Publications (3)4.57 Total impact
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Article: YY1 is a novel potential therapeutic target for the treatment of HPV infection-induced cervical cancer by arsenic trioxide.
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ABSTRACT: YY1 is a zinc finger transcription factor involved in the regulation of cell growth, development, and differentiation. Although YY1 can regulate human papillomavirus-type (HPV) viral oncogenes E6 and E7, it remains unknown if YY1 plays a key role in carcinoma progression of HPV-infected cells. Here we sought to determine whether YY1 is upregulated in the cervical cancer tissues and YY1 inhibition contributes to apoptosis of cervical cancer cells, which is at least partly p53 dependent. Therefore, YY1 can be a potential therapeutic target for cervical cancer treatment by arsenic trioxide (As2O3). The expression level of YY1 was examined and analyzed by Western blot in pathologically confirmed primary cervical cancer samples, in the adjacent normal samples, as well as in normal cervix samples. The effects of YY1 inhibition by specific small interfering RNA in HeLa cells were determined by Western blot analysis of p53 level, cell growth curve, colony formation assay, and apoptosis. The contribution of YY1 to As2O3-induced p53 activation and apoptosis was also examined by Western blot and cell cycle analysis. Here we report that the expression level of YY1 is significantly elevated in the primary cancer tissues. In HPV-positive HeLa cells, small interfering RNA-mediated YY1 inhibition induced apoptosis and increased the expression of p53. Treatment of HeLa cells with As2O3, a known anti-cervical cancer agent, reduced both protein and mRNA levels of YY1 in HeLa cells. YY1 knockdown significantly further enhanced As2O3-induced apoptosis. These results demonstrated that the expression of YY1 is upregulated in cervical carcinomas and that YY1 plays a critical role in the progression of HPV-positive cervical cancer. In addition, YY1 inhibition induces p53 activation and apoptosis in HPV-infected HeLa cells. Thus, YY1 is an As2O3 target and could serve as a potential drug sensitizer for anti-cervical cancer therapy.International Journal of Gynecological Cancer 08/2011; 21(6):1097-104. · 1.65 Impact Factor -
Article: Interplay between MDM2, MDMX, Pirh2 and COP1: the negative regulators of p53.
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ABSTRACT: MDM2, Pirh2 and COP1 are important E3 ubiquitin ligases, which directly interact with p53 and target p53 for proteasome-mediated degradation. MDMX, the MDM2 homologous protein, inhibits p53-mediated transcription activity. The interplay between MDM2, MDMX, Pirh2 and COP1 has not been reported, except the interaction between MDM2 and MDMX. Here, we reported that there were interactions between these four proteins independently of p53. The protein levels of MDM2, MDMX, Pirh2 and COP1 changed when any two of them were co-transfected. Our data also showed that the integrity of MDM2 RING finger domain was crucial for its ability to elevate the protein levels of COP1 and Pirh2. Any two of these four proteins could inhibit p53-mediated transcriptional activity synergistically. Furthermore, COP1 inhibited MDM2 self-ubiquitination and interfered with MDMX ubiquitination by MDM2. Our results suggest that MDM2, MDMX, Pirh2 and COP1 might inhibit p53 activity synergistically in vivo.Molecular Biology Reports 03/2010; 38(1):229-36. · 2.93 Impact Factor -
Article: [Location of the probe dots in gene chip image with the medialness function].
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ABSTRACT: For acquisition of the gene chip information, how to correctly locate the probe dots in the chip's scanning image is the base of the chip information processing. Here we present a new approach for locating the probe dots in the gene chip image. First, a medialness function, which is good at detection of circle area with radius given in advance, is used for calculating the medialness map in which the center of circle sample area of the gene chip image is disclosed prominently. Then, a method to locate the probe dots center is given based on the medialness map and the 2D space configuration of the probe dots. The experiments show that the new approach correctly locates the probe dots while against noise affection robustly.Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi 02/2002; 19(1):97-100, 116.
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Institutions
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2011
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Fudan University
- Institute of Genetics
Shanghai, Shanghai Shi, China
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