EC359: A First-in-Class Small-Molecule Inhibitor for Targeting Oncogenic LIFR Signaling in Triple-Negative Breast Cancer
Leukemia inhibitory factor receptor (LIFR) and its ligand LIF play a critical role in cancer progression, metastasis, stem cell maintenance, and therapy resistance. Here, we describe a rationally designed first-in-class inhibitor of LIFR, EC359, which directly interacts with LIFR to effectively bloc...
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| Veröffentlicht in: | Molecular cancer therapeutics 2019-08, Vol.18 (8), p.1341-1354 |
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| creator | Viswanadhapalli, Suryavathi Luo, Yiliao Sareddy, Gangadhara R Santhamma, Bindu Zhou, Mei Li, Mengxing Ma, Shihong Sonavane, Rajni Pratap, Uday P Altwegg, Kristin A Li, Xiaonan Chang, Annabel Chávez-Riveros, Alejandra Dileep, Kalarickal V Zhang, Kam Y J Pan, Xinlei Murali, Ramachandran Bajda, Marek Raj, Ganesh V Brenner, Andrew J Manthati, Vijaya Rao, Manjeet K Tekmal, Rajeshwar R Nair, Hareesh B Nickisch, Klaus J Vadlamudi, Ratna K |
| description | Leukemia inhibitory factor receptor (LIFR) and its ligand LIF play a critical role in cancer progression, metastasis, stem cell maintenance, and therapy resistance. Here, we describe a rationally designed first-in-class inhibitor of LIFR, EC359, which directly interacts with LIFR to effectively block LIF/LIFR interactions. EC359 treatment exhibits antiproliferative effects, reduces invasiveness and stemness, and promotes apoptosis in triple-negative breast cancer (TNBC) cell lines. The activity of EC359 is dependent on LIF and LIFR expression, and treatment with EC359 attenuated the activation of LIF/LIFR-driven pathways, including STAT3, mTOR, and AKT. Concomitantly, EC359 was also effective in blocking signaling by other LIFR ligands (CTF1, CNTF, and OSM) that interact at LIF/LIFR interface. EC359 significantly reduced tumor progression in TNBC xenografts and patient-derived xenografts (PDX), and reduced proliferation in patient-derived primary TNBC explants. EC359 exhibits distinct pharmacologic advantages, including oral bioavailability, and
stability. Collectively, these data support EC359 as a novel targeted therapeutic that inhibits LIFR oncogenic signaling.
. |
| doi_str_mv | 10.1158/1535-7163.MCT-18-1258 |
| format | Article |
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stability. Collectively, these data support EC359 as a novel targeted therapeutic that inhibits LIFR oncogenic signaling.
.</description><identifier>ISSN: 1535-7163</identifier><identifier>EISSN: 1538-8514</identifier><identifier>DOI: 10.1158/1535-7163.MCT-18-1258</identifier><identifier>PMID: 31142661</identifier><language>eng</language><publisher>United States</publisher><subject>Cell Line, Tumor ; Humans ; Leukemia Inhibitory Factor ; Leukemia Inhibitory Factor Receptor alpha Subunit ; Receptors, OSM-LIF ; Signal Transduction ; Triple Negative Breast Neoplasms</subject><ispartof>Molecular cancer therapeutics, 2019-08, Vol.18 (8), p.1341-1354</ispartof><rights>2019 American Association for Cancer Research.