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Du, Yong,Yan, Shu-Mei,Gu, Wan-Yi,He, Fan,Huang, Li-Yun,Li, Mei,Yuan, Yan,Chen, Ren-Hui,Zhong, Qian,Li, Man-Zhi,Li, Yong,Zeng, Mu-Sheng Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.12
FADS1 (fatty acid desaturase 1) plays a crucial role in fatty acid metabolism, and it was recently reported to be involved in tumorigenesis. However, the role of FADS1 expression in esophageal squamous cell carcinoma (ESCC) remains unknown. In the current study, we investigated the expression and clinical pathologic and prognostic significance of FADS1 in ESCC. Immunohistochemical analyses revealed that 58.2% (146/251) of the ESCC tissues had low levels of FADS1 expression, whereas 41.8% (105/251) exhibited high levels of FADS1 expression. In positive cases, FADS1 expression was detected in the cytoplasm of cells. Correlation analyses demonstrated that FADS1 expression was significantly correlated with tumor location (p=0.025) but not with age, gender, histological grade, tumor status, nodal status or TNM staging. Furthermore, patients with tumors expressing high levels of FADS1had a longer disease-free survival time (p<0.001) and overall survival time (p <0.001). Univariate and multivariate analyses revealed that, along with nodal status, FADS1 expression was an independent and significant predictive factor (p<0.001). In conclusion, our study suggested that FADS1 might be a valuable biomarker and potential therapeutic target for ESCC.
Dan Zong,Li Yin,Qian Zhong,Wen-jie Guo,Jian-hua Xu,Ning Jiang,Zhi-rui Lin,Man-zhi Li,Ping Han,Lin Xu,Xia He,Mu-sheng Zeng 대한암학회 2016 Cancer Research and Treatment Vol.48 No.1
Purpose The purpose of this study was to investigate the function of Zinc finger protein 488 (ZNF488) in nasopharyngeal carcinoma (NPC). Materials and Methods The endogenous expression of ZNF488 in NPC tissues, normal nasopharyngeal epithelium tissues and NPC cell lines were detected by quantitative reverse transcription polymerase chain reaction. ZNF488 over-expressing and knock-down NPC cell line models were estab- lished through retroviral vector pMSCV mediated over-expression and small interfering RNA (siRNA) mediated knock-down. The invasion and migration capacities were evaluated by wound healing and transwell invasion assays in ZNF488 over-expressing and control cell lines. Soft-agar colony formation and a xenograft experiment were performed to study tumorigenic ability in vitro and in vivo. Immunofluorescence and western blotting analysis were used to examine protein changes followed by ZNF488 over-expression. Microarray analysis was performed to explore gene expression profilings, while luciferase reporter assay to evaluate the transcriptive activity of Tcf/Lef. Results ZNF488 was over-expressed in NPC tissues compared with normal tissues, especially higher in 5-8F and S18, which are well-established high metastatic NPC clones. Functional studies indicate that over-expression of ZNF488 provokes invasion, whereas knock-down of ZNF488 alleviates invasive capability. Moreover, over-expression of ZNF488 promotes NPC tumor growth both in vitro and in vivo. Our data further show that over-expression of ZNF488 induces epithelial mesenchymal transition (EMT) by activating the WNT/β -catenin signaling pathway. Conclusion Our data strongly suggest that ZNF488 acts as an oncogene, promoting invasion and tumorigenesis by activating the Wnt/β -catenin pathway to induce EMT in NPC.
