Abstract
Aim. Sirtuin 1 (SIRT1) can induce autophagy through deacetylation of Beclin-1 and other autophagy mediators. However, the relationship between SIRT1 and autophagy in GC has not been defined. Therefore, the aim of this study was to confirm the prognostic value of SIRT1 and Beclin-1 and their relationship in GC patients. Methods. Transmission electron microscopy (TEM) was performed to examine the autophagy in GC patients. Immunohistochemistry was used to examine the expression of SIRT1, Beclin-1 in GC, and adjacent nonneoplastic mucosa. Results. In 7 out of 8 GC patients' samples examined by TEM, more autophagic vesicles were observed in GC tissues compared to adjacent nonneoplastic mucosa tissue. A positive correlation between SIRT1 and Beclin-1 expression was observed. Furthermore, Beclin-1 or SIRT1 expression alone or their combined expression were significantly correlated with advanced clinicopathological parameters. High Beclin-1 and SIRT1 expression alone and their combined high expression predicted shorter overall survival and relapse-free survival. Both high Beclin-1 and SIRT1 expressions were independent prognostic factors for poor survival of GC. Conclusions. Based on our results we can conclude that SIRT1 and Beclin-1 expression alone or in combination can be used as prognostic indicator and may represent new therapeutic targets in GC.
Highlights
Gastric cancer (GC) is the fourth most common cancer and the third leading cause of cancer-related deaths worldwide [1]
To determine whether the level of autophagy was different in GC compared to adjacent nonneoplastic mucosa (NNM) tissues, we have examined the number of autophagic vesicles in tissues of 8 GC patients (Figure 1(a)) using Transmission electron microscopy (TEM)
In 7 out of 8 GC patients, a higher number of autophagic vesicles were present in GC tissue compared to adjacent NNM tissue (Figure 1(b), p < 0.01)
Summary
Gastric cancer (GC) is the fourth most common cancer and the third leading cause of cancer-related deaths worldwide [1]. Autophagy is a cellular degradation and recycling process by which cells dispose of superfluous or nonfunctional components. These components are sent to the lysosome for degradation and new substrates for energy generation and biosynthesis are generated through this process [3]. It has been shown that autophagy may have a dual role depending upon specific physiological conditions. Autophagy can result in cell survival or can induce cell death during tumorigenesis and/or therapy [4]. In GC, anticancer drugs, which induce autophagy, can both suppress [5] or promote tumor cell growth [6]. The role of autophagy in the progression of GC is still poorly understood
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