American Association for Cancer Research
15357163mct160915-sup-176629_2_unknown_upload_4035089_kpk253.docx (21.96 kB)

Supplementary Table 5 from Dual Inhibition of NOX2 and Receptor Tyrosine Kinase by BJ-1301 Enhances Anticancer Therapy Efficacy via Suppression of Autocrine-Stimulatory Factors in Lung Cancer

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journal contribution
posted on 2023-04-03, 15:51 authored by Jaya Gautam, Jin-Mo Ku, Sushil Chandra Regmi, Hyunyoung Jeong, Ying Wang, Suhrid Banskota, Myo-Hyeon Park, Tae-gyu Nam, Byeong-Seon Jeong, Jung-Ae Kim

The Absolute mRNA expression (Ct andã…¿Ct values*) of NOX isoforms and regulatory subunits in A549 and H1299 cells


National Research Foundation of Korea (NRF)



NADPH oxidase–derived reactive oxygen species (ROS) potentiate receptor tyrosine kinase (RTK) signaling, resulting in enhanced angiogenesis and tumor growth. In this study, we report that BJ-1301, a hybrid of pyridinol and alpha-tocopherol, exerts anticancer effects by dual inhibition of NADPH oxidase and RTK activities in endothelial and lung cancer cells. BJ-1301 suppresses ROS production by blocking translocation of NADPH oxidase cytosolic subunits to the cell membrane, thereby inhibiting activation. The potency of RTK inhibition by BJ-1301 was lower than that of sunitinib (a multi-RTK inhibitor), but the inhibition of downstream signaling pathways (e.g., ROS generation) and subsequent biological changes (e.g., NOX2 induction) by BJ-1301 was superior. Consistently, BJ-1301 inhibited cisplatin-resistant lung cancer cell proliferation more than sunitinib did. In xenograft chick or mouse tumor models, BJ-1301 inhibited lung tumor growth, to an extent greater than that of sunitinib or cisplatin. Treatments with BJ-1301 induced regression of tumor growth, potentially due to downregulation of autocrine-stimulatory ligands for RTKs, such as TGFα and stem cell factor, in tumor tissues. Taken together, the current study demonstrates that BJ-1301 is a promising anticancer drug for the treatment of lung cancer. Mol Cancer Ther; 16(10); 2144–56. ©2017 AACR.