Background: The level of heat shock protein 60 (Hsp60) is elevated in tumor cells compared with normal prostate epithelium. Hsp60 is involved in tumor growth, invasion, and metastasis and is considered as a biomarker for cancer diagnosis and prognosis.
Aim: To study the level of antibodies against prokaryotic homolog of human Hsp60 (GroEL) in prostate cancer (PCa) patients as an additional risk marker for the prediction of biochemical recurrence after radical prostatectomy (RP).
Patients and methods: A total of 55 patients with localized and locally advanced PCa, who had undergone RP between July 2013 and May 2014 were enrolled. Level of antibodies to GroEL and human Hsp60 was determined by enzyme-linked immunosorbent assay before surgery. Serum samples of blood donors with low reactivity to GroEL and human Hsp60 were used as controls. The relationship between IgG antibodies against bacterial Hsp60 and human Hsp60 and clinicopathological features were analyzed. The biochemical recurrence (BCR) free survival rate was estimated by the Kaplan - Meier method. The univariate and multivariate Cox regression models were used to evaluate the risk factors of BCR-free survival rate.
Results: There were significant differences in anti-GroEL IgG levels between control and PCa patients while no significant differences in anti-human Hsp60 IgG levels between control and PCa patients were detected. During the follow-up period, 40/55 (72.7%) patients developed BCR. The time from surgery to BCR was from 18 to 72 months. Elevated IgG antibodies against bacterial Hsp60 in patients who had undergone RP were associated with early occurrence of biochemical relapse and lower 5-year BCR-free survival rate respectively (p < 0.001). The multivariate analysis indicated that IgG to GroEL (hazard ratio = 2.465; 95% confidence interval: 1.311-4.634, p < 0.05) could be independent prognostic factor in the patients who had developed BCR.
Conclusion: Elevated levels of IgG antibodies against GroEL before surgery can predict early occurrence of BCR after RP and can serve as an additional independent risk biomarker of a BCR after RP.