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COPT& TRAIN-PRO-N.DRIVER-ESC-GUIDA.ISDN-AM.DRIVER.DIM2.PRODS.CHE.GUEVARA-TRAIN.CHE.GUEVARA.ROCAKE.GUEVARA.PLUS.1.60.CRACKDVD.ENG..one.0199104.ref045]\]. One study to map protein-protein interactions of CHD6 in CTD-complex demonstrated the colocalization of CHD6 and other CTD-complex proteins TLE1/TLE3 in discrete nuclear foci. It was assumed that this might represent the subnuclear localization of the entire CTD-complex \[[@pone.0199104.ref046]\].
In our study, many cancer-related genes have been regulated in SW620 in response to knockdown of CHD6. We provide evidence that CHD6 plays an important role in the growth and survival of colon cancer cells by regulating the expression of a range of genes. We show that CHD6 expression is reduced in CRC samples compared to normal colon. Furthermore, we identify unique target genes that are most likely to be drivers of its oncogenic function, including DYRK1A and HRAS. DYRK1A, a key regulator of cell-cycle progression, was recently identified as a novel oncogene in CRC \[[@pone.0199104.ref047]\]. Its expression was elevated in CRC tissues compared to normal colon and colorectal adenoma. The increased protein levels of DYRK1A were correlated with depth of invasion, which resulted in prolonged survival of patients. Furthermore, the knockdown of DYRK1A inhibited the proliferation of CRC cells by induction of a G0/G1 cell-cycle arrest. HRAS was identified as a candidate oncogene in CRC by overexpression experiments. HRAS induces a G1 arrest through p16INK4a in CRC cell lines, and transcriptional profiling of HRAS-dependent cell lines showed its effects on cell-cycle regulation \[[@pone.0199104.ref048]\]. In contrast to our results, a recent study showed that the oncogenic effects of HRAS depend on the C-terminal activation loop phosphorylation by PLCgamma-mediated signaling, but not on its transcriptional activity \[[
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