Zhao Yf
Zhengzhou University
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Featured researches published by Zhao Yf.
Biochemical and Biophysical Research Communications | 2013
Gongquan Li; Shuijun Zhang; Hongbo Fang; Bing Yan; Zhao Yf; Feng Ls; Xiuxian Ma; Xuexiang Ye
Small-molecule Bcl-2/Bcl-xL inhibitor Navitoclax represents a promising cancer therapeutic since preclinical and clinical studies with Navitoclax have demonstrated strong anticancer activity in several types of cancers. However, because Navitoclax has a low binding affinity to Mcl-1, anticancer activity by Navitoclax is often attenuated by the elevated expression of Mcl-1 in hepatocellular carcinoma (HCC) and other cancers, posing a serious problem for its potential clinical utilities. Therefore, approaches that suppress the expression of Mcl-1 are urgently needed to overcome Navitoclax-resistance in these cancers. Here, we reported that aspirin markedly suppressed Mcl-1 expression, and significantly enhanced Navitoclax-mediated cell viability inhibition and apoptosis induction in HCC cells. We further showed that aspirin robustly enhanced Navitoclax-triggered cytosolic cytochrome c release, activation of initiator caspase-9 and effector caspase-3, and cleavage of PARP. Importantly, the cell death induction by the combination could be rescued by a cell-permeable caspase-9 inhibitor Z-LEHD-FMK, indicative of an indispensable role of mitochondrial apoptosis pathway during the combination effect. Taken together, our study suggests that aspirin can be used to enhance Navitoclax-mediated anticancer activity via suppression of Mcl-1. Since aspirin is one of the most commonly used medicines, our findings therefore have translational impacts on Navitoclax-based therapy for HCC.
PLOS ONE | 2012
Shuijun Zhang; Gongquan Li; Zhao Yf; Guangzhi Liu; Yu Wang; Xiuxian Ma; Dexu Li; Yang Wu; Jianfeng Lu
Background The members of inhibitor of apoptosis proteins (IAPs) family are key negative regulators of apoptosis. Overexpression of IAPs are found in hepatocellular carcinoma (HCC), and can contribute to chemotherapy resistance and recurrence of HCC. Small-molecule Second mitochondria-derived activator of caspases (Smac) mimetics have recently emerged as novel anticancer drugs through targeting IAPs. The specific aims of this study were to 1) examine the anticancer activity of Smac mimetics as a single agent and in combination with chemotherapy in HCC cells, and 2) investigate the mechanism of anticancer action of Smac mimetics. Methods Four HCC cell lines, including SMMC-7721, BEL-7402, HepG2 and Hep3B, and 12 primary HCC cells were used in this study. Smac mimetic SM-164 was used to treat HCC cells. Cell viability, cell death induction and clonal formation assays were used to evaluate the anticancer activity. Western blotting analysis and a pancaspase inhibitor were used to investigate the mechanisms. Results Although SM-164 induced complete cIAP-1 degradation, it displayed weak inhibitory effects on the viability of HCC cells. Nevertheless, SM-164 considerably potentiated Apo2 ligand or TNF-related apoptosis-inducing ligand (APO2L/TRAIL)- and Doxorubicin-mediated anticancer activity in HCC cells. Mechanistic studies demonstrated that SM-164 in combination with chemotherapeutic agents resulted in enhanced activation of caspases-9, -3 and cleavage of poly ADP-ribose polymerase (PARP), and also led to decreased AKT activation. Conclusions Smac mimetics can enhance chemotherapeutic-mediated anticancer activity by enhancing apoptosis signaling and suppressing survival signaling in HCC cells. This study suggests Smac mimetics are potential therapeutic agents for HCC.
Transplantation Proceedings | 2015
Shengli Cao; Bing Yan; Yantao Lu; Gong Zhang; Jie Li; Wenzhi Guo; Zhao Yf; Shusheng Zhang
BACKGROUND C/EBP homologous protein (CHOP) is an important marker in endoplasmic reticulum stress (ERS)-associated cell apoptosis. The role of CHOP-induced renal apoptosis remains unclear in rats with brain death (BD). The present study aims to investigate the possible implication of CHOP-mediated, ERS-related BD-induced apoptosis in rats. MATERIALS AND METHODS Forty male Sprague-Dawley rats were divided randomly into 4 experimental groups. We examined activation of ERS and apoptosis-related protein expression using Western blot and immunohistochemical staining. In addition, apoptosis is assessed by terminal deoxynucleotide transferase-mediated dUTP nick-end labeling assay. RESULTS Kidneys harvested after BD show increased ERS- and apoptosis-related protein markers compared with kidneys of non-BD rats. Salubrinal (Sal) significantly increased levels of p-eIF2a and decreased the activity of CHOP at 6 hours after BD compared with vehicle-treated dimethylsulfoxide. CONCLUSIONS Treating the BD donor with Sal influences renal apoptosis compared with vehicle-treated BD rats. Our results indicate that targeting the CHOP pathway provides a promising therapeutic approach for kidney injury associated with donor BD.
