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FCN3 functions as a tumor suppressor of lung adenocarcinoma through induction of endoplasmic reticulum stress.
Jang, Haeyeon; Jun, Yukyung; Kim, Suyeon; Kim, Eunjeong; Jung, Yeonjoo; Park, Byung Jo; Lee, Jinseon; Kim, Jhingook; Lee, Sanghyuk; Kim, Jaesang.
Afiliación
  • Jang H; Department of Life Science, Ewha Womans University, Seoul, Republic of Korea.
  • Jun Y; Ewha Research Center for Systems Biology, Ewha Womans University, Seoul, Republic of Korea.
  • Kim S; Ewha-JAX Cancer Immunotherapy Research Center, Seoul, Republic of Korea.
  • Kim E; Center for Supercomputing Applications, Division of National Supercomputing, Korea Institute of Science and Technology Information, Daejeon, Republic of Korea.
  • Jung Y; Department of Life Science, Ewha Womans University, Seoul, Republic of Korea.
  • Park BJ; Ewha Research Center for Systems Biology, Ewha Womans University, Seoul, Republic of Korea.
  • Lee J; Department of Life Science, Ewha Womans University, Seoul, Republic of Korea.
  • Kim J; Ewha Research Center for Systems Biology, Ewha Womans University, Seoul, Republic of Korea.
  • Lee S; Department of Life Science, Ewha Womans University, Seoul, Republic of Korea.
  • Kim J; Ewha Research Center for Systems Biology, Ewha Womans University, Seoul, Republic of Korea.
Cell Death Dis ; 12(4): 407, 2021 04 15.
Article en En | MEDLINE | ID: mdl-33859174
ABSTRACT
In this study, we report a novel function of FCN3 (Ficolin 3), a secreted lectin capable of activating the complement pathway, as a tumor suppressor of lung adenocarcinoma (LUAD). First, the expression of FCN3 was strongly down-regulated in cancer tissues compared to matched normal lung tissues, and down-regulation of FCN3 was shown to be significantly correlated with increased mortality among LUAD patients. Interestingly, while ectopic expression of FCN3 led to cell cycle arrest and apoptosis in A549 and H23 cells derived from LUAD, the secreted form of the protein had no effect on the cells. Rather, we found evidence indicating that activation of the unfolded protein response from endoplasmic reticulum (ER) stress is induced by ectopic expression of FCN3. Consistently, inhibition of ER stress response led to enhanced survival of the LUAD cells. Of note, the fibrinogen domain, which is not secreted, turned out to be both necessary and sufficient for induction of apoptosis when localized to ER, consistent with our proposed mechanism. Collectively, our data indicate that FCN3 is a tumor suppressor gene functioning through induction of ER stress.
Asunto(s)

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Estrés del Retículo Endoplásmico / Adenocarcinoma del Pulmón / Lectinas / Neoplasias Pulmonares Límite: Animals / Female / Humans Idioma: En Revista: Cell Death Dis Año: 2021 Tipo del documento: Article

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Estrés del Retículo Endoplásmico / Adenocarcinoma del Pulmón / Lectinas / Neoplasias Pulmonares Límite: Animals / Female / Humans Idioma: En Revista: Cell Death Dis Año: 2021 Tipo del documento: Article