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- 저자 : Luyao Yuan (검색결과 2 건)
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Weijiu Huang,Shanshan Yuan,Linjiang Chai,Luyao Jiang,Haiding Liu,Fangjun Wang,Dongzhe Wang,Junjun Wang 대한금속·재료학회 2019 METALS AND MATERIALS International Vol.25 No.2
A medium-strained (13% cold-drawing) 316L austenitic stainless steel rod was subjected to annealing between 750 and1100 °C. Electron backscatter diffraction and electron channeling contrast imaging techniques were jointly employed toinvestigate the development of microstructures and grain boundary character distribution during the annealing treatments. Results show that annealing at temperatures below 900 °C does not evidently change microstructures of the as-drawn specimen. Full recrystallization is observed after the temperature reaches 1000 °C and the deformation microstructures are replacedby fine and uniform recrystallized grains. A large number of annealing twins (with Σ3 misorientation) are produced by therecrystallization, leading to markedly increased fractions of special boundaries (fSB). The maximum fSB is found to be 67.3%in the present study. In addition, for the recrystallized grains, rapid growth is noticed at relatively high temperatures due toeasy migration of grain boundaries.
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Selumetinib overcomes gefitinib primary and acquired resistance by regulating MIG6/STAT3 in NSCLC
Xiaoping Song,Lina Wang,Wei Tang,Luyao Yuan,Qingchao Liu,Jing Li,Daidi Fan 대한약학회 2023 Archives of Pharmacal Research Vol.46 No.12
Gefitinib, as the first-generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), has achieved great advances in the treatment of non-small cell lung cancer (NSCLC), but drug resistance will inevitably occur. Therefore, exploring the resistance mechanism of gefitinib and developing new combination treatment strategies are of great importance. In our study, the results showed that selumetinib (AZD6244) synergistically inhibited the proliferation of NSCLC with gefitinib. Selumetinib also enhanced gefitinib-induced apoptosis and migration inhibition ability in gefitinib-resistant lung cancer cell lines. Subsequently, the negative regulation between MIG6 and STAT3 was observed and verified through the STRING database and western blotting assays. Sustained activation of STAT3 was significantly downregulated when co-treatment with selumetinib in gefitinib-resistant cells. However, the downregulation of p-STAT3, resulting from the combination of selumetinib and gefitinib was counteracted by the deletion of MIG6, suggesting that selumetinib enhanced gefitinib sensitivity by regulating MIG6/STAT3 in NSCLC. In contrast, p-STAT3 was further inhibited after treatment with gefitinib and selumetinib when MIG6 was overexpressed. Furthermore, the combined administration of selumetinib and gefitinib effectively promoted the sensitivity of lung cancer xenografts to gefitinib in vivo, and the tumor inhibition rate reached 81.49%, while the tumor inhibition rate of the gefitinib monotherapy group was only 31.95%. Overall, MIG6/STAT3 negative regulation plays an important role in the sustained activation of STAT3 and the resistance to EGFR-TKIs. Our study also suggests that EGFR-TKIs combined with MEK1/2 inhibitors, such as selumetinib, may be beneficial to those NSCLC patients who develop a primary or acquired resistance to EGFR-TKIs, providing theoretical support for combining TKIs and selumetinib in clinical cancer treatment.
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