Format

Send to

Choose Destination
J Cell Commun Signal. 2018 Mar;12(1):83-90. doi: 10.1007/s12079-017-0438-y. Epub 2017 Dec 7.

Assessment of TANK-binding kinase 1 as a therapeutic target in cancer.

Author information

1
Cancer Biology Graduate Program, Hamon Center for Therapeutic Oncology Research and Department of Surgery, UT Southwestern Medical Center, 6000 Harry Hines Blvd., Dallas, TX, 75390-8593, USA.
2
Cancer Biology Graduate Program, Hamon Center for Therapeutic Oncology Research and Department of Surgery, UT Southwestern Medical Center, 6000 Harry Hines Blvd., Dallas, TX, 75390-8593, USA. rolf.brekken@utsouthwestern.edu.
3
Department of Pharmacology, UT Southwestern Medical Center, Dallas, TX, USA. rolf.brekken@utsouthwestern.edu.

Abstract

TANK-binding kinase 1 (TBK1) is central to multiple biological processes that promote tumorigenesis including cell division, autophagy, innate immune response and AKT-pro survival signaling. TBK1 is well studied and most known for its function in innate immunity. However, the serine threonine protein kinase received significant attention as a synthetic lethal partner and effector of the major oncogene, RAS. This review summarizes newly identified cancer promoting functions of TBK1 and evaluates the therapeutic potential of targeting TBK1 in cancer.

KEYWORDS:

Autophagy; Cancer therapeutic target; Pancreatic cancer; RAS; TBK1

Supplemental Content

Full text links

Icon for Springer Icon for PubMed Central
Loading ...
Support Center