PT - JOURNAL ARTICLE AU - OYAMA, YASUHIRO AU - NAGAO, SHINJIRO AU - NA, LIN AU - YANAI, KOSUKE AU - UMEBAYASHI, MASAYO AU - NAKAMURA, KATSUYA AU - NAGAI, SHUNTARO AU - FUJIMURA, AKIKO AU - YAMASAKI, AKIO AU - NAKAYAMA, KAZUNORI AU - MORISAKI, TAKASHI AU - ONISHI, HIDEYA TI - TrkB/BDNF Signaling Could Be a New Therapeutic Target for Pancreatic Cancer AID - 10.21873/anticanres.15205 DP - 2021 Aug 01 TA - Anticancer Research PG - 4047--4052 VI - 41 IP - 8 4099 - http://ar.iiarjournals.org/content/41/8/4047.short 4100 - http://ar.iiarjournals.org/content/41/8/4047.full SO - Anticancer Res2021 Aug 01; 41 AB - Background/Aim: Tropomyosin-related kinase B (TrkB)/brain-derived neurotrophic factor (BDNF) signaling plays a role in inducing malignant phenotypes in several aggressive types of cancers. To create a conclusive therapy targeting TrkB/BDNF signaling in solid refractory cancers, the biological significance of TrkB/BDNF signaling was analyzed in pancreatic ductal adenocarcinoma (PDAC) cells. Materials and Methods: Three PDAC cell lines were used as target cells to investigate proliferation and invasiveness. Small interfering RNA (siRNA) and the TrkB tyrosine kinase inhibitor k252a were used as TrkB/BDNF signaling inhibitors. Results: All PDAC cell lines expressed TrkB and BDNF. When TrkB and BDNF were inhibited by siRNA or k252a, the invasiveness of PANC-1 and SUIT-2 cells significantly decreased. When TrkB was inhibited by siRNA or k252a, proliferation was significantly inhibited in PDAC cells. Conclusion: TrkB/BDNF signaling may be a new therapeutic target for PDAC. Therapies targeting TrkB/BDNF signaling may be a conclusive cancer therapy for refractory solid cancer.