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AS01. Basic/Translational science
PR002/#853  Catecholamines promote ovarian cancer progression through secretion of CXC-chemokines
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  1. Ha Kyun Chang1,
  2. Hyun Jung Kim2,
  3. Sung Jong Lee3 and
  4. Kyun Heo2
  1. 1Korea University Ansan Hostpital, Department of Obstetrics and Gynecology, Ansan, Korea, Republic of
  2. 2Kookmin University, Department of Biopharmaceutical Chemistry, Seoul, Korea, Republic of
  3. 3Seoul St. Mary’s Hospital, Obstetrics and Gynecology, Seoul, Korea, Republic of

Abstract

Introduction Catecholamines such as adrenaline (epinephrine) and noradrenaline (norepinephrine) are hormones that play a critical role in the body’s ‘fight or flight’ response, which is the physiological response to stress. Considerable evidence has accumulated in the last decade to support the notion that chronic stress is closely related to the growth, metastasis, and angiogenesis of ovarian cancer. The purpose of this study was to identify factors that increase the progression of ovarian cancer and to determine the possibility of inhibiting ovarian cancer progression using novel therapeutics.

Methods In this study, we analyzed the conditioned media in SKOV3 ovarian cancer cell line treated with catecholamine to identify secreted proteins responding to chronic stress.

Results We observed that epinephrine and norepinephrine enhanced the secretion and mRNA expression of CXC-chemokines (CXCL1, 2, 3, and 8). Neutralizing antibody to CXCL8 and CXCL8 receptor (CXCR2) inhibitors significantly reduced catecholamine-mediated invasion of SKOV3 cells. Finally, we found that the concentration of CXCL1 and CXCL8 in the plasma of ovarian cancer patients increased with stage progression.

Conclusion/Implications Therefore, not only can CXCL1 and CXCL8 be used as diagnostic markers for ovarian cancer, but their inhibition also holds promise as a potential therapeutic option for suppressing ovarian cancer progression. Taken together, these findings suggest that stress-related catecholamines may influence ovarian cancer progression through the secretion of CXC-chemokines.

Abstract PR002/#853 Figure 1
Abstract PR002/#853 Figure 1
Abstract PR002/#853 Figure 2
Abstract PR002/#853 Figure 2

https://doi.org/10.1136/ijgc-2023-IGCS.45

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