Journal of Cellular and Molecular Medicine | 2016
Wenzhi Guo; Shengli Cao; Bing Yan; Gong Zhang; Jie Li; Zhao Yf; Shuijun Zhang
To investigate whether the mitochondrial apoptotic pathway mediates myocardial cell injuries in rats under brain death (BD), and observe the effects and mechanisms of the c‐Jun N‐terminal kinase (JNK) inhibitor SP600125 on cell death in the heart. Forty healthy male Sprague‐Dawley (SD) rats were randomized into four groups: sham group (dural external catheter with no BD); BD group (maintain the induced BD state for 6 hrs); BD + SP600125 group (intraperitoneal injection of SP600125 10 mg/kg 1 hr before inducing BD, and maintain BD for 6 hrs); and BD + Dimethyl Sulphoxide (DMSO) group (intraperitoneal injection of DMSO 1 hr before inducing BD, and maintain BD for 6 hrs). Real‐time quantitative PCR was used to evaluate mRNA levels of Cyt‐c and caspase‐3. Western blot analysis was performed to examine the levels of mitochondrial apoptosis‐related proteins p‐JNK, Bcl‐2, Bax, Cyt‐c and Caspase‐3. TUNEL assay was employed to evaluate myocardial apoptosis. Compared with the sham group, the BD group exhibited increased mitochondrial apoptosis‐related gene expression, accompanied by the elevation of p‐JNK expression and myocardial apoptosis. As the vehicle control, DMSO had no treatment effects. The BD + SP600125 group had decreased p‐JNK expression, and reduced mitochondrial apoptosis‐related gene expression. Furthermore, the apoptosis rate of myocardial cells was reduced. The JNK inhibitor SP600125 could protect myocardial cells under BD through the inhibition of mitochondrial apoptosis‐related pathways.
Journal for ImmunoTherapy of Cancer | 2013
Meng Wang; Xinfeng Chen; Zhiqin Li; Zhen Zhang; Dongli Yue; Yan-hong Liu; Dong Jiang; Yu-ling Sun; Zhao Yf; Shuhuan Wu; Jiansheng Li; Yi Zhang
Results 87.3% of HCC tumor tissue samples expressed at least 1 CTAs. HCC adjacent non-cancerous tissues did not express CTAs. 78.9% tumor tissue samples expressed MAGE-A3 mRNA, 33.8% samples expressed MAGE-A4 mRNA, 74.6% samples expressed MAGE-C2 mRNA and 14.1% samples expressed NY-ESO-1 mRNA. The expression of CTAs showed correlation with Ki67(r=0.27, P=0.02) and tumor stages (r=0.31, P=0.01), no correlation with clinical parameters such as age, gender, ALT, HLAA2 positive, CA125, CA199, HBV or HCV infection and tumor size (P>0.05). The expression of MAGE-A3 showed correlation with the high expressions of CEA in serum (r=0.30, P=0.03), AFP in serum (r=0.26, P=0.03) and lymph node metastases (r=0.30, P=0.01).
Hepatobiliary & Pancreatic Diseases International | 2004
Xu Pq; Ma Xx; Ye Xx; Feng Ls; Dang Xw; Zhao Yf; Zhang Sj; Zhao Ls; Tang Z; Lu Xb
Hepatobiliary & Pancreatic Diseases International | 2005
Zhao Yf; Zhai Wl; Zhang Sj; Chen Xp
Hepatobiliary & Pancreatic Diseases International | 2004
Feng Ls; Peng Qp; Li K; Ma Xx; Zhao Yf; Ye Xx; Xu Pq; Chen Xp
International Journal of Clinical and Experimental Pathology | 2015
Meng Wang; Jiansheng Li; Liping Wang; Xinfeng Chen; Zhen Zhang; Dongli Yue; Yu Ping; Xiaojuan Shi; Lan Huang; Tengfei Zhang; Li Yang; Zhao Yf; Xiuxian Ma; Dexu Li; Zhengjun Fan; Longshuan Zhao; Zhe Tang; Wenlong Zhai; Bin Zhang; Yi Zhang
Hepatobiliary & Pancreatic Diseases International | 2003
Zhang Sj; Zhu Cj; Zhao Yf; Jieshou Li; Guo Wz