Aurora kinase blockade drives de novo addiction of cervical squamous cell carcinoma to druggable EGFR signalling
Oncogenic signalling confers tumour-progression advantages; thus, its pharmacological blockade is the best strategy for cancer chemotherapy. However, drug resistance and heterogeneous dependency of tumour hamper their therapeutic potential, suggesting the necessity for a new ubiquitous modality base...
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| Veröffentlicht in: | Oncogene 2022-04, Vol.41 (16), p.2326-2339 |
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| creator | Komatsu, Masayuki Nakamura, Kanako Takeda, Takashi Chiwaki, Fumiko Banno, Kouji Aoki, Daisuke Takeshita, Fumitaka Sasaki, Hiroki |
| description | Oncogenic signalling confers tumour-progression advantages; thus, its pharmacological blockade is the best strategy for cancer chemotherapy. However, drug resistance and heterogeneous dependency of tumour hamper their therapeutic potential, suggesting the necessity for a new ubiquitous modality based on evading drug resistance. Here, we proposed a
de
novo
ad
diction to
on
cogenic signalling (Dead-On) concept, wherein specific blockade of target molecules forces cancer cells to develop dependency on an oncogenic signalling. In cervical squamous cell carcinoma cells, Aurora A/B dual blockade elicited rapid addiction to EGFR–Erk signalling, and its pharmacological/genetic inhibition synergistically enhanced anti-cancer activities in vitro, in vivo, and in a patient-derived organoid model. The signal activation was independent of EGFR genetic status, it was triggered by receptor accumulation on the plasma membrane
via
Rab11-mediated endocytic recycling machinery. These findings support our novel Dead-On concept which may lead to drug discovery as well as expand the adaptation of approved targeted drugs. |
| doi_str_mv | 10.1038/s41388-022-02256-3 |
| format | Article |
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de
novo
ad
diction to
on
cogenic signalling (Dead-On) concept, wherein specific blockade of target molecules forces cancer cells to develop dependency on an oncogenic signalling. In cervical squamous cell carcinoma cells, Aurora A/B dual blockade elicited rapid addiction to EGFR–Erk signalling, and its pharmacological/genetic inhibition synergistically enhanced anti-cancer activities in vitro, in vivo, and in a patient-derived organoid model. The signal activation was independent of EGFR genetic status, it was triggered by receptor accumulation on the plasma membrane
via
Rab11-mediated endocytic recycling machinery. These findings support our novel Dead-On concept which may lead to drug discovery as well as expand the adaptation of approved targeted drugs.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/s41388-022-02256-3</identifier><identifier>PMID: 35250028</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/31 ; 13/95 ; 42/89 ; 631/67/1059/602 ; 631/67/1517/1371 ; 631/80/313/1461 ; 631/80/86/2368 ; 64/60 ; 96/1 ; Addictions ; Apoptosis ; Aurora kinase ; Cancer ; Carcinoma, Squamous Cell - drug therapy ; Carcinoma, Squamous Cell - genetics ; Cell Biology ; Cell Line, Tumor ; Cervical cancer ; Cervix ; Chemotherapy ; Drug resistance ; Drug Resistance, Neoplasm - genetics ; Epidermal growth factor receptors ; ErbB Receptors - metabolism ; Extracellular signal-regulated kinase ; Female ; Human Genetics ; Humans ; Internal Medicine ; Kinases ; Medicine ; Medicine & Public Health ; Oncogenes ; Oncology ; Organoids ; Signal Transduction ; Squamous cell carcinoma ; Tumors ; Uterine Cervical Neoplasms - drug therapy ; Uterine Cervical Neoplasms - genetics</subject><ispartof>Oncogene, 2022-04, Vol.41 (16), p.2326-2339</ispartof><rights>The Author(s), under exclusive licence to Springer Nature Limited 2022</rights><rights>2022. The Author(s), under exclusive licence to Springer Nature Limited.</rights><rights>The Author(s), under exclusive licence to Springer Nature Limited 2022.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-ff04027f716aa89de050a47f424366126c03293304f566ca106ac143e6c30f693</citedby><cites>FETCH-LOGICAL-c375t-ff04027f716aa89de050a47f424366126c03293304f566ca106ac143e6c30f693</cites><orcidid>0000-0003-1180-1746 ; 0000-0002-9443-0364 ; 0000-0002-2200-8359 ; 0000-0002-0914-9157 ; 0000-0003-2610-2833 ; 0000-0002-9596-8326 ; 0000-0001-6686-5742</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27928,27929</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35250028$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Komatsu, Masayuki</creatorcontrib><creatorcontrib>Nakamura, Kanako</creatorcontrib><creatorcontrib>Takeda, Takashi</creatorcontrib><creatorcontrib>Chiwaki, Fumiko</creatorcontrib><creatorcontrib>Banno, Kouji</creatorcontrib><creatorcontrib>Aoki, Daisuke</creatorcontrib><creatorcontrib>Takeshita, Fumitaka</creatorcontrib><creatorcontrib>Sasaki, Hiroki</creatorcontrib><title>Aurora kinase blockade drives de novo addiction of cervical squamous cell carcinoma to druggable EGFR signalling</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Oncogenic signalling confers tumour-progression advantages; thus, its pharmacological blockade is the best strategy for cancer chemotherapy. However, drug resistance and heterogeneous dependency of tumour hamper their therapeutic potential, suggesting the necessity for a new ubiquitous modality based on evading drug resistance. Here, we proposed a
