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Peer Reviewed Papers, Books, Chapters

Year Title Citation Authors Review type Summary Keywords File filename File mime type
1. 2010 Src regulates hVPS34 to mediate activation of S6K1 and cellular transformation. Submitted
2. 2009 Rac1 contributes to trastuzumab-resistance of breast cancer cells: Rac1 as a potential therapeutic target for the treatment of trastuzumab-resistant breast cancer. Mol Cancer Ther. 2009 Jun; 8(6): 1557-69.
3. 2009 Mechanism of E-cadherin lysosomal degradation Nat Rev Cancer 9:143.
4. 2008 Cdc42 regulates E-cadherin ubiquitination and degradation through an epidermal growth factor receptor to Src-mediated pathway J. Biol. Chem. 283:5127-37.
5. 2007 Cdc42: downstream effector and regulator of ErbB1 as strategic target for anti-cancer therapeutic development in breast cancer Future Drug (Expert Review of Anticancer Therapy) 7: 147-157
6. 2006 Growth and motility inhibition of breast cancer cells by EGFR degradation is correlated with inactivation of Cdc42 Cancer Research 66: 3520-30
7. 2005 Development and regulation of monoclonal antibody product: Challenges and opportunities. Cancer and Metastasis Reviews 24: 569-584
8. 2005 Cdc42 and Ras cooperate to mediate cellular transformation by intersectin-L J. Biol. Chem. 280: 22883-91
9. 2003 Epidermal growth factor-dependent regulation of Cdc42 is mediated by the Src tyrosine kinase. J. Biol. Chem. 278: 49293-49300.
10. 2003 Activated Cdc42 sequesters c-Cbl and prevents EGF receptor degradation. Cell 114: 715-725
11. 2002 Antiapoptotic cdc42 mutants are potent activators of cellular transformation. Biochemistry 41: 12350-12358.
12. 2000 Cdc42 stimulates RNA splicing via the S6 kinase and a novel S6 kinase target, the nuclear cap-binding complex J. Biol. Chem. 275: 37307-37310.
13. 2000 The g-subunit of the coatomer complex binds Cdc42 to mediate transformation. Nature 405: 800-804
14. 2000 Activation of phospholipase D1 by Cdc42 requires the Rho insert region J. Biol. Chem. 275:15665-15668
15. 1998 Transformation activity of Cdc42 requires a region unique to Rho-related proteins. J. Biol. Chem. 273: 16655-16658
16. 1997 Interactions between Cdc42Hs and Rho-GDI is mediated through the Rho insert region J. Biol. Chem. 272: 26153-26158
17. 1996 Phosphatidylinositol-4,5-bisphosphate provides an alternative to guanine nucleotide exchange factors by stimulating the dissociation of GDP from Cdc42Hs. J. Biol. Chem. 271: 23815-23819.
18. 1996 Use of a fluorescence spectroscopic read-out to characterize the interactions of Cdc42Hs with its target/effector, mPAK-3 Biochemistry 36: 1173-1180
19. 1996 Identification of a putative effector for Cdc42Hs with high sequence similarity to IQGAP2. J. Biol. Chem. 271: 21732-21737.
