Nanotechnology provides various nanomaterials with tremendous functionalities for cancer diagnostics and therapeutics.Recently, theranostics has been developed as an alternative strategy for efficient cancer treatment...Nanotechnology provides various nanomaterials with tremendous functionalities for cancer diagnostics and therapeutics.Recently, theranostics has been developed as an alternative strategy for efficient cancer treatment through combination of imaging diagnosis and therapeutic interventions under the guidance of diagnostic results. Ultrasound(US) imaging shows unique advantages with excellent features of real-time imaging, low cost, high safety and portability, making US contrast agents(UCAs)an ideal platform for construction of cancer theranostic agents. This review focuses on the development of nanomaterials incorporated multifunctional UCAs serving as theranostic agents for cancer diagnostics and therapeutics, via conjugation of superparamagnetic iron oxide nanoparticles(SPIOs), Cu S nanoparticles, DNA, si RNA, gold nanoparticles(GNPs), gold nanorods(GNRs), gold nanoshell(GNS), graphene oxides(GOs), polypyrrole(PPy) nanocapsules, Prussian blue(PB) nanoparticles and so on to different types of UCAs. The cancer treatment could be more effectively and accurately carried out under the guidance and monitoring with the help of the achieved theranostic agents. Furthermore, nanomaterials incorporated theranostic agents based on UCAs can be designed and constructed by demand for personalized and accurate treatment of cancer, demonstrating their great potential to address the challenges of cancer heterogeneity and adaptation, which can provide alternative strategies for cancer diagnosis and therapeutics.展开更多
Unlike the previous circulating strains that were not associated with significant human pathology,recent circulating Zika virus(ZIKV)strains isolated during the 2015–2016Brazilian Outbreak are highly suspected to cau...Unlike the previous circulating strains that were not associated with significant human pathology,recent circulating Zika virus(ZIKV)strains isolated during the 2015–2016Brazilian Outbreak are highly suspected to cause neuropathology,including disorders of fetal brain development and Guillain-Barrésyndrome(Broutet et al.,2016).Studies have revealed that recent ZIKV strains can be spread through maternal-fetal(Calvet et al.,2016)and sexual(Hills et al.,2016)transmission,in addition to the traditional展开更多
Hepatitis B virus(HBV)can cause chronic hepatitis B,which may lead to cirrhosis and liver cancer.Type I interferon(IFN)is an approved drug for the treatment of chronic hepatitis B.However,the fundamental mechanisms of...Hepatitis B virus(HBV)can cause chronic hepatitis B,which may lead to cirrhosis and liver cancer.Type I interferon(IFN)is an approved drug for the treatment of chronic hepatitis B.However,the fundamental mechanisms of antiviral action by type I IFN and the downstream signaling pathway are unclear.TRIM25 is an IFN-stimulated gene(ISG)that has an important role in RIG-I ubiquitination and activation.Whether TRIM25 is induced in liver cells by type I IFN to mediate anti-HBV function remains unclear.Here we report that interleukin-27(IL-27)has a critical role in IFN-induced TRIM25 upregulation.TRIM25 induction requires both STAT1 and STAT3.In TRIM25 knockout HepG2 cells,type I IFN production was consistently attenuated and HBV replication was increased,whereas overexpression of TRIM25 in HepG2 cells resulted in elevated IFN production and reduced HBV replication.More interestingly,we found that TRIM25 expression was downregulated in HBV patients and the addition of serum samples from HBV patients could inhibit TRIM25 expression in HepG2 cells,suggesting that HBV might have involved a mechanism to inhibit antiviral ISG expression and induce IFN resistance.Collectively,our results demonstrate that type I IFN-induced TRIM25 is an important factor in inhibiting HBV replication,and the IFN-IL-27-TRIM25 axis may represent a new target for treating HBV infection.展开更多
Hepatitis B virus(HBV)and its associated chronic infection remain serious health threats worldwide.However,there is still no impactful approach for clinical treatment of hepatitis B patients.Therefore,developing a bet...Hepatitis B virus(HBV)and its associated chronic infection remain serious health threats worldwide.However,there is still no impactful approach for clinical treatment of hepatitis B patients.Therefore,developing a better understanding of the interactions between HBV and its host is particularly important.HBV infection has been reported to induce type-III but not type-I or type-II interferon(IFN).In this study,we identified CBFβ,an HIV enhancer,as an HBV restriction factor that is specifically induced by type-III IFN in the early stages of HBV infection.Type-III IFN-induced IL-10 played an important role in the production of CBFβ.Interestingly,the interaction between CBFβ-and HBV-encoded regulatory protein X(HBx)enhanced the stability of CBFβ,but notably blocked HBx-mediated promotion of HBV replication.CBFβexpression was lower in HBV patients than in healthy persons,and the addition of serum from HBV patients inhibited CBFβexpression in HepG2 cells.On the contrary,HBV via HBsAg inhibited type-III IFN-induced CBFβexpression and decreased the anti-HBV activity of type-III IFN,suggesting that HBV inhibits antiviral interferon-stimulated gene(ISG)expression and induces IFN resistance.Collectively,our results demonstrate that type-III IFN-triggered and IL-10-induced CBFβare crucial factors for inhibiting HBV replication,and the HBx–CBFβ–HBsAg axis reveals a new molecular mechanism of interaction between HBV and its hosts.展开更多
基金financially supported by the National Natural Science Foundation of China(Grant No.81501585)the Natural Science Foundation of Jiangsu Province of China(Grant No.BK20150348)+1 种基金the Natural Science Foundation of the Jiangsu Higher Education Institutions of China(Grant No.15KJB310019)China Postdoctoral Science Foundation(Grant No.2015M570475 and 2016T90496)
文摘Nanotechnology provides various nanomaterials with tremendous functionalities for cancer diagnostics and therapeutics.Recently, theranostics has been developed as an alternative strategy for efficient cancer treatment through combination of imaging diagnosis and therapeutic interventions under the guidance of diagnostic results. Ultrasound(US) imaging shows unique advantages with excellent features of real-time imaging, low cost, high safety and portability, making US contrast agents(UCAs)an ideal platform for construction of cancer theranostic agents. This review focuses on the development of nanomaterials incorporated multifunctional UCAs serving as theranostic agents for cancer diagnostics and therapeutics, via conjugation of superparamagnetic iron oxide nanoparticles(SPIOs), Cu S nanoparticles, DNA, si RNA, gold nanoparticles(GNPs), gold nanorods(GNRs), gold nanoshell(GNS), graphene oxides(GOs), polypyrrole(PPy) nanocapsules, Prussian blue(PB) nanoparticles and so on to different types of UCAs. The cancer treatment could be more effectively and accurately carried out under the guidance and monitoring with the help of the achieved theranostic agents. Furthermore, nanomaterials incorporated theranostic agents based on UCAs can be designed and constructed by demand for personalized and accurate treatment of cancer, demonstrating their great potential to address the challenges of cancer heterogeneity and adaptation, which can provide alternative strategies for cancer diagnosis and therapeutics.
