Glucocorticoids induce differentiation and chemoresistance in ovarian cancer by promoting ROR1-mediated stemness
Glucocorticoids are routinely used in the clinic as anti-inflammatory and immunosuppressive agents as well as adjuvants during cancer treatment to mitigate the undesirable side effects of chemotherapy. However, recent studies have indicated that glucocorticoids may negatively impact the efficacy of...
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Published in | Cell death & disease Vol. 11; no. 9; p. 790 |
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Main Authors | , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Nature Publishing Group UK
23.09.2020
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Abstract | Glucocorticoids are routinely used in the clinic as anti-inflammatory and immunosuppressive agents as well as adjuvants during cancer treatment to mitigate the undesirable side effects of chemotherapy. However, recent studies have indicated that glucocorticoids may negatively impact the efficacy of chemotherapy by promoting tumor cell survival, heterogeneity, and metastasis. Here, we show that dexamethasone induces upregulation of ROR1 expression in ovarian cancer (OC), including platinum-resistant OC. Increased ROR1 expression resulted in elevated RhoA, YAP/TAZ, and BMI-1 levels in a panel of OC cell lines as well as primary ovarian cancer patient-derived cells, underlining the translational relevance of our studies. Importantly, dexamethasone induced differentiation of OC patient-derived cells ex vivo according to their molecular subtype and the phenotypic expression of cell differentiation markers. High-throughput drug testing with 528 emerging and clinical oncology compounds of OC cell lines and patient-derived cells revealed that dexamethasone treatment increased the sensitivity to several AKT/PI3K targeted kinase inhibitors, while significantly decreasing the efficacy of chemotherapeutics such as taxanes, as well as anti-apoptotic compounds such as SMAC mimetics. On the other hand, targeting ROR1 expression increased the efficacy of taxane drugs and SMAC mimetics, suggesting new combinatorial targeted treatments for patients with OC. |
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AbstractList | Glucocorticoids are routinely used in the clinic as anti-inflammatory and immunosuppressive agents as well as adjuvants during cancer treatment to mitigate the undesirable side effects of chemotherapy. However, recent studies have indicated that glucocorticoids may negatively impact the efficacy of chemotherapy by promoting tumor cell survival, heterogeneity, and metastasis. Here, we show that dexamethasone induces upregulation of ROR1 expression in ovarian cancer (OC), including platinum-resistant OC. Increased ROR1 expression resulted in elevated RhoA, YAP/TAZ, and BMI-1 levels in a panel of OC cell lines as well as primary ovarian cancer patient-derived cells, underlining the translational relevance of our studies. Importantly, dexamethasone induced differentiation of OC patient-derived cells ex vivo according to their molecular subtype and the phenotypic expression of cell differentiation markers. High-throughput drug testing with 528 emerging and clinical oncology compounds of OC cell lines and patient-derived cells revealed that dexamethasone treatment increased the sensitivity to several AKT/PI3K targeted kinase inhibitors, while significantly decreasing the efficacy of chemotherapeutics such as taxanes, as well as anti-apoptotic compounds such as SMAC mimetics. On the other hand, targeting ROR1 expression increased the efficacy of taxane drugs and SMAC mimetics, suggesting new combinatorial targeted treatments for patients with OC. Abstract Glucocorticoids are routinely used in the clinic as anti-inflammatory and immunosuppressive agents as well as adjuvants during cancer treatment to mitigate the undesirable side effects of chemotherapy. However, recent studies have indicated that glucocorticoids may negatively impact the efficacy of chemotherapy by promoting tumor cell survival, heterogeneity, and metastasis. Here, we show that dexamethasone induces upregulation of ROR1 expression in