Yu, Min,Men, Hai-Tao,Niu, Zhi-Min,Zhu, Yu-Xi,Tan, Ben-Xu,Li, Long-Hao,Jiang, Juan Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.14
Background: The aim of this study was to analyze the prognostic implications of pretreatment circulating endothelial cells (CECs) and circulating endothelial progenitor cells (CEPCs) for the survival of patients with lung cancer. Materials and Methods: Relevant literature was identified using Medline and EMBASE. Patient clinical characteristics, overall survival (OS) and progression-free survival (PFS) together with CEC and CEPC positive rates before treatment were extracted. STATA 12.0 was used for our analysis and assessment of publication bias. Results: A total of 13 articles (8 for CEC and 5 for CEPC, n=595 and n=244) were pooled for the global meta-analysis. The odds ratio (OR) for OS predicted by pretreatment CECs was 1.641 [0.967, 2.786], while the OR for PFS was 1.168 [0.649, 2.100]. The OR for OS predicted by pretreatment CEPCs was 12.673 [5.274, 30.450], while the OR for PFS was 4.930 [0.931, 26.096]. Subgroup analyses were conducted according to clinical staging. Odds ratio (OR) showed the high level of pretreatment CECs only correlated with the OS of patients with advanced lung cancer (stage III-IV). Conclusions: High counts of CECs seem to be associated only with worse 1-year OS in patients with lung cancer, while high level of pretreatment CEPCs correlate with both worse PFS and OS.
Shao-Mei Yang,Fu-Nan Li,Zhi-Ning Huang,Zhong-Shi Zhou,Jin Hou,Man-Yi Zheng,Li-Juan Wang,Yu Jiang,Xin-Yi Zhou,Qiu-Yue Chen,Shan-Hua Li 대한약학회 2015 Archives of Pharmacal Research Vol.38 No.10
To identify novel therapeutic agents to treatcancer, we synthesized a series of diaryl ether derivatives. Structure–activity relationship studies revealed that thepresence of a chlorine or hydroxyl at the para-position onthe phenyl ring (5h or 5k) significantly enhanced antitumoractivity. Compound 5h had stronger growth inhibitory activityin HepG2, A549, and HT-29 cells than compound 5k,with IC50 values of 2.57, 5.48, and 30.04 lM, respectively. Compound 5h also inhibited the growth of other cells lines,including Hep3B, PLC/PRF5, SMMC-7721, HeLa, andA375, with IC50 values of 2.76, 4.26, 29.66, 18.86, and10.21 lM, respectively. The antitumor activity of compound5h was confirmed by a colony forming assay. Further,our results indicated that the antitumor activity ofcompound 5h may be mediated by enhancing expression ofp21 and cl-caspase3, and leading to apoptosis of cancercells.
QTLs Mapping for Agronomic Traits in RIL of Japonica Cultivar x Japonica Weody Rice
Young Chan Cho,Im Soo Choi,Man Kee Baek,Soon Wook Kwon,Jung Pil Suh,Myung Kyu Oh,Zhi Kang Li,Hung Goo Hwang,Yeon Gyu Kim,Young Tae Lee 한국육종학회 2006 한국육종학회지 Vol.38 No.4
A population ofrecombinant inbred lines derived from a cross between Ilpumbyeo, a blast-susceptibleyopowca cultivarofhigh eating-quality and high yield potential, and GL33, a blast-resistance/apowca weedy rice was used to identifv QTLs affect-ing importan
Lu, Feng-Bin,Chen, Da-Zhi,Chen, Lu,Hu, En-De,Wu, Jin-Lu,Li, Hui,Gong, Yue-Wen,Lin, Zhuo,Wang, Xiao-Dong,Li, Ji,Jin, Xiao-Ya,Xu, Lan-Man,Chen, Yong-Ping Korean Society for Molecular and Cellular Biology 2019 Molecules and cells Vol.42 No.12
MicroRNA-223-3p (miR-223-3p) is one of the potential microRNAs that have been shown to alleviate inflammatory responses in pre-clinical investigations and is highly encased in exosomes derived from bone mesenchymal stem cells (MSC-exosomes). MSC-exosomes are able to function as carriers to deliver microRNAs into cells. Autoimmune hepatitis is one of the challenging liver diseases with no effective treatment other than steroid hormones. Here, we examined whether MSC-exosomes can transfer miR-223-3p to treat autoimmune hepatitis in an experimental model. We found that MSC-exosomes were successfully incorporated with miR-223-3p and delivered miR-223-3p into macrophages. Moreover, there was no toxic effect of exosomes on the macrophages. Furthermore, treatments of either exosomes or exosomes with miR-223-3p successfully attenuated inflammatory responses in the liver of autoimmune hepatitis and inflammatory cytokine release in both the liver and macrophages. The mechanism may be related to the regulation of miR-223-3p level and STAT3 expression in the liver and macrophages. These results suggest that MSC-exosomes can be used to deliver miR-223-3p for the treatment of autoimmune hepatitis.
