OSI-906 restores the sensitivity of ovarian clear cell carcinoma to cisplatin by targeting the IGF1R/AKT pathway
Among the various histologic subtypes of ovarian cancers (OCs), ovarian clear cell carcinoma (OCCC) represents a great challenge due to its disease aggressiveness and resistance to chemotherapy. IGF1 is overexpressed in epithelial ovarian cancer (EOC), and IGF1 pathway activation is related to the c...
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| Veröffentlicht in: | Medical oncology (Northwood, London, England) London, England), 2022-02, Vol.39 (2), p.26-26, Article 26 |
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| creator | Liu, Li Liang, Changyan Zhuo, Chenya Jiang, Huiyun Ye, Huixia Ruan, Tianyuan Song, Jiao Jiang, Senwei Zhang, Yu Li, Xiaomao |
| description | Among the various histologic subtypes of ovarian cancers (OCs), ovarian clear cell carcinoma (OCCC) represents a great challenge due to its disease aggressiveness and resistance to chemotherapy. IGF1 is overexpressed in epithelial ovarian cancer (EOC), and IGF1 pathway activation is related to the chemoresistance of various cancers. In this study, we found that the expression level of IGF1 was higher in OCCC than in the most common type of OC, high-grade serous adenocarcinoma (HGSC). Then, we investigated the role of IGF1 pathway activation in the progression of OCCC, observing that activation of the IGF1 pathway using IGF1 promoted the proliferation and migration of ES2 cells, while inactivation of the IGF1 pathway using the selective IGF1R inhibitor OSI-906 reversed the alteration mediated by IGF1. Based on the role of the IGF1 pathway in cancer chemoresistance, we proposed that OSI-906 may restore the sensitivity of OCCC to cisplatin. We first validated that IGF1 increased the IC50 value of cisplatin in ES2 cells, while OSI-906 decreased it. Then we confirmed that IGF1 decreased the apoptosis rate of ES2 cells induced by cisplatin, while OSI-906 increased it. Finally, we conducted animal experiments to investigate whether OSI-906 helps cisplatin control the growth of OCCC. As expected, OSI-906 increased the effect of cisplatin in attenuating the growth of OCCC in vivo. Therefore, we conclude that using OSI-906 may be an effective method to restore the sensitivity of OCCC to cisplatin by targeting the IGF1R/AKT pathway. |
| doi_str_mv | 10.1007/s12032-021-01592-w |
| format | Article |
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IGF1 is overexpressed in epithelial ovarian cancer (EOC), and IGF1 pathway activation is related to the chemoresistance of various cancers. In this study, we found that the expression level of IGF1 was higher in OCCC than in the most common type of OC, high-grade serous adenocarcinoma (HGSC). Then, we investigated the role of IGF1 pathway activation in the progression of OCCC, observing that activation of the IGF1 pathway using IGF1 promoted the proliferation and migration of ES2 cells, while inactivation of the IGF1 pathway using the selective IGF1R inhibitor OSI-906 reversed the alteration mediated by IGF1. Based on the role of the IGF1 pathway in cancer chemoresistance, we proposed that OSI-906 may restore the sensitivity of OCCC to cisplatin. We first validated that IGF1 increased the IC50 value of cisplatin in ES2 cells, while OSI-906 decreased it. Then we confirmed that IGF1 decreased the apoptosis rate of ES2 cells induced by cisplatin, while OSI-906 increased it. Finally, we conducted animal experiments to investigate whether OSI-906 helps cisplatin control the growth of OCCC. As expected, OSI-906 increased the effect of cisplatin in attenuating the growth of OCCC in vivo. Therefore, we conclude that using OSI-906 may be an effective method to restore the sensitivity of OCCC to cisplatin by targeting the IGF1R/AKT pathway.</description><identifier>ISSN: 1357-0560</identifier><identifier>EISSN: 1559-131X</identifier><identifier>DOI: 10.1007/s12032-021-01592-w</identifier><identifier>PMID: 34982265</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adenocarcinoma, Clear Cell - drug therapy ; Adenocarcinoma, Clear Cell - metabolism ; Adenocarcinoma, Clear Cell - pathology ; Animal research ; Animals ; Antineoplastic Agents - therapeutic use ; Apoptosis ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Chemotherapy ; Cisplatin - therapeutic use ; Drug Resistance ; Female ; Hematology ; Imidazoles - pharmacology ; Internal Medicine ; Medicine ; Medicine & Public Health ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Oncology ; Original Paper ; Ovarian cancer ; Ovarian Neoplasms - drug therapy ; Ovarian Neoplasms - metabolism ; Ovarian Neoplasms - pathology ; Pathology ; Proto-Oncogene Proteins c-akt - drug effects ; Proto-Oncogene Proteins c-akt - metabolism ; Pyrazines - pharmacology ; Receptor, IGF Type 1 - drug effects ; Receptor, IGF Type 1 - metabolism ; Signal Transduction - drug effects</subject><ispartof>Medical oncology (Northwood, London, England), 2022-02, Vol.39 (2), p.26-26, Article 26</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>2021. Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-8519f73c1f7c0ffcea0e8f3d9d6709308f65f8e24140c0ae1ed6f29fd2ba894a3</citedby><cites>FETCH-LOGICAL-c419t-8519f73c1f7c0ffcea0e8f3d9d6709308f65f8e24140c0ae1ed6f29fd2ba894a3</cites><orcidid>0000-0001-6374-1488 ; 0000-0002-3687-0070</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12032-021-01592-w$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12032-021-01592-w$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34982265$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Li</creatorcontrib><creatorcontrib>Liang, Changyan</creatorcontrib><creatorcontrib>Zhuo, Chenya</creatorcontrib><creatorcontrib>Jiang, Huiyun</creatorcontrib><creatorcontrib>Ye, Huixia</creatorcontrib><creatorcontrib>Ruan, Tianyuan</creatorcontrib><creatorcontrib>Song, Jiao</creatorcontrib><creatorcontrib>Jiang, Senwei</creatorcontrib><creatorcontrib>Zhang, Yu</creatorcontrib><creatorcontrib>Li, Xiaomao</creatorcontrib><title>OSI-906 restores the sensitivity of ovarian clear cell carcinoma to cisplatin by targeting the IGF1R/AKT pathway</title><title>Medical oncology (Northwood, London, England)</title><addtitle>Med Oncol</addtitle><addtitle>Med Oncol</addtitle><description>Among the various histologic subtypes of ovarian cancers (OCs), ovarian clear cell carcinoma (OCCC) represents a great challenge due to its disease aggressiveness and resistance to chemotherapy. IGF1 is overexpressed in epithelial ovarian cancer (EOC), and IGF1 pathway activation is related to the chemoresistance of various cancers. In this study, we found that the expression level of IGF1 was higher in OCCC than in the most common type of OC, high-grade serous adenocarcinoma (HGSC). Then, we investigated the role of IGF1 pathway activation in the progression of OCCC, observing that activation of the IGF1 pathway using IGF1 promoted the proliferation and migration of ES2 cells, while inactivation of the IGF1 pathway using the selective IGF1R inhibitor OSI-906 reversed the alteration mediated by IGF1. Based on the role of the IGF1 pathway in cancer chemoresistance, we proposed that OSI-906 may restore the sensitivity of OCCC to cisplatin. We first validated that IGF1 increased the IC50 value of cisplatin in ES2 cells, while OSI-906 decreased it. Then we confirmed that IGF1 decreased the apoptosis rate of ES2 cells induced by cisplatin, while OSI-906 increased it. Finally, we conducted animal experiments to investigate whether OSI-906 helps cisplatin control the growth of OCCC. As expected, OSI-906 increased the effect of cisplatin in attenuating the growth of OCCC in vivo. Therefore, we conclude that using OSI-906 may be an effective method to restore the sensitivity of OCCC to cisplatin by targeting the IGF1R/AKT pathway.</description><subject>Adenocarcinoma, Clear Cell - drug therapy</subject><subject>Adenocarcinoma, Clear Cell - metabolism</subject><subject>Adenocarcinoma, Clear Cell - pathology</subject><subject>Animal research</subject><subject>Animals</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Apoptosis</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Chemotherapy</subject><subject>Cisplatin - therapeutic use</subject><subject>Drug Resistance</subject><subject>Female</subject><subject>Hematology</subject><subject>Imidazoles - pharmacology</subject><subject>Internal Medicine</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Oncology</subject><subject>Original Paper</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms - drug therapy</subject><subject>Ovarian Neoplasms - metabolism</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Pathology</subject><subject>Proto-Oncogene Proteins c-akt - drug effects</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Pyrazines - pharmacology</subject><subject>Receptor, IGF Type 1 - drug effects</subject><subject>Receptor, IGF Type 1 - metabolism</subject><subject>Signal Transduction - drug effects</subject><issn>1357-0560</issn><issn>1559-131X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kV9PHCEUxUmjqdb2C_TBkPjSF_QCAzM8GlPtpiYm_kn6RlgGVszsMALrZr99cdfWpA99gZvc3z33wEHoK4VTCtCeZcqAMwKMEqBCMbL-gA6pEIpQTn_t1ZqLloCQcIA-5fwElRRMfUQHvFEdY1IcounmbkYUSJxcLrEeuDw6nN2YQwkvoWxw9Di-mBTMiO3gTMLWDQO2JtkwxqXBJWIb8jSYEkY83-Bi0sLVerFVml1d0tuz85_3eDLlcW02n9G-N0N2X97uI_Rw-f3-4ge5vrmaXZxfE9tQVUgnqPItt9S3Fry3zoDrPO9VL1tQHDovhe8ca2gDFoyjrpeeKd-zuelUY_gR-rbTnVJ8XtXH6WXIr9bN6OIqayapFIoLxit68g_6FFdprO62VNN2VMlKsR1lU8w5Oa-nFJYmbTQF_ZqH3uWh6y_rbR56XYeO36RX86Xr_478CaACfAfk2hoXLr3v_o_sb1d_lec</recordid><startdate>20220201</startdate><enddate>20220201</enddate><creator>Liu, Li</creator><creator>Liang, Changyan</creator><creator>Zhuo, Chenya</creator><creator>Jiang, Huiyun</creator><creator>Ye, Huixia</creator><creator>Ruan, Tianyuan</creator><creator>Song, Jiao</creator><creator>Jiang, Senwei</creator><creator>Zhang, Yu</creator><creator>Li, Xiaomao</creator><general>Springer US</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-6374-1488</orcidid><orcidid>https://orcid.org/0000-0002-3687-0070</orcidid></search><sort><creationdate>20220201</creationdate><title>OSI-906 restores the sensitivity of ovarian clear cell carcinoma to cisplatin by targeting the IGF1R/AKT pathway</title><author>Liu, Li ; 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IGF1 is overexpressed in epithelial ovarian cancer (EOC), and IGF1 pathway activation is related to the chemoresistance of various cancers. In this study, we found that the expression level of IGF1 was higher in OCCC than in the most common type of OC, high-grade serous adenocarcinoma (HGSC). Then, we investigated the role of IGF1 pathway activation in the progression of OCCC, observing that activation of the IGF1 pathway using IGF1 promoted the proliferation and migration of ES2 cells, while inactivation of the IGF1 pathway using the selective IGF1R inhibitor OSI-906 reversed the alteration mediated by IGF1. Based on the role of the IGF1 pathway in cancer chemoresistance, we proposed that OSI-906 may restore the sensitivity of OCCC to cisplatin. We first validated that IGF1 increased the IC50 value of cisplatin in ES2 cells, while OSI-906 decreased it. Then we confirmed that IGF1 decreased the apoptosis rate of ES2 cells induced by cisplatin, while OSI-906 increased it. Finally, we conducted animal experiments to investigate whether OSI-906 helps cisplatin control the growth of OCCC. As expected, OSI-906 increased the effect of cisplatin in attenuating the growth of OCCC in vivo. Therefore, we conclude that using OSI-906 may be an effective method to restore the sensitivity of OCCC to cisplatin by targeting the IGF1R/AKT pathway.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>34982265</pmid><doi>10.1007/s12032-021-01592-w</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-6374-1488</orcidid><orcidid>https://orcid.org/0000-0002-3687-0070</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma, Clear Cell - drug therapy Adenocarcinoma, Clear Cell - metabolism Adenocarcinoma, Clear Cell - pathology Animal research Animals Antineoplastic Agents - therapeutic use Apoptosis Cell Line, Tumor Cell Movement Cell Proliferation Chemotherapy Cisplatin - therapeutic use Drug Resistance Female Hematology Imidazoles - pharmacology Internal Medicine Medicine Medicine & Public Health Mice Mice, Inbred BALB C Mice, Nude Oncology Original Paper Ovarian cancer Ovarian Neoplasms - drug therapy Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology Pathology Proto-Oncogene Proteins c-akt - drug effects Proto-Oncogene Proteins c-akt - metabolism Pyrazines - pharmacology Receptor, IGF Type 1 - drug effects Receptor, IGF Type 1 - metabolism Signal Transduction - drug effects |
| title | OSI-906 restores the sensitivity of ovarian clear cell carcinoma to cisplatin by targeting the IGF1R/AKT pathway |
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