ovarian cancer (OC), including platinum-resistant OC. Increased ROR1 expression resulted in elevated RhoA, YAP/TAZ, and BMI-1 levels in a panel of OC cell lines as well as primary ovarian cancer patient-derived cells, underlining the translational relevance of our studies. Importantly, dexamethasone induced differentiation of OC patient-derived cells ex vivo according to their molecular subtype and the phenotypic expression of cell differentiation markers. High-throughput drug testing with 528 emerging and clinical oncology compounds of OC cell lines and patient-derived cells revealed that dexamethasone treatment increased the sensitivity to several AKT/PI3K targeted kinase inhibitors, while significantly decreasing the efficacy of chemotherapeutics such as taxanes, as well as anti-apoptotic compounds such as SMAC mimetics. On the other hand, targeting ROR1 expression increased the efficacy of taxane drugs and SMAC mimetics, suggesting new combinatorial targeted treatments for patients with OC. |
ArticleNumber | 790 |
Author | Barker, Harlan Karvonen, Hanna Kallioniemi, Olli Niininen, Wilhelmiina Koivisto-Korander, Riitta Arjama, Mariliina Loukovaara, Mikko Murumägi, Astrid Kaleva, Laura Lassus, Heini Bützow, Ralf Ungureanu, Daniela Tapper, Johanna Pakarinen, Päivi |
Author_xml | – sequence: 1 givenname: Hanna orcidid: 0000-0002-7815-0709 surname: Karvonen fullname: Karvonen, Hanna organization: Faculty of Medicine and Health Technology, Tampere University – sequence: 2 givenname: Mariliina surname: Arjama fullname: Arjama, Mariliina organization: Institute for Molecular Medicine Finland, FIMM, University of Helsinki – sequence: 3 givenname: Laura surname: Kaleva fullname: Kaleva, Laura organization: Faculty of Medicine and Health Technology, Tampere University – sequence: 4 givenname: Wilhelmiina surname: Niininen fullname: Niininen, Wilhelmiina organization: Faculty of Medicine and Health Technology, Tampere University – sequence: 5 givenname: Harlan orcidid: 0000-0003-4125-2522 surname: Barker fullname: Barker, Harlan organization: Faculty of Medicine and Health Technology, Tampere University, Fimlab Ltd., Tampere University Hospital – sequence: 6 givenname: Riitta surname: Koivisto-Korander fullname: Koivisto-Korander, Riitta organization: Department of Obstetrics and Gynecology, University of Helsinki, Helsinki University Hospital – sequence: 7 givenname: Johanna surname: Tapper fullname: Tapper, Johanna organization: Department of Obstetrics and Gynecology, University of Helsinki, Helsinki University Hospital – sequence: 8 givenname: Päivi surname: Pakarinen fullname: Pakarinen, Päivi organization: Department of Obstetrics and Gynecology, University of Helsinki, Helsinki University Hospital – sequence: 9 givenname: Heini surname: Lassus fullname: Lassus, Heini organization: Department of Obstetrics and Gynecology, University of Helsinki, Helsinki University Hospital – sequence: 10 givenname: Mikko surname: Loukovaara fullname: Loukovaara, Mikko organization: Department of Obstetrics and Gynecology, University of Helsinki, Helsinki University Hospital – sequence: 11 givenname: Ralf surname: Bützow fullname: Bützow, Ralf organization: Department of Pathology, University of Helsinki and HUSLAB, Helsinki University Hospital – sequence: 12 givenname: Olli surname: Kallioniemi fullname: Kallioniemi, Olli organization: Institute for Molecular Medicine Finland, FIMM, University of Helsinki, Science for Life Laboratory, Department of Oncology and Pathology, Karolinska Institutet – sequence: 13 givenname: Astrid surname: Murumägi fullname: Murumägi, Astrid organization: Institute for Molecular Medicine Finland, FIMM, University of Helsinki – sequence: 14 givenname: Daniela surname: Ungureanu fullname: Ungureanu, Daniela email: daniela.ungureanu@helsinki.fi organization: Faculty of Medicine and Health Technology, Tampere University, Applied Tumor Genomics Research Program, Faculty of Medicine, University of Helsinki |
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Title | Glucocorticoids induce differentiation and chemoresistance in ovarian cancer by promoting ROR1-mediated stemness |
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