Trkb/bdnf signaling could be a new therapeutic target for pancreatic cancer

YASUHIRO OYAMA, SHINJIRO NAGAO, LIN NA, KOSUKE YANAI, MASAYO UMEBAYASHI, KATSUYA NAKAMURA, Shuntaro Nagai, AKIKO FUJIMURA, AKIO YAMASAKI, KAZUNORI NAKAYAMA, TAKASHI MORISAKI, HIDEYA ONISHI

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)4047-4052
Number of pages6
JournalAnticancer research
Volume41
Issue number8
DOIs
Publication statusPublished - Aug 2021

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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