1158/1541-7786.c.6545405Direct OA link when available
- Concepts
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Antagonist, VEGF receptors, Prostate, Interleukin 8, Prostate cancer, Cancer research, Medicine, Internal medicine, Oncology, Pharmacology, Receptor, Cancer, InflammationTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.formation | 118 |
| abstract_inverted_index.including | 34 |
| abstract_inverted_index.increased | 143, 152 |
| abstract_inverted_index.induction | 77 |
| abstract_inverted_index.prolonged | 137 |
| abstract_inverted_index.providing | 240 |
| abstract_inverted_index.resistant | 248 |
| abstract_inverted_index.response. | 30 |
| abstract_inverted_index.signaling | 2, 5, 232 |
| abstract_inverted_index.sustained | 129 |
| abstract_inverted_index.treatment | 11, 243 |
| abstract_inverted_index.Subsequent | 134 |
| abstract_inverted_index.angiogenic | 116 |
| abstract_inverted_index.associated | 141 |
| abstract_inverted_index.attenuated | 115 |
| abstract_inverted_index.concurrent | 206 |
| abstract_inverted_index.confirming | 176 |
| abstract_inverted_index.expression | 100, 154, 183 |
| abstract_inverted_index.functional | 178 |
| abstract_inverted_index.impediment | 26 |
| abstract_inverted_index.importance | 89, 179 |
| abstract_inverted_index.inhibition | 207 |
| abstract_inverted_index.inhibitors | 6 |
| abstract_inverted_index.mechanisms | 82 |
| abstract_inverted_index.represents | 23 |
| abstract_inverted_index.resistance | 17, 32 |
| abstract_inverted_index.resolution | 198 |
| abstract_inverted_index.subsequent | 76 |
| abstract_inverted_index.treatment, | 139 |
| abstract_inverted_index.<i>in | 124, 161 |
| abstract_inverted_index.AR-targeted | 54 |
| abstract_inverted_index.accelerated | 148 |
| abstract_inverted_index.adaptation. | 70 |
| abstract_inverted_index.catastrophe | 64 |
| abstract_inverted_index.endothelial | 111 |
| abstract_inverted_index.endothelium | 104 |
| abstract_inverted_index.mechanisms, | 33 |
| abstract_inverted_index.preclinical | 221 |
| abstract_inverted_index.sensitivity | 217 |
| abstract_inverted_index.therapeutic | 236 |
| abstract_inverted_index.xenografts. | 133 |
| abstract_inverted_index.Coinhibition | 163 |
| abstract_inverted_index.Enzalutamide | 114 |
| abstract_inverted_index.characterize | 72 |
| abstract_inverted_index.coinhibition | 188 |
| abstract_inverted_index.cytotoxicity | 121 |
| abstract_inverted_index.enzalutamide | 61, 138, 219, 229 |
| abstract_inverted_index.highlighting | 87 |
| abstract_inverted_index.underpinning | 95 |
| abstract_inverted_index.(AR)-targeted | 21 |
| abstract_inverted_index.Understanding | 31 |
| abstract_inverted_index.angiogenesis, | 79 |
| abstract_inverted_index.enzalutamide, | 86, 175, 239 |
| abstract_inverted_index.reoxygenation, | 135 |
| abstract_inverted_index.hypoxia-induced | 210, 231 |
| abstract_inverted_index.transcriptional | 156 |
| abstract_inverted_index.microenvironment | 69 |
| abstract_inverted_index.vitro</i>, | 125 |
| abstract_inverted_index.vitro</i>. | 162 |
| abstract_inverted_index.hypoxia-regulated | 92 |
| abstract_inverted_index.microenvironment, | 47 |
| abstract_inverted_index.treatment-induced | 73 |
| abstract_inverted_index.castrate-resistant | 13 |
| abstract_inverted_index.enzalutamide-resistant | 185 |
| abstract_inverted_index.enzalutamide-sensitive | 200 |
| abstract_inverted_index.CD34<sup>+</sup> | 102 |
| abstract_inverted_index.disease.</p></div> | 249 |
| abstract_inverted_index.<div>Abstract<p>Inhibiting | 0 |
| abstract_inverted_index.resistance.</p>Implications:<p>Targeting | 230 |
| cited_by_percentile_year | |
| countries_distinct_count | 0 |
| institutions_distinct_count | 14 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.4699999988079071 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.36582767 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |