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Abstract 1830: Role of heat shock factor 1 (HSF1) on metabolic reprogramming of T -cells

Heat shock transcription factor 1 (HSF1) is normally activated in response to a variety of environmental stressors. Higher levels of HSF1 expression has been shown in many tumor types and this is associated with poor prognosis. Previous data from our laboratory indicate that genetic inactivation of HSF1 significantly delays ERBB2-induced mammary tumorigenesis and hepatocellular carcinoma induced by chemical carcinogen in mouse models. We have also shown that HSF1 is involved in controlling cellular bioenergetics. CD8-positive T cells plays an important role in anti-tumor immunity response. Our preliminary results show that genetic inactivation of HSF1 in T-cells leads to reduced oxygen consumption rate (OCR) as well as Extracellular Acidification Rate (ECAR). We have also observed that deletion of HSF1 from T cells delayed in-vitro activation of purified CD8-positive T cells upon stimulation with anti-CD3 and anti-CD28. Above characteristics corresponds to reduced cellular glycolysis and T cell proliferation. Further studies will be directed towards exploring the effects of HSF1 deletion in T cell activation induced anti-tumor immunity. This study is supported by the NCI grants; NCICA062130 and NCICA132640. Citation Format: Bhaumik D. Pandya, Nahid M. Mivechi, Dimitrios Moskophidis. Role of heat shock factor 1 (HSF1) on metabolic reprogramming of T -cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1830.