Abstract
Response gene to complement 32 (RGC32) is a transcription factor that regulates the expression of multiple genes involved in cell growth, viability and tissue-specific differentiation. However, the role of RGC32 in tumorigenesis and tumor progression in colorectal cancer (CRC) has not been fully elucidated. Here, we showed that the expression of RGC32 was significantly up-regulated in human CRC tissues versus adjacent normal tissues. RGC32 expression was significantly correlated with invasive and aggressive characteristics of tumor cells, as well as poor survival of CRC patients. We also demonstrated that RGC32 overexpression promoted proliferation, migration and tumorigenic growth of human CRC cells in vitro and in vivo. Functionally, RGC32 facilitated epithelial-mesenchymal transition (EMT) in CRC via the Smad/Sip1 signaling pathway, as shown by decreasing E-cadherin expression and increasing vimentin expression. In conclusion, our findings suggested that overexpression of RGC32 facilitates EMT of CRC cells by activating Smad/Sip1 signaling.
Highlights
In this study, we report that overexpression of RGC32 is related to poor overall survival in patients with Colorectal cancer (CRC)
The results indicated that the expression of RGC32 was higher in CRC tissues (C) than in adjacent normal colorectal tissues (N) (6.952 ± 1.355 versus 3.025 ± 0.7769, P < 0.05) (Fig. 1A)
The results showed that the expression of RGC32 was markedly increased in 170/183 of the CRC tissues
Summary
We report that overexpression of RGC32 is related to poor overall survival in patients with CRC. We demonstrate that RGC32 promotes cell proliferation, motility, and invasion of CRC. We speculate that up-regulation of the expression of RGC32 contributes to EMT in CRC by activating the Smad/Sip[1] signaling pathway. We suggest that RGC32 protein, a valuable CRC prognostic marker, plays an important role in the development and progression of human CRC
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