Anti-ERCC6L (full length) polyclonal antibody

Excision repair cross-complementation group 6 like (ERCC6L), a recently discovered DNA helicase, has been demonstrated to be highly expressed in a variety of human cancer types. However, the precise role of ERCC6L in colorectal cancer (CRC) remains unclear. The current study aimed to investigate the potential role of ERCC6L in the development and progression of CRC. Reverse transcription-quantitative polymerase chain reaction, western blot analysis and immunohistochemistry were used to detect the expression level of ERCC6L in 30 matched pairs of CRC and adjacent noncancerous tissues. The function of ERCC6L in cell proliferation, cycle, apoptosis, invasion and colony formation was examined in CRC cell lines. ERCC6L was revealed to be highly expressed in CRC tissues and cell lines compared with normal controls (P<0.05). The expression level of ERCC6L was significantly associated with tumor size (P<0.05), but not with other clinical features, including age, gender, differentiation and clinical stage. It was identified that reducing ERCC6L expression using small interfering RNA significantly inhibited the proliferation and colony-forming ability of CRC cell lines. Flow cytometric analysis demonstrated that ERCC6L knockdown in CRC cells inhibited cell cycle progression and increased the number of cells in the G0/G1 phase without affecting apoptosis. Furthermore, ERCC6L knockdown markedly decreased the number of invading CRC cells compared with control cells. These results suggest that ERCC6L promotes the growth and invasion of CRC cells, and ERCC6L may be a potential new target for cancer therapy.

Accurate duplication and transmission of identical genetic information into offspring cells lies at the heart of a cell division cycle. During the last stage of cellular division, namely mitosis, the fully replicated DNA molecules are condensed into X-shaped chromosomes, followed by a chromosome separation process called sister chromatid disjunction. This process allows for the equal partition of genetic material into two newly born daughter cells. However, emerging evidence has shown that faithful chromosome segregation is challenged by the presence of persistent DNA intertwining structures generated during DNA replication and repair, which manifest as so-called ultra-fine DNA bridges (UFBs) during anaphase. Undoubtedly, failure to disentangle DNA linkages poses a severe threat to mitosis and genome integrity. This review will summarize the possible causes of DNA bridges, particularly sister DNA inter-linkage structures, in an attempt to explain how they may be processed and how they influence faithful chromosome segregation and the maintenance of genome stability.