Posted: Wednesday, February 2, 2022
Researchers have identified a novel gene signature that may help predict prognosis, immune microenvironment, and chemotherapy sensitivity in patients with bladder cancer, according to a study published in the journal Human Genomics. Fu et al, of the First Affiliated Hospital of Nanchang University, China, used the Cancer Genome Atlas database to study differences in the expression of unfolded protein response–related (UPR) genes in bladder cancer samples and normal bladder samples.
“[Unfolded protein response] plays a critical role in the occurrence and progression of tumors. Our study demonstrated the value of a set of UPR genes as a prognostic biomarker in [bladder cancer],” the study authors stated.
The researchers analyzed the expression of 251 UPR genes from the UALCAN database in bladder cancer and normal bladder tissue samples. Of those samples, 44 were differentially expressed in bladder cancer. Examination of mRNA expression and promoter methylation level of seven UPR genes revealed that four of them were increased in cancer tissues compared with normal bladder tissues, whereas three were decreased in cancer tissues compared with normal bladder tissues.
The researcher discovered that these seven UPR genes correlated with disease progression and outcomes of patients with bladder cancer and could therefore be considered a prognostic signature for survival, with patients categorized into high-risk and low-risk groups. By using the Genomics of Drug Sensitivity database to estimate the half maximal inhibitory concentration of common chemotherapy drugs, the researchers found that patients with high-risk scores tended to be more sensitive to certain drugs than patients with low-risk scores.
By establishing and validating a risk model based on the seven UPR genes identified in the study, the researchers believe that these genes may have reliable potential for clinical application in the treatment of bladder cancer.
Disclosure: The study authors reported no conflicts of interest.