Introduction Autophagy is a physiological cellular process for degradation and recycle of useless proteins, however it maintains survival of cancer cells with defects in apoptosis. This study aimed to evaluate autophagy status and the clinical significance in serous ovarian carcinoma (SOC).
Methods Tissue microarray including 72 SOC, 10 serous adenoma, and 13 borderline serous tumors was used for immunohistochemical analysis. Immunoreactivity of LC3, Beclin-1, p62 and TFEB were semi-quantitatively scored. Clinicopathological parameters were obtained from medical records. Kaplan-Meier estimate and the Cox regression were used for survival analysis.
Results LC3 and TFEB were present in 31.9% and 20.8% of SOC. Beclin-1 and p62 were significantly upregulated in SOC compared with controls (70.8% and 95.8%; p = 0.03 and p < 0.001, respectively). Significant correlation was observed among LC3, Beclin-1 and p62. A simultaneous accumulation of Beclin-1 and p62 represents coexistence of induction and last stage of autophagy, suggesting autophagy activation with impairment of autophagy flux. In univariate analysis, the presence of TFEB, suboptimality, advanced FIGO stage, and chemoresistance were significantly associated with worse disease-free survival and overall survival (OS). Multivariate analysis showed that surgical optimality and chemoresistance were independent predictor for OS. The expressions of p62 and TFEB were positively correlated with FIGO stage (p = 0.017 and p = 0.015, respectively) and Beclin-1 expression was lower in high-grade tumor than low-grade tumor (p = 0.001).
Conclusion/Implications A dysregulation of autophagy was found in SOC. Beclin-1, p62 and TFEB were associated with aggressiveness and poor prognosis of SOC.
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