Abstract
Dehydrogenase/reductase (SDR family) member 9 (DHRS9) is aberrantly expressed in colorectal cancer (CRC), but its prognostic value is unknown. The aim of the work was to investigate the prognostic significance of DHRS9 expression in CRC. We found that DHRS9 was frequently downregulated in CRC clinical samples at both the messenger RNA (mRNA) and protein levels. Decreased expression of DHRS9 was significantly correlated with increased lymph node metastasis (p = 0.032), advanced tumor–node–metastasis (TNM) stage (p = 0.021), increased disease recurrence (p = 0.001), and death (p = 0.014). Kaplan–Meier analysis indicated that low DHRS9 expression predicted poor disease-free survival (p = 0.003) and disease-specific survival (p = 0.021). Cox multivariate analysis revealed that reduced expression of DHRS9 was an independent unfavorable prognostic indicator for CRC. Furthermore, combination of DHRS9 with TNM stage was a more powerful predictor of poor prognosis than either of the two parameters alone. Our results suggest that decreased expression of DHRS9 correlates with tumor progression and may serve as a potential prognostic biomarker in CRC.
Highlights
Colorectal cancer (CRC) is one of the most commonly diagnosed cancers worldwide, with an estimated 1.4 million cases and 693,900 deaths occurring in 2012 [1]
The expression levels of Dehydrogenase/reductase (SDR family) member 9 (DHRS9) messenger RNA (mRNA) in 58 paired human CRC tissues and corresponding adjacent normal mucosa tissues were quantified by real-time quantitative polymerase chain reaction (qPCR) method
Representative staining of DHRS9 in CRC tissues is shown in Fig. 1c, and positive expression of DHRS9 was observed in the cytoplasm
Summary
Colorectal cancer (CRC) is one of the most commonly diagnosed cancers worldwide, with an estimated 1.4 million cases and 693,900 deaths occurring in 2012 [1]. Consistent with the data from the adenoma and carcinoma samples, they found that colon-cancer-derived cell lines expressed low or undetectable levels of DHRS9 and displayed poor conversion of retinol to retinoic acid when compared to normal epithelial cells. Mechanistic investigations revealed that reintroduction of the tumor suppressor adenomatous polyposis coli (APC) into the APC-deficient colon carcinoma cell line HT29 resulted in increased mRNA expression of DHRS9 via the transcription factor CDX2 [15]. Since lack of retinoic acid biosynthesis has been proposed as a mechanism contributing to the development of colon adenomas and carcinomas, we hypothesized that dysregulation of DHRS9 expression may be associated with aggressive clinical behavior of CRC. The clinical relevance of DHRS9 expression in CRC has not been investigated
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