CCN1 sensitizes esophageal cancer cells to TRAIL-mediated apoptosis
Abstract TRAIL is one of the best anti-cancer molecules in our body. It kills a variety of cancer cells that are resistant to conventional chemotherapy, without causing much negative impact on normal cells, because its death receptors are almost exclusively found on cancer cells. However, some cancer cells are not sensitive to TRAIL treatment, even though they express its death receptors. A second molecule is needed to help TRAIL to complete its mission. Finding such molecules now becomes a top priority in cancer research. Our study shows that CCN1 is such a molecule. CCN1 was highly expressed in the esophageal epithelium of the patients suffering from gastroesophageal reflux disease, but faded away as the situation worsened towards adenocarcinoma. Treating the tumor cells with CCN1 resulted in apoptosis, while the same treatment to the normal cells only nourished cell growth. It was TRAIL that mediated this process. Apparently, CCN1 altered the expression profile of TRAIL and its receptors in tumor cells, namely, activating TRAIL and its death receptors and shutting down its decoy receptors. CCN1 and TRAIL worked as a team to put the cancer cells to death, as elimination of either one failed apoptosis. Highlights EAC cells express all three decoy receptors of TRAIL. CCN1 is barely detectable in EAC cells. CCN1 inhibits expression of TRAIL decoy receptors in EAC cells. CCN1 induces apoptosis in EAC cells. TRAIL mediates CCN1-induced EAC cell apoptosis. Graphical abstract [DISPLAY OMISSION]
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