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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| Veröffentlicht in: | Cell death & disease 2020-09, Vol.11 (9), p.790-790, Article 790 |
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| creator | Karvonen, Hanna Arjama, Mariliina Kaleva, Laura Niininen, Wilhelmiina Barker, Harlan Koivisto-Korander, Riitta Tapper, Johanna Pakarinen, Päivi Lassus, Heini Loukovaara, Mikko Bützow, Ralf Kallioniemi, Olli Murumägi, Astrid Ungureanu, Daniela |
| description | 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. |
| doi_str_mv | 10.1038/s41419-020-03009-4 |
| format | Article |
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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. 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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. 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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><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32989221</pmid><doi>10.1038/s41419-020-03009-4</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0003-4125-2522</orcidid><orcidid>https://orcid.org/0000-0002-7815-0709</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 13/89 13/95 14/34 631/67/395 631/67/71 692/699/67/70 82/29 96/1 96/106 96/31 Antibodies Biochemistry Biomedical and Life Sciences Carcinoma, Ovarian Epithelial - drug therapy Carcinoma, Ovarian Epithelial - pathology Cell Biology Cell Culture Cell Differentiation - drug effects Cell Line, Tumor Drug Resistance, Neoplasm - drug effects Female Gene Expression Regulation, Neoplastic - drug effects Glucocorticoids - metabolism Glucocorticoids - pharmacology Humans Immunology Life Sciences Neoplastic Stem Cells - drug effects Neoplastic Stem Cells - metabolism Ovarian Neoplasms - drug therapy Ovarian Neoplasms - genetics Receptor Tyrosine Kinase-like Orphan Receptors - metabolism |
| title | Glucocorticoids induce differentiation and chemoresistance in ovarian cancer by promoting ROR1-mediated stemness |
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