| Note | |
| Entity | Various carcinomas and melanoma |
| Note | RPS27 overexpression has been reported in many cancers including prostate cancer (Fernandez-Pol et al., 1997), colorectal cancer (Ganger et al., 1997), liver cancer (Ganger et al., 2001), breast cancer (Atsuta et al., 2002), head and neck squamous cell cancer (HNSCC) (Stack et al., 1999; Stack et al., 2004; Lee et al., 2004), gastric cancer (Wang, et al., 2006), as well as, melanoma (Santa Cruz et al., 1997).
Since high serum levels of RPS27 have been found in cancer patients, especially in head and neck squamous cell carcinoma (HNSCC), the protein can be used as a tumor marker (Fernandez-Pol et al., 1996; Lee et al., 2004; Stack et al. 2004). |
| Prognosis | It was reported that RPS27 levels correlate with tumor stage in patients with gastric cancer, thus high levels serve as a poor prognostic indicator (Wang et al., 2006). |
| Oncogenesis | The mechanism behind RPS27 overexpression is currently under investigation. One explanation recently offered arises from the relationship between RPS27, MDM2 and p53: RPS27 is a p53 repressible protein (He and Sun, 2007; Li et al., 2007). A 2011 study found that it competes with p53 for a central acidic binding domain on MDM2. Once bound, MDM2 is stimulated to ubiquinate and degrade the RPS27 or p53, whichever it is bound to. When RPS27 levels are elevated, it can out-compete p53 for MDM2 binding and subsequent degradation, thus stabilizing p53 levels. This would be an appropriate cellular response to genotoxic stress. The same study also found that mutant p53 cannot suppress RPS27, only the wild-type can. Since mutated p53 is found in almost 50% of all human cancers, RPS27 overexpression logically follows. Furthermore, stabilization of mutant p53 levels associated with RPS27 abundance could provide malignant cells with a growth advantage (Xiong et al., 2011).
RPS27 knockdown was found to enhance spontaneous apoptosis of tumor cells via caspase-3 activation (Wang et al., 2006; Yang et al., 2011).
HNSCC: some have questioned if RPS27 overexpression is the cause or result of cancer. A 2010 study overexpressed RPS27 in a line of HNSCC cells to study the impact on tumor behavior. They found that RPS27 overexpression resulted in reduced cancer cell growth, proliferation rate and angiogenesis. RPS27 overexpression was also found to reduce the mRNA of Paxillin, a focal adhesion protein up regulated in HNSCC and many other cancer cells. RPS27 induced Paxillin repression offers a possible explanation for the decreased HNSCC growth (Dai et al., 2010). |
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