Virtual Library

Start Your Search

Q. Zhang



Author of

  • +

    P1.03 - Chemotherapy/Targeted Therapy (ID 689)

    • Event: WCLC 2017
    • Type: Poster Session with Presenters Present
    • Track: Chemotherapy/Targeted Therapy
    • Presentations: 1
    • +

      P1.03-017 - Benzyl Isothiocyanate Induces Protective Autophagy in Human Lung Cancer Cells through Endoplasmic Reticulum Stress-Mediated Mechanism (ID 7882)

      09:30 - 09:30  |  Author(s): Q. Zhang

      • Abstract

      Background:
      Benzyl isothiocyanate (BITC) inhibits the growth of various human cancer cells, however, the mechanism underlying growth inhibitory effect of BITC is not fully understood. In the present study, we investigated the effect of BITC on autophagy induction in human lung cancer cells in vitro and in vivo.

      Method:
      Autophagy was characterized by detection of the formation of acidic vesicular organelles (AVOs), the accumulation of microtubule-associated protein 1 light chain 3-II (LC3-II), the punctuate pattern of LC3, and expression of Atg5. Endoplasmic reticulum (ER) stress was determined by measurement of cytosolic calcium level, and phorphorylation of ER stress marker proteins PERK and eIF2α. The effect of BITC on lung tumor growth was examined by lung cancer cell xenograft experiments.

      Result:
      Our data showed that BITC inhibited the growth of human lung cancer cells. BITC induced autophagy in lung cancer cells, pretreatment with autophagy inhibitor 3-MA enhanced the inhibitory effect of BITC. ER stress was also caused by BITC, suppression of ER stress by ER stress inhibitor 4-PBA attenuated autophagy induction, and further potentiated the cell growth inhibition by BITC. Xenograft experiments showed that BITC inhibited lung tumor growth in vivo, and induced both autophagy and ER stress in lung tumor cells.

      Conclusion:
      Our results indicated that BITC inhibits lung cancer cell growth both in vitro and in vivo. BITC induces autophagy in lung cancer cells, and autophagy plays a protective role in the inhibition effect of BITC. The autophagy induction is mediated by ER stress response.