Published online Jul 15, 2021. doi: 10.4251/wjgo.v13.i7.693
Peer-review started: March 4, 2021
First decision: April 17, 2021
Revised: April 19, 2021
Accepted: June 1, 2021
Article in press: June 1, 2021
Published online: July 15, 2021
Processing time: 127 Days and 19 Hours
Cryptotanshinone (CTS) exhibits antitumor effects in a variety of tumors. Cytotoxin-associated gene A (CagA) is one of the main pathogenic factors in Helicobacter pylori (H. pylori) related gastric cancer (GC). However, the effects of CTS on CagA-induced development of GC and CagA+ H. pylori strains caused gastric mucosal lesions is unknown.
To identify the effect and mechanism of CTS on CagA associated GC.
We assessed the role of CTS in CagA induced proliferation and metastasis of GC cells, and in CagA+ H. pylori strains caused pathological changes of gastric mucosa of mice.
The proliferation and metastasis of GC cells were evaluated by CCK-8 and Transwell assays, respectively, and the expression of SHP2 and phosphorylated SHP2 was detected using western blotting. Enzyme-linked immunosorbent assay was used to determine the immunoglobulin G (IgG) level against CagA in patient serum. Mice were divided into four groups and administered H. pylori strains (CagA+ or CagA-) and CTS (or PBS) intragastrically, and the establishment of the chronic infection model was verified using polymerase chain reaction and sequencing of isolated strains. Hematoxylin and eosin staining was used to assess mucosal erosion in the stomach and toxicity to the liver and kidney.
CTS significantly inhibited the CagA-induced abnormal proliferation, migration, and invasion of GC cells. Moreover, the expression of p-SHP2 protein in tumor tissue was related to the expression of IgG against CagA in the serum of GC patients. Additionally, CTS suppressed the protein expression levels of both SHP2 and p-SHP2 in GC cells. CTS suppressed CagA+ H. pylori strain-induced mucosal erosion in the stomach of mice but had no obvious effect on the CagA- H. pylori strain group.
CTS inhibited CagA-induced proliferation and epithelial-mesenchymal transition of GC cells in vitro, and CagA+ H. pylori strains caused mucosal erosion of the stomach in vivo by decreasing the expression of SHP2 protein.
CTS might be an adjuvant agent in anti-H. pylori therapy, decreasing the incidence of H. pylori associated GC.