A comparison of EphA3 immunohistochemical scores for tumor and matched normal intestinal tissues revealed that the protein was downregulated in 82/164 (50.0%), unchanged in 52/164 (31.7%), and upregulated in 30/164 (18.3%) cases of CRC.
Our findings reveal the mechanisms underlying the oncogenic activities of EphA3 in colorectal cells, which could provide novel targets for the prevention, early diagnosis, and treatment of colorectal cancer.
We report here a thorough study to address the physiological role of the putative lung cancer tumor suppressor EPH receptor A3 (EPHA3), a gene that is frequently mutated in human lung adenocarcinomas.
Moreover, EPHA3 gene copy numbers and/or expression levels were decreased in tumors from large cohorts of patients with lung cancer (eg, the gene was deleted in 157 of 371 [42%] primary lung adenocarcinomas).
A comparison of EphA3 immunohistochemical scores for tumor and matched normal intestinal tissues revealed that the protein was downregulated in 82/164 (50.0%), unchanged in 52/164 (31.7%), and upregulated in 30/164 (18.3%) cases of CRC.
The isolated compounds were evaluated for their cancer chemopreventive potential by using quinone reductase induction and nuclear factor-kappa B inhibition tests in Hepa 1c1c7 and HEK-293/NF-<i>κ</i>B-Luc cells, respectively.