@Article{096504017X14835311718295,
AUTHOR = {Huimin Wang, Hexin Chen, Hang Zhou, Wenfa Yu, Zhenmin Lu},
TITLE = {Cyclin-Dependent Kinase Inhibitor 3 Promotes Cancer Cell Proliferation  and Tumorigenesis in Nasopharyngeal Carcinoma by Targeting p27},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {9},
PAGES = {1431--1440},
URL = {http://www.techscience.com/or/v25n9/56928},
ISSN = {1555-3906},
ABSTRACT = {Nasopharyngeal carcinoma (NPC) is a common malignancy of the head and neck that arises from the nasopharynx epithelium and is highly invasive. Cyclin-dependent kinase inhibitor 3 (CDKN3) belongs to the dualspecificity protein phosphatase family, which plays a key role in regulating cell division. Abnormal expression 
of CDKN3 has been found in numerous types of cancer. In the current study, we explored the possible role 
of CDKN3 in cell proliferation, ability to invade, and radiosensitivity in NPC cells. We reported that CDKN3 
was upregulated and p27 was downregulated in NPC tissues and is associated with a worse prognosis for 
patients. In addition, downregulation of CDKN3 and upregulation of p27 decreased cell proliferation, induced 
cell cycle arrest, increased apoptosis, decreased cell invasion, and enhanced radiosensitivity. Silencing of p27 
significantly inhibited the effects of the knockdown of CDKN3. Moreover, downregulation of CDKN3 and 
upregulation of p27 inhibited the increase in tumor volume and weight in implanted tumors, decreased the 
phosphorylation of Akt, and increased the expression of cleaved caspase 3 in tumors. CDKN3 expression was 
also inversely correlated with p27 expression in NPC patients. Knockdown of CDKN3 increased p27 expression. Silencing of p27 markedly inhibited the effects of CDKN3 on cell proliferation, cell cycle progression, 
apoptosis, invasion, and radiosensitivity. These results demonstrate that upregulation of p27 is involved in 
the knockdown of CDKN3-induced decrease in cell proliferation, increase in cell cycle arrest and apoptosis, 
decrease in invasion, and increase in radiosensitivity. The results demonstrate that the CDKN3/p27 axis may 
be a novel target in the treatment of NPC.},
DOI = {10.3727/096504017X14835311718295}
}