PT  - JOURNAL ARTICLE
AU  - Xiao-Mei Deng
AU  - Wei Li
AU  - Xiao Zhang
AU  - Chuan-Xin Wang
AU  - Zhao-Gang Dong
AU  - Xin Zhang
AU  - Gui-Xi Zheng
AU  - Xu-Hua Zhang
AU  - Ni Zheng
AU  - Li-Li Wang
AU  - Lu-Tao Du
AU  - Shun Wang
TI  - RNA Interference of Human Papillomavirus Type 16 E7 Increases HLA Class I Antigen Expression in HaCaT-E7 Cells
AID  - 10.1097/IGC.0b013e3181ffcca1
DP  - 2011 Jan 01
TA  - International Journal of Gynecologic Cancer
PG  - 28--34
VI  - 21
IP  - 1
4099  - http://ijgc.bmj.com/content/21/1/28.short
4100  - http://ijgc.bmj.com/content/21/1/28.full
SO  - Int J Gynecol Cancer2011 Jan 01; 21
AB  - Background: High-risk human papillomaviruses (HPVs) are the major causative agents of cervical cancer. The E7 protein of high-risk HPV disturbs cell cycle control and down-regulates components of the antigen presentation pathway, suggesting an ideal target for development of the immunotherapy in HPV-positive cervical cancers. We previously reported that HPV16 E7 could down-regulate cell-surface HLA class I antigen accompanying decreased expression of transporter associated with antigen processing 1 (TAP-1). The purpose of this study was to determine whether knockdown of HPV16 E7 could up-regulate surface HLA class I antigen expression in HPV16 E7 expressing HaCaT cells (HaCaT-E7).Methods: An E7-specific small interfering RNA (siRNA) was transfected into the HaCaT-E7 cells, and the expression of HPV16 E7 was measured by real-time reverse transcriptase polymerase chain reaction and Western blot. With the use of flow cytometry analysis, the levels of cell surface HLA class I antigen and intracellular TAP-1 expression were detected.Results: It was found that transfection of HPV16 E7-siRNA reduced HPV16 E7 expression as measured on messenger RNA and protein levels. The flow cytometry analysis showed that, compared with mock transfection, a statistically significant increase of approximately 75% in surface HLA class I levels was observed in HaCaT-E7 cells at 72 hours after transfection of E7 siRNA. Moreover, he knockdown of E7 in HaCaT-E7 cells could result in an increase of intracellular TAP-1 expression, which is essential for the expression of HLA class I at cell surface.Conclusions: Our study showed that the knockdown of HPV16 E7 could increase cell surface HLA class I antigen expression in HaCaT-E7 cells. In addition, for HPV-positive human cervical cancer, our observations indicate that the HPV E7 gene is a target of choice.