To determine the function of COX‑1 in cancer development, short hairpin RNA knockdown of COX‑1 was employed in HCT116 and HT29 CRC cells in the present study.
Apart from assigning the mechanistic role to the MT-CO1 variants and their perturbed expression in cancer development, the present study provides novel insights into the functional role of somatic mutations within MT-CO1 promoting cancer phenotype.
Patients affected by T3-T4/N0-N+/M0 GC/GEJ cancer were treated with the COI regimen for 4 cycles followed by restaging and gastroresection with D2 lymphadenectomy.
Gastrin and CCK(B)-R mRNA were detected in the cancer tissue and the resection margin and similarly COX-2 mRNA was expressed in most of cancers and their resection margin but not in intact colonic mucosa where only COX-1 was detected.
Both gastrin and CCKB-R mRNA were detected in the cancer tissue and at the resection margin and similarly COX-2 mRNA was expressed in most cancers and resection margin but not in bronchial mucosa where only COX-1 was found.
Since gastrin is recognized as a effective gastric mitogen, it could be capable to induce COX-2, a potent tumor growth promoting and angiogenic factor, we decided 1) to compare the seroprevalence of HP and its cytotoxic protein, CagA, in gastric cancer patients with those in age- and gender-matched controls; 2) to determine the gene expression of gastrin and its receptors (CCK(B)-R) in gastric cancer, 3) to assess the plasma levels, gastric lumen and tumor tissue contents of gastrin and 4) to examine the mRNA and enzyme protein expression of COX-1 and COX-2 in cancer tissue and intact gastric mucosa before and after HP eradication.
In the following article, the phenotypes of the two Ptgs (genes coding for COX-1 and COX-2) knockouts are summarized, and recent studies to investigate the effects of COX deficiency on cancer susceptibility, inflammatory response, gastric ulceration, and female reproductive processes are discussed.