Yong-Ping Chen,Feng-Bin Lu,Da-Zhi Chen,Lu Chen,En-De Hu,Jin-Lu Wu,Hui Li,Yue-Wen Gong,Zhuo Lin,Xiao-Dong Wang,Ji Li,Xiao-Ya Jin,Lan-Man Xu 한국분자세포생물학회 2019 Molecules and cells Vol.42 No.12
MicroRNA-223-3p (miR-223-3p) is one of the potential microRNAs that have been shown to alleviate inflammatory responses in pre-clinical investigations and is highly encased in exosomes derived from bone mesenchymal stem cells (MSC-exosomes). MSC-exosomes are able to function as carriers to deliver microRNAs into cells. Autoimmune hepatitis is one of the challenging liver diseases with no effective treatment other than steroid hormones. Here, we examined whether MSC-exosomes can transfer miR-223-3p to treat autoimmune hepatitis in an experimental model. We found that MSC-exosomes were successfully incorporated with miR-223-3p and delivered miR-223-3p into macrophages. Moreover, there was no toxic effect of exosomes on the macrophages. Furthermore, treatments of either exosomes or exosomes with miR-223-3p successfully attenuated inflammatory responses in the liver of autoimmune hepatitis and inflammatory cytokine release in both the liver and macrophages. The mechanism may be related to the regulation of miR-223-3p level and STAT3 expression in the liver and macrophages. These results suggest that MSC-exosomes can be used to deliver miR-223-3p for the treatment of autoimmune hepatitis.
Ying-Jie Chen,Jia-Ying Wu,Yu-Yi Deng,Ying Wu,Xiao-Qi Wang,Amy Sze-man Li,Lut Yi Wong,Xiuqiong Fu,Zhi-Ling Yu,Chun Liang 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.3
Sorafenib is effective in treating hepatoma, but most patients develop resistance to it. STAT3signaling has been implicated in sorafenib resistance. Artesunate (ART) and 20(R)-ginsenoside Rg3 (Rg3)have anti-hepatoma effects and can inhibit STAT3 signaling in cancer cells. This study aimed to evaluatethe effects of Rg3 in combination with ART (Rg3-plus-ART) in overcoming sorafenib resistance, and toexamine the involvement of STAT3 signaling in these effects. Methods: Sorafenib-resistant HepG2 cells (HepG2-SR) were used to evaluate the in vitro anti-hepatomaeffects of Rg3-plus-ART. A HepG2-SR hepatoma-bearing BALB/c-nu/nu mouse model was used to assessthe in vivo anti-hepatoma effects of Rg3-plus-ART. CCK-8 assays and Annexin V-FITC/PI double stainingwere used to examine cell proliferation and apoptosis, respectively. Immunoblotting was employed toexamine protein levels. ROS generation was examined by measuring DCF-DA fluorescence. Results: Rg3-plus-ART synergistically reduced viability of, and evoked apoptosis in HepG2-SR cells, andsuppressed HepG2-SR tumor growth in mice. Mechanistic studies revealed that Rg3-plus-ART inhibitedactivation/phosphorylation of Src and STAT3 in HepG2-SR cultures and tumors. The combination alsodecreased the STAT3 nuclear level and induced ROS production in HepG2-SR cultures. Furthermore, overactivation of STAT3 or removal of ROS diminished the anti-proliferative effects of Rg3-plus-ART, andremoval of ROS diminished Rg3-plus-ART's inhibitory effects on STAT3 activation in HepG2-SR cells. Conclusions: Rg3-plus-ART overcomes sorafenib resistance in experimental models, and inhibition of Src/STAT3 signaling and modulation of ROS/STAT3 signaling contribute to the underlying mechanisms. Thisstudy provides a pharmacological basis for developing Rg3-plus-ART into a novel modality for treatingsorafenib-resistant hepatoma.