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c477t-5ff7313819de587b30ed5fe267e43858ff544c8705295dee4645be457e37f6253</citedby><cites>FETCH-LOGICAL-c477t-5ff7313819de587b30ed5fe267e43858ff544c8705295dee4645be457e37f6253</cites><orcidid>0000-0002-6056-6992 ; 0000-0002-8384-2793 ; 0000-0001-5152-5235 ; 0000-0003-4964-3720 ; 0000-0001-6032-0354 ; 0000-0002-3985-253X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3343,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31142661$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Viswanadhapalli, Suryavathi</creatorcontrib><creatorcontrib>Luo, Yiliao</creatorcontrib><creatorcontrib>Sareddy, Gangadhara R</creatorcontrib><creatorcontrib>Santhamma, Bindu</creatorcontrib><creatorcontrib>Zhou, Mei</creatorcontrib><creatorcontrib>Li, Mengxing</creatorcontrib><creatorcontrib>Ma, Shihong</creatorcontrib><creatorcontrib>Sonavane, Rajni</creatorcontrib><creatorcontrib>Pratap, Uday P</creatorcontrib><creatorcontrib>Altwegg, Kristin A</creatorcontrib><creatorcontrib>Li, Xiaonan</creatorcontrib><creatorcontrib>Chang, Annabel</creatorcontrib><creatorcontrib>Chávez-Riveros, Alejandra</creatorcontrib><creatorcontrib>Dileep, Kalarickal V</creatorcontrib><creatorcontrib>Zhang, Kam Y J</creatorcontrib><creatorcontrib>Pan, Xinlei</creatorcontrib><creatorcontrib>Murali, Ramachandran</creatorcontrib><creatorcontrib>Bajda, Marek</creatorcontrib><creatorcontrib>Raj, Ganesh V</creatorcontrib><creatorcontrib>Brenner, Andrew J</creatorcontrib><creatorcontrib>Manthati, Vijaya</creatorcontrib><creatorcontrib>Rao, Manjeet K</creatorcontrib><creatorcontrib>Tekmal, Rajeshwar R</creatorcontrib><creatorcontrib>Nair, Hareesh B</creatorcontrib><creatorcontrib>Nickisch, Klaus J</creatorcontrib><creatorcontrib>Vadlamudi, Ratna K</creatorcontrib><title>EC359: A First-in-Class Small-Molecule Inhibitor for Targeting Oncogenic LIFR Signaling in Triple-Negative Breast Cancer</title><title>Molecular cancer therapeutics</title><addtitle>Mol Cancer Ther</addtitle><description>Leukemia inhibitory factor receptor (LIFR) and its ligand LIF play a critical role in cancer progression, metastasis, stem cell maintenance, and therapy resistance. Here, we describe a rationally designed first-in-class inhibitor of LIFR, EC359, which directly interacts with LIFR to effectively block LIF/LIFR interactions. EC359 treatment exhibits antiproliferative effects, reduces invasiveness and stemness, and promotes apoptosis in triple-negative breast cancer (TNBC) cell lines. The activity of EC359 is dependent on LIF and LIFR expression, and treatment with EC359 attenuated the activation of LIF/LIFR-driven pathways, including STAT3, mTOR, and AKT. Concomitantly, EC359 was also effective in blocking signaling by other LIFR ligands (CTF1, CNTF, and OSM) that interact at LIF/LIFR interface. EC359 significantly reduced tumor progression in TNBC xenografts and patient-derived xenografts (PDX), and reduced proliferation in patient-derived primary TNBC explants. EC359 exhibits distinct pharmacologic advantages, including oral bioavailability, and
stability. Collectively, these data support EC359 as a novel targeted therapeutic that inhibits LIFR oncogenic signaling.
