Data from Key Survival Factor, Mcl-1, Correlates with Sensitivity to Combined Bcl-2/Bcl-xL Blockade Article Swipe
Michelle M. Williams
,
Linus Lee
,
Donna J. Hicks
,
Meghan M. Joly
,
David L. Elion
,
Bushra Rahman
,
Courtney McKernan
,
Violeta Sánchez
,
Justin M. Balko
,
Thomas Stricker
,
Mónica V. Estrada
,
Rebecca S. Cook
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/1541-7786.c.6539923
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/1541-7786.c.6539923
An estimated 40,000 deaths will be attributed to breast cancer in 2016, underscoring the need for improved therapies. Evading cell death is a major hallmark of cancer, driving tumor progression and therapeutic resistance. To evade apoptosis, cancers use antiapoptotic Bcl-2 proteins to bind to and neutralize apoptotic activators, such as Bim. Investigation of antiapoptotic Bcl-2 family members in clinical breast cancer datasets revealed greater expression and more frequent gene amplification of MCL1 as compared with BCL2 or BCL2L1 (Bcl-xL) across three major molecular breast cancer subtypes, Luminal (A and B), HER2-enriched, and Basal-like. While Mcl-1 protein expression was elevated in estrogen receptor α (ERα)-positive and ERα-negative tumors as compared with normal breast, Mcl-1 staining was higher in ERα+ tumors. Targeted Mcl-1 blockade using RNAi increased caspase-mediated cell death in ERα+ breast cancer cells, resulting in sustained growth inhibition. In contrast, combined blockade of Bcl-2 and Bcl-xL only transiently induced apoptosis, as cells rapidly acclimated through Mcl-1 upregulation and enhanced Mcl-1 activity, as measured in situ using Mcl-1/Bim proximity ligation assays. Importantly, MCL1 gene expression levels correlated inversely with sensitivity to pharmacologic Bcl-2/Bcl-xL inhibition in luminal breast cancer cells, whereas no relationship was seen between the gene expression of BCL2 or BCL2L1 and sensitivity to Bcl-2/Bcl-xL inhibition. These results demonstrate that breast cancers rapidly deploy Mcl-1 to promote cell survival, particularly when challenged with blockade of other Bcl-2 family members, warranting the continued development of Mcl-1–selective inhibitors for targeted tumor cell killing.Implications: Mcl-1 levels predict breast cancer response to inhibitors targeting other Bcl-2 family members, and demonstrate the key role played by Mcl-1 in resistance to this drug class. Mol Cancer Res; 15(3); 259–68. ©2016 AACR.
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Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1158/1541-7786.c.6539923
- OA Status
- gold
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4392689616
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4392689616Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1158/1541-7786.c.6539923Digital Object Identifier
- Title
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Data from Key Survival Factor, Mcl-1, Correlates with Sensitivity to Combined Bcl-2/Bcl-xL BlockadeWork 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
-
Michelle M. Williams, Linus Lee, Donna J. Hicks, Meghan M. Joly, David L. Elion, Bushra Rahman, Courtney McKernan, Violeta Sánchez, Justin M. Balko, Thomas Stricker, Mónica V. Estrada, Rebecca S. CookList of authors in order
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https://doi.org/10.1158/1541-7786.c.6539923Publisher landing page
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YesWhether a free full text is available
- OA status
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goldOpen access status per OpenAlex
- OA URL
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https://doi.org/10.1158/1541-7786.c.6539923Direct OA link when available
- Concepts
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Bcl-xL, Blockade, Sensitivity (control systems), Key (lock), Factor (programming language), Chemistry, Computer science, Medicine, Internal medicine, Apoptosis, Engineering, Receptor, Electronic engineering, Programmed cell death, Biochemistry, Computer security, Programming languageTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.predict | 243 |
| abstract_inverted_index.promote | 216 |
| abstract_inverted_index.protein | 95 |
| abstract_inverted_index.rapidly | 152, 212 |
| abstract_inverted_index.results | 207 |
