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.