title: Mechanisms underlying cancer growth and apoptosis by DEK overexpression in colorectal cancer.
abstract: Our previous study indicated that DEK protein was overexpressed in colorectal carcinoma (CRC) compared with the normal colorectal mucosa. DEK was also significantly correlated with the prognostic characteristics of patients with CRC, demonstrating that DEK played an important role in CRC progression. In this work, we evaluate the effects of DEK on biological behaviors in CRC and explore the related molecular mechanisms. The results showed that DEK was overexpressed in human CRC tissues, and was correlated with the Ki-67 index and the apoptotic index. DEK depletion by RNAi in SW-620 and HCT116 cells significantly decreased cell proliferation, but increased cell apoptosis. Upregulation of DEK was involved in the p53/MDM, Bcl-2 family, and caspase pathways. Our study demonstrates that DEK promotes the growth of CRC, and could be a therapeutic target in CRC.
authors.affiliation: Department of Pathology & Cancer Research Center, Yanbian University Medical College, Yanji, China; Department of Medical Imaging, College of Medicine, Eastern Liaoning University, Dandong, China.
authors.forename: Lijuan
authors.initials: L
authors.lastname: Lin
authors.affiliation: Department of Pathology & Cancer Research Center, Yanbian University Medical College, Yanji, China.
authors.forename: Junjie
authors.initials: J
authors.lastname: Piao
authors.affiliation: Department of Pathology, Dandong Centre Hospital, Dandong, China.
authors.forename: Yibing
authors.initials: Y
authors.lastname: Ma
authors.affiliation: Department of Pathology & Cancer Research Center, Yanbian University Medical College, Yanji, China.
authors.forename: Tiefeng
authors.initials: T
authors.lastname: Jin
authors.affiliation: The Key Laboratory of Pathobiology, Ministry of Education, Bethune Medical College, Jilin University, Changchun, China.
authors.forename: Chengshi
authors.initials: C
authors.lastname: Quan
authors.affiliation: Department of Pathology & Cancer Research Center, Yanbian University Medical College, Yanji, China.
authors.forename: Jienan
authors.initials: J
authors.lastname: Kong
authors.affiliation: The Key Laboratory of Pathobiology, Ministry of Education, Bethune Medical College, Jilin University, Changchun, China.
authors.forename: Yulin
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Pathology & Cancer Research Center, Yanbian University Medical College, Yanji, China.
authors.forename: Zhenhua
authors.initials: Z
authors.lastname: Lin
mesh_terms: D017209:Apoptosis; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D002868:Chromosomal Proteins, Non-Histone / Q000378:metabolism*; D015179:Colorectal Neoplasms / Q000201:enzymology* / Q000473:pathology*; D018450:Disease Progression; D020869:Gene Expression Profiling; D045325:HCT116 Cells; D006801:Humans; D007150:Immunohistochemistry; D007413:Intestinal Mucosa / Q000473:pathology; D019394:Ki-67 Antigen / Q000378:metabolism; D008856:Microscopy, Fluorescence; D015513:Oncogene Proteins / Q000378:metabolism*; D000075223:Poly-ADP-Ribose Binding Proteins; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D034741:RNA, Small Interfering / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: C000595707:BCL2 protein, human; D002868:Chromosomal Proteins, Non-Histone; C084738:DEK protein, human; D019394:Ki-67 Antigen; D015513:Oncogene Proteins; D000075223:Poly-ADP-Ribose Binding Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D034741:RNA, Small Interfering; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53