20. BACKGROUND: The prognosis of pancreatic carcinoma (PC) remains poor and the American Joint Committee on Cancer (AJCC) 8th staging system for survival prediction in PC patients after curative resection is still limited. Pubmed BACKGROUND: The prognosis of pancreatic carcinoma (PC) remains poor and the American Joint Committee on Cancer (AJCC) 8th staging system for survival prediction in PC patients after curative resection is still limited. Thus, the aim of this study is to refine a valuable prognostic model and novel staging system for PC with curative resection. METHODS: The data of 3,458 patients used in this study were retrieved from the Surveillance, Epidemiology, and End Results database registry of National Cancer Institute. The prognostic value of lymph node ratio (LNR) was analyzed in the primary cohort and prognostic nomogram based on the LNR was established to create a novel staging system. Then, analyses were conducted to evaluate the application of the formulated nomogram staging system and the AJCC 8th staging system. The predictive performance of model was further validated in the internal validation cohort. RESULTS: Significant positive correlations were found between LNR and all factors except for surgical procedures. The results of univariate and multivariate analyses showed that LNR was identified as an independent prognostic indicator for overall survival (OS) in both primary and validation cohorts (all P < 0.001). A prognostic nomogram based on the LNR was formulated to obtain superior discriminatory abilities. Compared with the AJCC 8th staging system, the formulated nomogram staging system showed higher hazard ratios of stage II, III, and IV disease (reference to stage I disease) that were 1.637, 2.300, and 3.521, respectively, by univariate analyses in the primary cohort and the distinction between stage I, II, and III disease at the beginning or end of the survival curves was more apparent. All these results were further verified in the validation cohort. CONCLUSION: LNR can be considered as a useful independent prognostic indicator for PC patients after curative resection regardless of the surgical procedures. Compared with the AJCC 8th staging system, the formulated nomogram showed superior predictive accuracy for OS and its novel staging system revealed better risk stratification. AJCC; decision curve analysis; lymph node ratio; nomogram; pancreatic head carcinoma; prognosis
21. BACKGROUND: Glypican-3 (GPC3) is highly expressed in most of the hepatocellular carcinomas (HCCs), even in small HCCs. Pubmed BACKGROUND: Glypican-3 (GPC3) is highly expressed in most of the hepatocellular carcinomas (HCCs), even in small HCCs. It may be used as a potential biomarker for early detection of HCC. The aptamer is a promising targeting agent with unique advantages over antibody. This study was to introduce a novel GPC3 specific aptamer (AP613-1), to verify its specific binding property in vitro, and to evaluate its targeting efficiency in vivo by performing near-infrared (NIR) fluorescence imaging on an HCC xenograft model. METHODS: AP613-1 was generated from the systematic evolution of ligands by exponential enrichment. Flow cytometry and aptamer-based immunofluorescence imaging were performed to verify the binding affinity of AP613-1 to GPC3 in vitro. NIR Fluorescence images of nude mice with unilateral (n=12) and bilateral (n=4) subcutaneous xenograft tumors were obtained. Correlation between the tumor fluorescence intensities in vivo and ex vivo was analyzed. RESULTS: AP613-1 could specifically bind to GPC3 in vitro. In vivo and ex vivo tumors, fluorescence intensities were in excellent correlation (P<0.001, r=0.968). The fluorescence intensity is significantly higher in tumors given Alexa Fluor 750 (AF750) labeled AP613-1 than in those given AF750 labeled initial ssDNA library both in vivo (P<0.001) and ex vivo (P=0.022). In the mice with bilateral subcutaneous tumors injected with AF750 labeled AP613-1, Huh-7 tumors showed significantly higher fluorescence intensities than A549 tumors both in vivo (P=0.016) and ex vivo (P=0.004). CONCLUSIONS: AP613-1 displays a specific binding affinity to GPC3 positive HCC. Fluorescently labeled AP613-1 could be used as an imaging probe to subcutaneous HCC in xenograft models. Alexa Fluor 750 (AF750); GPC3; hepatocellular carcinoma (HCC); optical imaging; ssDNA aptamer
22. Sensitive skin (SS) is a condition of subjective cutaneous hyper-reactivity. Pubmed Sensitive skin (SS) is a condition of subjective cutaneous hyper-reactivity. The role of long non-coding RNAs (lncRNAs) in subjects with SS is unclear. Therefore, the aim of the present study was to provide a comprehensive profile of the mRNAs and lncRNAs in subjects with SS. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis presented the characteristics of associated protein-coding genes. In addition, a co-expression network of lncRNA and mRNA was constructed to identify potential underlying regulation targets; the results were verified by quantitative real-time PCR (qRT-PCR) and RNA-seq analyses in patients with SS and normal samples. Compared with the normal skin group, 266 novel lncRNAs and 6750 annotated lncRNAs were identified in the SS group. A total of 71 lncRNA transcripts and 2615 mRNA transcripts were differentially expressed (P < 0.05). The heat signature of the SS samples could be distinguished from the normal skin samples, whereas the majority of the genes that were present in enriched pathways were those that participated in focal adhesion, PI3K-Akt signaling, and cancer-related pathways. Five transcripts were selected for qRT-PCR analysis and the results were consistent with RNA-seq. The results suggested that LNC_000265 may play a role in the epidermal barrier structure of patient with SS. The data suggest novel genes and pathways that may be involved in the pathogenesis of SS and highlight potential targets that could be used for individualized treatment applications. RNA sequencing; lncRNA; mRNA; sensitive skin


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