OBJECTIVETo explore the expression of CDK6 in nasopharyngeal carcinoma (NPC) and explore its clinical significance.

METHODSImmunohistochemistry was used to examine the differential expression of CDK6 protein in 101 NPC and 30 nasopharyngeal tissues, and the correlation of CDK6 expression with the clinical characteristics was analyzed in NPC cases.

RESULTSImmunohistochemistry demonstrated that CDK6 protein was a co-expressed factor in the cytoplasm and cell nuclei. CDK6 was expressed predominantly in the cytoplasm in nasopharyngeal tissues, but in NPC tissues, CDK6 was co-expressed predominantly in the cytoplasm and nuclei. Compared to the nasopharyngeal tissues, NPC tissues showed significantly up-regulated CDK6 expression (P=0.009) in positive correlation with tumor size (P=0.020) and clinical stages (P=0.0039).

CONCLUSIONSIncreased CDK6 protein expression is an unfavorable factor that promotes the development and progression of NPC.

Carcinoma ; Cell Nucleus ; Cyclin-Dependent Kinase 6 ; metabolism ; Cytoplasm ; Disease Progression ; Humans ; Immunohistochemistry ; Nasopharyngeal Neoplasms ; metabolism ; Up-Regulation

OBJECTIVETo assess the effect of small interfering RNA (siRNA)-mediated suppression of CDK6 expression on the proliferation and cell cycles of nasopharyngeal carcinoma (NPC) cells in vitro.

METHODSQRT-PCR was used to examine the differential expression of CDK6 in 30 NPC tissues and 18 normal nasopharyngeal tissues. A siRNA targeting CDK6 was transfected in NPC CNE2 cells, and MTT assay and flow cytometry were used to analyze the changes in cell proliferation and cell cycle distribution. Western blotting was used to examine the expressions of the cell cycle-related factors.

RESULTSCompared with normal nasopharyngeal tissues, NPC tissues showed an increased expression of CDK6 mRNA. Knocking down CDK6 expression obviously inhibited tumor cell growth and cell cycle transition from G1 to S phase and caused reduced expressions of CDK4, CCND1, and E2F1 and enhanced expression of the tumor suppressor p21.

CONCLUSIONNPC tissues overexpress CDK6. Knocking down CDK6 expression inhibits the growth and cell cycle transition of NPC cells in vitro by inhibiting the expressions of CDK4, CCND1, and E2F1 and upregulating tumor suppressor p21 expression.

Carcinoma ; Cell Cycle ; Cell Line, Tumor ; Cell Proliferation ; Cyclin D1 ; metabolism ; Cyclin-Dependent Kinase 4 ; metabolism ; Cyclin-Dependent Kinase 6 ; genetics ; Cyclin-Dependent Kinase Inhibitor p21 ; metabolism ; E2F1 Transcription Factor ; metabolism ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Humans ; Nasopharyngeal Neoplasms ; pathology ; RNA, Messenger ; RNA, Small Interfering ; Transfection ; Up-Regulation