4.5 Article

Correlation of SATB1 overexpression with the progression of human rectal cancer

Journal

INTERNATIONAL JOURNAL OF COLORECTAL DISEASE
Volume 27, Issue 2, Pages 143-150

Publisher

SPRINGER
DOI: 10.1007/s00384-011-1302-9

Keywords

Special AT-rich sequence-binding protein 1; Human rectal cancer; Quantitative real-time PCR; Immunohistochemistry; KM12C cell lines

Funding

  1. National Natural Science Foundation of China [30830100]
  2. Ph.D. Programs Foundation of the Ministry of Education of China [20080610058]

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To date, the association between special AT-rich sequence-binding protein 1 (SATB1) and colorectal cancer (CRC) has not been reported. This study was aimed at investigating the expression and potential role of SATB1 in human rectal cancers. Ninety-three paired samples of rectal cancer and distant normal rectal tissue were analyzed by quantitative real-time PCR (qRT-PCR) and immunohistochemistry (IHC), and the correlations between SATB1 expression and clinicopathological parameters were evaluated. The expression profiles of SATB1 were also investigated in a panel of five human colon carcinoma cell lines. The general level of SATB1 mRNA in rectal cancer tissues was statistically significantly higher than that in normal mucosa (P = 0.043). The rate of positive SATB1 protein expression in rectal cancers (44.1%) was significantly higher than that in normal tissues (25.8%) by IHC analysis (P = 0.009). Overexpression of SATB1 mRNA was more predominant in patients with earlier onset of rectal cancer (P = 0.033). SATB1 expression correlated with invasive depth and tumor node metastasis (TNM) stage at both protein and mRNA levels (P < 0.05). Furthermore, SATB1 expression in the poorly metastatic KM12C cells was significantly lower than the highly metastatic KM12SM and KM12L4A cells and higher than the HCT116 and SW480 cells (P = 0.001). These results were further confirmed by Western blotting. Our results indicate that SATB1 may play an important role in the progression of human rectal cancer, which represents a possible new mechanism underlying CRC.

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