고려대학교 혈액종양내과 의국입니다.

고려대학교 암 연구소(http://www.kucancer.org)가 주최하는 2019년 3월 세미나 일정을 안내합니다.

* 일시 : 2019년 3월 13일 (수) 오후 12시

* 장소 : 고려대학교 의과대학 문숙의학관 1층 윤병주홀

* 연자 : 송 나 영 교수님

* 소속 : 연세대학교

* 주제 : Role of IKKα in Microenvironment and Its Impact on Pathogenesis.

ABSTRACT:

The IκB kinase (IKK) complex, composed of IKKα, IKKβ, and NEMO (IKKγ), is essential for the activation of NF-κB. IKKα regulates canonical and noncanonical NF-κB signaling as well as NF-κB–independent functions. My research interest is the role of IKKα in tumorigenesis, particularly via regulation of tumor microenvironment, in terms of oxidative stress, immune system and microbiome. Recently, I have found that IKKα plays a crucial role in Kras-driven lung adenocarcinoma development. Disruption of lung epithelial IKKα leads to oxidative stress by producing reactive oxygen species (ROS) while inhibiting antioxidant gene expression, which contributes to cell proliferation and helps Kras-driven lung adenocarcinomas to escape from senescence. In addition to tumor intrinsic oxidative stress, lung epithelial IKKα loss increases accumulation of ROS in tumor-associated macrophages which promotes induction of regulatory T cells, creating an immunosuppressive microenvironment. Taken together, these data suggest that IKKα is a tumor suppressor in lung adenocarcinoma development by regulating major redox signals and immune responses. Then, my research focus has moved toward a relationship between IKKα and microbiome, due to that IKKα is crucial for integrity of epithelium where microbes thrive. I have found that epithelial IKKα loss can provoke bacterial-fungal symbiosis which contributes to tumor promotion. My talk will cover the crosstalk between epithelial IKKα and bacterial-fungal interaction in more details.

REFERENCE:
Song, N.-Y., … Karin, M., Hu, Y. IKKα inactivation promotes Kras-initiated lung adenocarcinoma development through disrupting major redox regulatory pathways. PNAS. 115(4):E812-E821, 2018.