Dear Colleagues,

It is my great honor to call for manuscript submissions to a Special Issue of IJMS entitled “TNIK in Cancer Progression and Therapeutic Opportunities”. TNIK (Traf2- and Nck-interacting kinase) was originally identified as a new member of the germinal center kinase (GCK) family. TNIK is a multifunctional protein that regulates the c‐Jun N‐terminal kinase (JNK) and nuclear factor‐κB (NF‐κB) signaling pathways. However, its transcriptional co-activator function with Wnt/β-catenin signal target genes is now attracting the broader attention of academic and industrial researchers. Colorectal cancer cells are highly dependent on the expression of TNIK for proliferation. Tnik-deficient mice are resistant to colon tumorigenesis. The TNIK gene is localized in chromosome region 3q26, where gene amplification often occurs in various cancers. Increased TNIK expression is associated with poor outcomes in patients with hepatocellular, colorectal, and pancreatic cancers. Various TNIK inhibitors with different chemical structures are now under preclinical development aimed at clinical application. Therefore, I think it is timely to summarize current knowledge of this fascinating, but mysterious, protein kinase.

Original and review articles dealing with the basic and translational aspects of TNIK are all welcome. We look forward to hearing from you.

Dr. Tesshi Yamada
Guest Editor

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• TNIK
• Wnt signaling
• β-catenin
• cancer
• gene amplification
• therapeutics