.</description><subject>Cell Line, Tumor</subject><subject>Humans</subject><subject>Leukemia Inhibitory Factor</subject><subject>Leukemia Inhibitory Factor Receptor alpha Subunit</subject><subject>Receptors, OSM-LIF</subject><subject>Signal Transduction</subject><subject>Triple Negative Breast Neoplasms</subject><issn>1535-7163</issn><issn>1538-8514</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkU1vEzEQhi0Eoh_wE0A-cnFZf3s5IJVVUyKlrdSGs-U4462R4w32poJ_z4a0VTmMZjTzzjsjPQh9oM0ZpdJ8ppJLoqniZ1fdklBDKJPmFTqe-oYYScXrf_VBc4ROav3ZNNS0jL5FR5xSwZSix-j3Rcdl-wWf41ksdSQxky65WvHdxqVEroYEfpcAz_N9XMVxKDhMsXSlhzHmHt9kP_SQo8eL-ewW38U-u7QfxIyXJW4TkGvo3RgfAH8r4OqIO5c9lHfoTXCpwvvHfIp-zC6W3XeyuLmcd-cL4oXWI5EhaE65oe0apNEr3sBaBmBKg-BGmhCkEN7oRrJWrgGEEnIFQmrgOigm-Sn6evDd7lYbWHvIY3HJbkvcuPLHDi7a_yc53tt-eLBKaS1bPhl8ejQow68d1NFuYvWQkssw7KpljDOheavVJJUHqS9DrQXC8xna2D01uydi90TsRM3SqTFRm_Y-vvzxeesJE_8L5yOTOQ</recordid><startdate>20190801</startdate><enddate>20190801</enddate><creator>Viswanadhapalli, Suryavathi</creator><creator>Luo, Yiliao</creator><creator>Sareddy, Gangadhara R</creator><creator>Santhamma, Bindu</creator><creator>Zhou, Mei</creator><creator>Li, Mengxing</creator><creator>Ma, Shihong</creator><creator>Sonavane, Rajni</creator><creator>Pratap, Uday P</creator><creator>Altwegg, Kristin A</creator><creator>Li, Xiaonan</creator><creator>Chang, Annabel</creator><creator>Chávez-Riveros, Alejandra</creator><creator>Dileep, Kalarickal V</creator><creator>Zhang, Kam Y J</creator><creator>Pan, Xinlei</creator><creator>Murali, Ramachandran</creator><creator>Bajda, Marek</creator><creator>Raj, Ganesh V</creator><creator>Brenner, Andrew J</creator><creator>Manthati, Vijaya</creator><creator>Rao, Manjeet K</creator><creator>Tekmal, Rajeshwar R</creator><creator>Nair, Hareesh B</creator><creator>Nickisch, Klaus J</creator><creator>Vadlamudi, Ratna K</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6056-6992</orcidid><orcidid>https://orcid.org/0000-0002-8384-2793</orcidid><orcidid>https://orcid.org/0000-0001-5152-5235</orcidid><orcidid>https://orcid.org/0000-0003-4964-3720</orcidid><orcidid>https://orcid.org/0000-0001-6032-0354</orcidid><orcidid>https://orcid.org/0000-0002-3985-253X</orcidid></search><sort><creationdate>20190801</creationdate><title>EC359: A First-in-Class Small-Molecule Inhibitor for Targeting Oncogenic LIFR Signaling in Triple-Negative Breast Cancer</title><author>Viswanadhapalli, Suryavathi ; 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Here, we describe a rationally designed first-in-class inhibitor of LIFR, EC359, which directly interacts with LIFR to effectively block LIF/LIFR interactions. EC359 treatment exhibits antiproliferative effects, reduces invasiveness and stemness, and promotes apoptosis in triple-negative breast cancer (TNBC) cell lines. The activity of EC359 is dependent on LIF and LIFR expression, and treatment with EC359 attenuated the activation of LIF/LIFR-driven pathways, including STAT3, mTOR, and AKT. Concomitantly, EC359 was also effective in blocking signaling by other LIFR ligands (CTF1, CNTF, and OSM) that interact at LIF/LIFR interface. EC359 significantly reduced tumor progression in TNBC xenografts and patient-derived xenografts (PDX), and reduced proliferation in patient-derived primary TNBC explants. EC359 exhibits distinct pharmacologic advantages, including oral bioavailability, and
stability. Collectively, these data support EC359 as a novel targeted therapeutic that inhibits LIFR oncogenic signaling.
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| subjects | Cell Line, Tumor Humans Leukemia Inhibitory Factor Leukemia Inhibitory Factor Receptor alpha Subunit Receptors, OSM-LIF Signal Transduction Triple Negative Breast Neoplasms |
| title | EC359: A First-in-Class Small-Molecule Inhibitor for Targeting Oncogenic LIFR Signaling in Triple-Negative Breast Cancer |
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