Published online Apr 21, 2020. doi: 10.3748/wjg.v26.i15.1775
Peer-review started: December 11, 2019
First decision: January 13, 2020
Revised: January 23, 2020
Accepted: March 19, 2020
Article in press: March 19, 2020
Published online: April 21, 2020
Processing time: 132 Days and 0.1 Hours
As a common digestive tract tumor, esophageal cancer is typically treated by radiotherapy. Poor responses to radiotherapy in most patients are prone to causing local radiotherapy failure. It is therefore essential to find new radiosensitizers to enhance the response of cancer cells to radiotherapy and increase the survival rate of esophageal cancer patients with radiation resistance. The long non-coding RNA (lncRNA) Rpph1 is highly expressed in human gastric cancer tissues, which also decreases breast cancer cell proliferation as well as tumorigenesis. In fact, the expression of lncRNA Rpph1 in esophageal cancer and its relationship with radio-sensitivity have not been thoroughly investigated.
LncRNA Rpph1 is found abnormally expressed in a variety of cancers. The possibility that Rpph1 impacts the radio-sensitivity of esophageal cancer cells requires more research.
This study was intended to reveal the value of lncRNA Rpph1 in esophageal cancer as well as its effect on cell sensitivity to radiotherapy.
We initially detected the expression of lncRNA Rpph1 in esophageal cancer tissue samples obtained surgically. Subsequently, siRNA-NC or siRNA-Rpph1 was transfected into esophageal cancer cell lines, and a blank control group was set where cells were not transfected with anything. Consequently, we analyzed the effect of Rpph1 on the biological behavior of esophageal cancer cells exposed to irradiation.
We found that Rpph1 is highly expressed in esophageal cancer. Rpph1 can be applied for the diagnosis of esophageal cancer and identify the pathological characteristics of patients. The results of 3-year survival supported patients with low Rpph1 expression over those with high Rpph1 expression (P < 0.05). Cytological studies indicated that silencing the expression of Rpph1 contributed to the enhancement of radio-sensitivity of esophageal cancer cells and cell apoptosis via regulating apoptosis-linked proteins, thus relieving the radiation-induced G2/M phase cell cycle arrest. It also helped restrain cell proliferation and migration and regulate the expression of epithelial-mesenchymal transition (EMT)-related proteins.
Rpph1 is highly expressed in esophageal cancer. Silencing Rpph1 expression has an influence on the biological behavior of tumor cells and the enhancement of radio-sensitivity.
This study revealed the value of Rpph1 in the diagnosis of esophageal cancer and concluded that silencing Rpph1 expression can enhance the radiotherapy of tumor cells, illuminating a new target for the future treatment of esophageal cancer.