Published online Nov 28, 2023. doi: 10.3748/wjg.v29.i44.5919
Peer-review started: July 20, 2023
First decision: October 9, 2023
Revised: October 23, 2023
Accepted: November 14, 2023
Article in press: November 14, 2023
Published online: November 28, 2023
Processing time: 130 Days and 2.8 Hours
The role of Tousled-like kinase 1 (TLK1) in in gastric cancer (GC) remains unclear.
To investigate the expression, biological function, and underlying mechanisms of TLK1 in GC.
We measured TLK1 protein expression levels and localized TLK1 in GC cells and tissues by western blot and immunofluorescence, respectively. We transfected various GC cells with lentiviruses to create TLK1 overexpression and knockdown lines and established the functional roles of TLK1 through in vitro colony formation, 5-ethynyl-2`-deoxyuridine, and Transwell assays as well as flow cytometry. We applied bioinformatics to elucidate the signaling pathways associated with TLK1. We performed in vivo validation of TLK1 functions by inducing subcutaneous xenograft tumors in nude mice.
TLK1 was significantly upregulated in GC cells and tissues compared to their normal counterparts and was localized mainly to the nucleus. TLK1 knockdown significantly decreased colony formation, proliferation, invasion, and migration but increased apoptosis in GC cells. TLK1 overexpression had the opposite effects. Bioinformatics revealed, and subsequent experiments verified, that the tumor growth factor-beta signaling pathway was implicated in TLK1-mediated GC progression. The in vivo assays confirmed that TLK1 promotes tumorigenesis in GC.
The findings of the present study indicated that TLK1 plays a crucial role in GC progression and is, therefore, promising as a therapeutic target against this disease.
Core Tip: We demonstrated that Tousled-like kinase 1 (TLK1) is highly expressed in gastric cancer (GC), localized mainly to the nucleus, significantly promotes GC cell proliferation, invasion, and migration, and inhibits apoptosis. TLK1 may facilitate GC progression by modulating tumor growth factor-beta expression. We believe that TLK1 could be a crucial therapeutic target for GC, and propose that future investigations evaluate the feasibility and practicality of targeting TLK1 in GC treatment.