BACKGROUND: To evaluate the expression of chromodomain helicase/adenosine triphosphatase DNA binding protein 1-like gene (CHD1L) in colorectal carcinoma (CRC) and its clinical significance. Its oncogenic ability was also investigated. MATERIALS AND METHODS: CHD1L amplification and overexpression were detected by fluorescence in situ hybridization, real-time reverse transcriptase-polymerase chain reaction, and immunohistochemistry in 86 patients with CRC. The correlation between the clinical characteristics and prognosis was also determined. To evaluate the tumorigenic ability of CHD1L, it was cloned into expression vector pcDNA3.1(+) and transfected into CRC cell line SW1116. Next, the changes in the biologic behavior of the CRC cells, including cell proliferation, adhesion, migration, and invasion, were examined. Apoptosis and the cell cycle of the CRC cells were detected using flow cytometry. RESULTS: We have demonstrated that CHD1L is frequently amplified and overexpressed in CRC. Overexpression of CHD1L correlated with a large tumor size, deep tumor invasion, and a high histologic grade. It also conferred worse disease-free survival. CHD1L-transfected cells possessed a strong oncogenic ability, increasing the tumorigenicity in nude mice, which could be effectively suppressed by small interfering RNA against CHD1L. Functional studies showed that overexpression of CHD1L could promote G1/S-phase cells and inhibit apoptosis. CONCLUSIONS: Our results suggest that CHD1L is the target oncogene within the 1q21 amplicon and plays a pivotal role in CRC pathogenesis.
BACKGROUND: To evaluate the expression of chromodomain helicase/adenosine triphosphatase DNA binding protein 1-like gene (CHD1L) in colorectal carcinoma (CRC) and its clinical significance. Its oncogenic ability was also investigated. MATERIALS AND METHODS:CHD1L amplification and overexpression were detected by fluorescence in situ hybridization, real-time reverse transcriptase-polymerase chain reaction, and immunohistochemistry in 86 patients with CRC. The correlation between the clinical characteristics and prognosis was also determined. To evaluate the tumorigenic ability of CHD1L, it was cloned into expression vector pcDNA3.1(+) and transfected into CRC cell line SW1116. Next, the changes in the biologic behavior of the CRC cells, including cell proliferation, adhesion, migration, and invasion, were examined. Apoptosis and the cell cycle of the CRC cells were detected using flow cytometry. RESULTS: We have demonstrated that CHD1L is frequently amplified and overexpressed in CRC. Overexpression of CHD1L correlated with a large tumor size, deep tumor invasion, and a high histologic grade. It also conferred worse disease-free survival. CHD1L-transfected cells possessed a strong oncogenic ability, increasing the tumorigenicity in nude mice, which could be effectively suppressed by small interfering RNA against CHD1L. Functional studies showed that overexpression of CHD1L could promote G1/S-phase cells and inhibit apoptosis. CONCLUSIONS: Our results suggest that CHD1L is the target oncogene within the 1q21 amplicon and plays a pivotal role in CRC pathogenesis.