de
novo
ad
diction to
on
cogenic signalling (Dead-On) concept, wherein specific blockade of target molecules forces cancer cells to develop dependency on an oncogenic signalling. In cervical squamous cell carcinoma cells, Aurora A/B dual blockade elicited rapid addiction to EGFR–Erk signalling, and its pharmacological/genetic inhibition synergistically enhanced anti-cancer activities in vitro, in vivo, and in a patient-derived organoid model. The signal activation was independent of EGFR genetic status, it was triggered by receptor accumulation on the plasma membrane
via
Rab11-mediated endocytic recycling machinery. These findings support our novel Dead-On concept which may lead to drug discovery as well as expand the adaptation of approved targeted drugs.</description><subject>13/31</subject><subject>13/95</subject><subject>42/89</subject><subject>631/67/1059/602</subject><subject>631/67/1517/1371</subject><subject>631/80/313/1461</subject><subject>631/80/86/2368</subject><subject>64/60</subject><subject>96/1</subject><subject>Addictions</subject><subject>Apoptosis</subject><subject>Aurora kinase</subject><subject>Cancer</subject><subject>Carcinoma, Squamous Cell - drug therapy</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cervical cancer</subject><subject>Cervix</subject><subject>Chemotherapy</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Epidermal growth factor receptors</subject><subject>ErbB Receptors - metabolism</subject><subject>Extracellular signal-regulated kinase</subject><subject>Female</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Kinases</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Oncogenes</subject><subject>Oncology</subject><subject>Organoids</subject><subject>Signal Transduction</subject><subject>Squamous cell carcinoma</subject><subject>Tumors</subject><subject>Uterine Cervical Neoplasms - 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Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Komatsu, Masayuki</au><au>Nakamura, Kanako</au><au>Takeda, Takashi</au><au>Chiwaki, Fumiko</au><au>Banno, Kouji</au><au>Aoki, Daisuke</au><au>Takeshita, Fumitaka</au><au>Sasaki, Hiroki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aurora kinase blockade drives de novo addiction of cervical squamous cell carcinoma to druggable EGFR signalling</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2022-04-15</date><risdate>2022</risdate><volume>41</volume><issue>16</issue><spage>2326</spage><epage>2339</epage><pages>2326-2339</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract>Oncogenic signalling confers tumour-progression advantages; thus, its pharmacological blockade is the best strategy for cancer chemotherapy. However, drug resistance and heterogeneous dependency of tumour hamper their therapeutic potential, suggesting the necessity for a new ubiquitous modality based on evading drug resistance. Here, we proposed a
de
novo
ad
diction to
on
cogenic signalling (Dead-On) concept, wherein specific blockade of target molecules forces cancer cells to develop dependency on an oncogenic signalling. In cervical squamous cell carcinoma cells, Aurora A/B dual blockade elicited rapid addiction to EGFR–Erk signalling, and its pharmacological/genetic inhibition synergistically enhanced anti-cancer activities in vitro, in vivo, and in a patient-derived organoid model. The signal activation was independent of EGFR genetic status, it was triggered by receptor accumulation on the plasma membrane
via
Rab11-mediated endocytic recycling machinery. These findings support our novel Dead-On concept which may lead to drug discovery as well as expand the adaptation of approved targeted drugs.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>35250028</pmid><doi>10.1038/s41388-022-02256-3</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0003-1180-1746</orcidid><orcidid>https://orcid.org/0000-0002-9443-0364</orcidid><orcidid>https://orcid.org/0000-0002-2200-8359</orcidid><orcidid>https://orcid.org/0000-0002-0914-9157</orcidid><orcidid>https://orcid.org/0000-0003-2610-2833</orcidid><orcidid>https://orcid.org/0000-0002-9596-8326</orcidid><orcidid>https://orcid.org/0000-0001-6686-5742</orcidid></addata></record> |
| fulltext | fulltext |
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| ispartof | Oncogene, 2022-04, Vol.41 (16), p.2326-2339 |
| issn | 0950-9232 1476-5594 |
| language | eng |
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| subjects | 13/31 13/95 42/89 631/67/1059/602 631/67/1517/1371 631/80/313/1461 631/80/86/2368 64/60 96/1 Addictions Apoptosis Aurora kinase Cancer Carcinoma, Squamous Cell - drug therapy Carcinoma, Squamous Cell - genetics Cell Biology Cell Line, Tumor Cervical cancer Cervix Chemotherapy Drug resistance Drug Resistance, Neoplasm - genetics Epidermal growth factor receptors ErbB Receptors - metabolism Extracellular signal-regulated kinase Female Human Genetics Humans Internal Medicine Kinases Medicine Medicine & Public Health Oncogenes Oncology Organoids Signal Transduction Squamous cell carcinoma Tumors Uterine Cervical Neoplasms - drug therapy Uterine Cervical Neoplasms - genetics |
| title | Aurora kinase blockade drives de novo addiction of cervical squamous cell carcinoma to druggable EGFR signalling |
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