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      • KCI등재SCOPUSSCIE

        Metallothionein MT1M Suppresses Carcinogenesis of Esophageal Carcinoma Cells through Inhibition of the Epithelial-Mesenchymal Transition and the SOD1/PI3K Axis

        Li, Dandan,Peng, Weiyan,Wu, Bin,Liu, Huan,Zhang, Ruizhen,Zhou, Ruiqin,Yao, Lijun,Ye, Lin Korean Society for Molecular and Cellular Biology 2021 Molecules and cells Vol.44 No.4

        Metallothionein (MT1M) belongs to a family of cysteinerich cytosolic protein and has been reported to be a tumor suppressor gene in multiple cancers. However, its role in esophageal carcinoma carcinogenesis remains unclear. In this study, MT1M expression was correlated with tumor type, stage, drinking and smoking history, as well as patient survival. We also studied the regulation and biological function of MT1M in esophageal squamous cell carcinoma (ESCC). We have found that MT1M is significantly downregulated in ESCC tissues compared with adjacent non-cancer tissues. Furthermore, restoration of expression by treatment with the demethylation agent A + T showed that MT1M downregulation might be closely related to hypermethylation in its promoter region. Over-expression of MT1M in ESCC cells significantly altered cell morphology, induced apoptosis, and reduced colony formation, cell viability, migration and epithelial-mesenchymal transition. Moreover, based on reactive oxygen species (ROS) levels, a superoxide dismutase 1 (SOD1) activity assay and protein analysis, we verified that the tumor-suppressive function of MT1M was at least partially caused by its upregulation of ROS levels, downregulation of SOD1 activity and phosphorylation of the SOD1 downstream pathway PI3K/AKT. In conclusion, our results demonstrated that MT1M was a novel tumor-suppressor in ESCC and may be disrupted by promoter CpG methylation during esophageal carcinogenesis.

      • SCISCIESCOPUS

        Biomimetic apatite formed on cobalt-chromium alloy: A polymer-free carrier for drug eluting stent

        Chen, Cen,Yao, Chenxue,Yang, Jingxin,Luo, Dandan,Kong, Xiangdong,Chung, Sung-Min,Lee, In-Seop Elsevier 2017 Colloids and surfaces Biointerfaces Vol.151 No.-

        <P><B>Abstract</B></P> <P>In this study, sirolimus (SRL) was loaded within biomimetic apatite formed on cobalt-chromium (Co-Cr) alloy, which has been reported for the first time, to inhibit the in-stent restenosis. Two different groups of loading SRL within biomimetic apatite were prepared: Group A (mono-layer of apatite/SRL) and Group B (bi-layer of apatite/SRL). Group A and Group B showed the biphasic pattern of SRL release up to 40 and 90days, respectively. The attachment of human artery smooth muscle cell (HASMC) for both Group A and Group B was significantly inhibited, and proliferation dramatically decreased with the release of SRL. Noteworthily, biomimetic apatite alone also suppressed the SMC proliferation. The porous biomimetic apatite uniformly covered Co-Cr stent without crack or webbings. After balloon expansion, the integrity of biomimetic apatite was sufficient to resist delamination or destruction. Thus, this study demonstrated that biomimetic apatite is a promising drug carrier for potential use in stents.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Biomimetic apatite is formed on Co-Cr alloy as a polymer-free drug carrier. </LI> <LI> To inhibit in-stent restenosis, sirolimus is loaded within apatite in two ways. </LI> <LI> Porous and biodegradable biomimetic apatite releases of sirolimus over 40days. </LI> <LI> Integrity of biomimetic apatite is sufficient for clamping and balloon expansion. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

      • KCI등재

        Hearing Improvement in A/J Mice via the Mouse Nerve Growth Factor

        Lixiang Gao,Ruli Ge,Gang Xie,Dandan Yao,Ping Li,Oumei Wang,Xiufang Ma,Fengchan Han 대한이비인후과학회 2017 Clinical and Experimental Otorhinolaryngology Vol.10 No.4

        Objectives. To investigate the otoprotective effects of mouse nerve growth factor (mNGF) in A/J mice. Methods. The mice at postnatal day 7 (P7) were randomly separated into a mNGF treated group (mNGF group) and a distilled water (for injection) treated group (control group). The mNGF dissolved in distilled water or distilled water alone was given to the mice once every other day from P7 by intramuscular injection in the hips. The otoprotective effects of mNGF in A/J mice were observed in a time course manner. The thresholds of auditory-evoked brainstem response (ABR) were tested from the age of the 3rd to the 8th week. Sections of the inner ears were stained by hematoxylin and eosin, and spiral ganglion neurons (SGNs) were observed at the age of the 3rd, the 6th, and the 8th week. Counts of whole mount outer hair cells (OHCs) in the cochleae were made at the age of 8 weeks. Expression of apoptosis related genes was determined by quantitative real-time polymerase chain reaction and Western blotting. Results. ABR thresholds of the mNGF group were significantly lower than those of the control group at the age of the 6th and the 8th week. Moreover, the mNGF preserved OHC and SGN in the mouse cochleae in this period. Further experiments showed that the expression of caspase genes (including caspase-3) was inhibited in the mouse inner ears in the mNGF group. Conclusion. The mNGF improves hearing in A/J mice by preserving SGN and OHC in the cochleae.

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