文摘Unlike the previous circulating strains that were not associated with significant human pathology,recent circulating Zika virus(ZIKV)strains isolated during the 2015–2016Brazilian Outbreak are highly suspected to cause neuropathology,including disorders of fetal brain development and Guillain-Barrésyndrome(Broutet et al.,2016).Studies have revealed that recent ZIKV strains can be spread through maternal-fetal(Calvet et al.,2016)and sexual(Hills et al.,2016)transmission,in addition to the traditional
基金This work was supported in part by the National Natural Science Foundation, China, Jilin Provincial Science and Technology Department of the Youth Fund Project, and Jilin University Bethune training program (grant no. 81401290, 20160520161JH, 470110000456 to GT)CAMS Initiative for Innovative Medicine (no. CAMS-I2M) to FXQ and GC.
文摘Hepatitis B virus(HBV)can cause chronic hepatitis B,which may lead to cirrhosis and liver cancer.Type I interferon(IFN)is an approved drug for the treatment of chronic hepatitis B.However,the fundamental mechanisms of antiviral action by type I IFN and the downstream signaling pathway are unclear.TRIM25 is an IFN-stimulated gene(ISG)that has an important role in RIG-I ubiquitination and activation.Whether TRIM25 is induced in liver cells by type I IFN to mediate anti-HBV function remains unclear.Here we report that interleukin-27(IL-27)has a critical role in IFN-induced TRIM25 upregulation.TRIM25 induction requires both STAT1 and STAT3.In TRIM25 knockout HepG2 cells,type I IFN production was consistently attenuated and HBV replication was increased,whereas overexpression of TRIM25 in HepG2 cells resulted in elevated IFN production and reduced HBV replication.More interestingly,we found that TRIM25 expression was downregulated in HBV patients and the addition of serum samples from HBV patients could inhibit TRIM25 expression in HepG2 cells,suggesting that HBV might have involved a mechanism to inhibit antiviral ISG expression and induce IFN resistance.Collectively,our results demonstrate that type I IFN-induced TRIM25 is an important factor in inhibiting HBV replication,and the IFN-IL-27-TRIM25 axis may represent a new target for treating HBV infection.
基金supported by the National Natural Science Foundation of China(Nos.31671436,31600133,31771533,and 31830051)the Priority Academic Program Development of Jiangsu Higher Education Institutions,the Natural Science Foundation of Jiangsu Province(No.BK20160314)+1 种基金the Fok Ying Tung Education Foundation for Young Teachers(No.151020)the Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences(Nos.2017NL31002 and 2017NL31004)
基金This work was supported by the National Natural Science Foundation,ChinaJilin Provincial Science and Technology Department of the Youth Fund Projectby the Jilin University Bethune training program(Grant No.81401290,20160520161JH,and 470110000456 to G.T.).
文摘Hepatitis B virus(HBV)and its associated chronic infection remain serious health threats worldwide.However,there is still no impactful approach for clinical treatment of hepatitis B patients.Therefore,developing a better understanding of the interactions between HBV and its host is particularly important.HBV infection has been reported to induce type-III but not type-I or type-II interferon(IFN).In this study,we identified CBFβ,an HIV enhancer,as an HBV restriction factor that is specifically induced by type-III IFN in the early stages of HBV infection.Type-III IFN-induced IL-10 played an important role in the production of CBFβ.Interestingly,the interaction between CBFβ-and HBV-encoded regulatory protein X(HBx)enhanced the stability of CBFβ,but notably blocked HBx-mediated promotion of HBV replication.CBFβexpression was lower in HBV patients than in healthy persons,and the addition of serum from HBV patients inhibited CBFβexpression in HepG2 cells.On the contrary,HBV via HBsAg inhibited type-III IFN-induced CBFβexpression and decreased the anti-HBV activity of type-III IFN,suggesting that HBV inhibits antiviral interferon-stimulated gene(ISG)expression and induces IFN resistance.Collectively,our results demonstrate that type-III IFN-triggered and IL-10-induced CBFβare crucial factors for inhibiting HBV replication,and the HBx–CBFβ–HBsAg axis reveals a new molecular mechanism of interaction between HBV and its hosts.