Published online Dec 21, 2022. doi: 10.3748/wjg.v28.i47.6769
Peer-review started: October 12, 2022
First decision: October 20, 2022
Revised: November 5, 2022
Accepted: November 30, 2022
Article in press: November 30, 2022
Published online: December 21, 2022
Processing time: 67 Days and 20.8 Hours
Gastric cancer (GC) is one of the most common malignant tumors with a high morbidity and mortality rate globally, especially in East Asian countries. Helicobacter pylori (H. pylori) infection is the most significant risk factor for GC. Studying their interaction can reveal the potential pathogenesis and therapeutic targets of GC.
Although substantial efforts have been done to link H. pylori infection and GC over the past decades, the molecular mechanisms of H. pylori-induced GC are not fully understood, which results in reduced treatment benefits.
The present study aimed to study the interaction of H. pylori infection, dickkopf-related protein (DKK) 1, and cytoskeleton-associated protein (CAKP) 4 in GC and the underlying molecular mechanisms.
RNA sequencing identified differentially expressed genes (DEGs) between H. pylori-infected and uninfected primary GC cells. Dual-luciferase reporter assay and co-immunoprecipitation determined the interaction of activator protein (AP)-1, DKK1 and CKAP4. Western blotting and immunohistochemistry detected the expression of DKK1, CKAP4 and phosphatidylinositol 3-kinase (PI3K) pathway-related proteins in GC cells and tissues. Functional experiments and tumorigenicity in nude mice detected the malignant behavior of GC cells in vitro and in vivo.
H. pylori infection upregulated JUN, FOSL1, DKK1 and CKAP4 expression in GC cells, H. pylori-infected gerbil gastric tissues, and human GC samples. JUN and FOSL1 formed activator protein-1 (AP-1) to transcriptionally activate DKK1. DKK1 bound to CKAP4, but not Wnt coreceptor, to promote GC cell growth, migration, invasion, and xenograft tumor growth in nude mice via activating the PI-3K/AKT/mammalian target of rapamycin (mTOR) pathway. Targeting PI3K inhibited DKK1-mediated CKAP4/PI3K signaling activity and the malignant behavior of GC cells.
H. pylori-induced AP-1 promotes the binding of DKK1 to CAKP4, which contributes to gastric tumorigenesis via the PI3K/AKT/mTOR pathway.
The findings suggest that the DKK1/CKAP4 interaction may be a therapeutic target for H. pylori-induced GC. The identification of small compounds and drugs targeting the DKK1/CKAP4 axis will be a crucial aspect of future studies. We will also investigate this possibility further.