| abstract_inverted_index.through | 154 |
| abstract_inverted_index.tumors. | 118 |
| abstract_inverted_index.whereas | 188 |
| abstract_inverted_index.(Bcl-xL) | 78 |
| abstract_inverted_index.Targeted | 119 |
| abstract_inverted_index.blockade | 121, 141, 223 |
| abstract_inverted_index.clinical | 58 |
| abstract_inverted_index.combined | 140 |
| abstract_inverted_index.compared | 73, 108 |
| abstract_inverted_index.datasets | 61 |
| abstract_inverted_index.elevated | 98 |
| abstract_inverted_index.enhanced | 158 |
| abstract_inverted_index.estrogen | 100 |
| abstract_inverted_index.frequent | 67 |
| abstract_inverted_index.hallmark | 24 |
| abstract_inverted_index.improved | 16 |
| abstract_inverted_index.ligation | 168 |
| abstract_inverted_index.measured | 162 |
| abstract_inverted_index.members, | 228, 253 |
| abstract_inverted_index.proteins | 40 |
| abstract_inverted_index.receptor | 101 |
| abstract_inverted_index.response | 246 |
| abstract_inverted_index.revealed | 62 |
| abstract_inverted_index.staining | 113 |
| abstract_inverted_index.targeted | 237 |
| abstract_inverted_index.259–68. | 272 |
| abstract_inverted_index.Mcl-1/Bim | 166 |
| abstract_inverted_index.activity, | 160 |
| abstract_inverted_index.apoptotic | 46 |
| abstract_inverted_index.continued | 231 |
| abstract_inverted_index.contrast, | 139 |
| abstract_inverted_index.estimated | 1 |
| abstract_inverted_index.increased | 124 |
| abstract_inverted_index.inversely | 176 |
| abstract_inverted_index.molecular | 82 |
| abstract_inverted_index.proximity | 167 |
| abstract_inverted_index.resulting | 133 |
| abstract_inverted_index.subtypes, | 85 |
| abstract_inverted_index.survival, | 218 |
| abstract_inverted_index.sustained | 135 |
| abstract_inverted_index.targeting | 249 |
| abstract_inverted_index.acclimated | 153 |
| abstract_inverted_index.apoptosis, | 35, 149 |
| abstract_inverted_index.attributed | 6 |
| abstract_inverted_index.challenged | 221 |
| abstract_inverted_index.correlated | 175 |
| abstract_inverted_index.expression | 64, 96, 173, 196 |
| abstract_inverted_index.inhibition | 182 |
| abstract_inverted_index.inhibitors | 235, 248 |
| abstract_inverted_index.neutralize | 45 |
| abstract_inverted_index.resistance | 263 |
| abstract_inverted_index.therapies. | 17 |
| abstract_inverted_index.warranting | 229 |
| abstract_inverted_index.<i>in | 163 |
| abstract_inverted_index.Basal-like. | 92 |
| abstract_inverted_index.activators, | 47 |
| abstract_inverted_index.demonstrate | 208, 255 |
| abstract_inverted_index.development | 232 |
| abstract_inverted_index.inhibition. | 137, 205 |
| abstract_inverted_index.progression | 29 |
| abstract_inverted_index.resistance. | 32 |
| abstract_inverted_index.sensitivity | 178, 202 |
| abstract_inverted_index.therapeutic | 31 |
| abstract_inverted_index.transiently | 147 |
| abstract_inverted_index.<i>Mol | 268 |
| abstract_inverted_index.Bcl-2/Bcl-xL | 181, 204 |
| abstract_inverted_index.Importantly, | 170 |
| abstract_inverted_index.particularly | 219 |
| abstract_inverted_index.relationship | 190 |
| abstract_inverted_index.underscoring | 12 |
| abstract_inverted_index.upregulation | 156 |
| abstract_inverted_index.ERα-negative | 105 |
| abstract_inverted_index.Investigation | 51 |
| abstract_inverted_index.amplification | 69 |
| abstract_inverted_index.antiapoptotic | 38, 53 |
| abstract_inverted_index.pharmacologic | 180 |
| abstract_inverted_index.HER2-enriched, | 90 |
| abstract_inverted_index.situ</i> | 164 |
| abstract_inverted_index.(ERα)-positive | 103 |
| abstract_inverted_index.caspase-mediated | 125 |
| abstract_inverted_index.Mcl-1–selective | 234 |
| abstract_inverted_index.<i>BCL2</i> | 75, 198 |
| abstract_inverted_index.<i>MCL1</i> | 71, 171 |
| abstract_inverted_index.<i>BCL2L1</i> | 77, 200 |
| abstract_inverted_index.ERα<sup>+</sup> | 117, 129 |
| abstract_inverted_index.<div>Abstract<p>An | 0 |
| abstract_inverted_index.AACR</i>.</p></div> | 274 |
| abstract_inverted_index.killing.</p><p><b>Implications:</b> | 240 |
| cited_by_percentile_year | |
| countries_distinct_count | 0 |
| institutions_distinct_count | 12 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.8600000143051147 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.36826184 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |