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Radiotherapy diagnostic biomarkers in radioresistant human H460 lung cancer stem-like cells
Yun, Hong Shik,Baek, Jeong-Hwa,Yim, Ji-Hye,Um, Hong-Duck,Park, Jong Kuk,Song, Jie-Young,Park, In-Chul,Kim, Jae-Sung,Lee, Su-Jae,Lee, Chang-Woo,Hwang, Sang-Gu TaylorFrancis 2016 Cancer Biology & Therapy Vol.17 No.2
<P><B>ABSTRACT</B></P><P>Tumor cell radioresistance is a major contributor to radiotherapy failure, highlighting the importance of identifying predictive biomarkers for radioresistance. In this work, we established a radioresistant H460 (RR-H460) cell line from parental radiosensitive H460 lung cancer cells by exposure to fractionated radiation. The radiation-resistant, anti-apoptotic phenotype of RR-H460 cell lines was confirmed by their enhanced clonogenic survival and increased expression of the radioresistance genes Hsp90 and Her-3. RR-H460 cells displayed characteristics of cancer stem-like cells (CSCs), including induction of the surface marker CD44 and stem cell markers Nanog, Oct4, and Sox2. RR-H460 cells also exhibited sphere formation and malignant behavior, further supporting a CSC phenotype. Using proteomic analyses, we identified 8 proteins that were up-regulated in RR-H460 CSC lines and therefore potentially involved in radioresistance and CSC-related biological processes. Notably, 4 of these—PAI-2, NOMO2, KLC4, and PLOD3—have not been previously linked to radioresistance. Depletion of these individual genes sensitized RR-H460 cells to radiotoxicity and additively enhancing radiation-induced apoptosis. Our findings suggest the possibility of integrating molecular targeted therapy with radiotherapy as a strategy for resolving the radioresistance of lung tumors.</P>
Kim, Gwan-Shik,Cheong, Dong-Kyun,Kim, Se-Won,Ko, Seong-Hee,Baek, Jeong-Hwa,Lee, Jong-Oh,Kim, Joong-Soo,Lee, Jong-Heun The Official Publication of Korean Academy of Oral 1994 International Journal of Oral Biology Vol.18 No.2
Transforming growth factor-β(TGF-β) is a multifunctional polypeptide with diverse effects on the proliferation, differentiation and other functions in a wide variety of cells. TGF-β is highly abundant in bone and is now recognized as an important growth regulator and modulator in bone metabolism, but its role in osteoclast differentiation remains controversial. The present study was undertaken to investigate the effects of TGF-β on osteoclast generation induced by prostaglandin E₂(PGE₂) or 1,25-dihydroxycholecalciferol(1,25-DHCC) in mouse bone marrow cutures. The number of osteoclast-like cells (OC-like cells) which retain osteoclast characteristics, including multinuclearity and positive staining for tartrate-resistant acid phosphatase, was increased by PGE₂and 1,25-DHCC in dose-dependent manner. OC-like cell formation in presence of 1,25-DHCC was partially inhibited by simultaneous addition of indomethacin, indicating the possible involvement of endogeneous PG in 1,25-DHCC-induced OC-like cell generation in mouse bone marrow cutures. TGF-β, by itself, failed to produce a significant efftect on OC-like cell formation. In contrast, PGE₂ or 1,25-DHCC-induced generation of OC-like cells was markedly modulated by TGF-β treatment with different profiles. TGF-β reduced the number of OC-like cells formed in presence of PGE₂over the concentration range tested and almost complete inhibition was seen at 1 ng/ml. However, TGF-β produced a biphasic effect on OC-like cell generation induced by 1,25-DHCC; at low concentration stimulated, whereas at higher concentration suppressed the formation of OC-like cell. And further treatment of cultures with indomethacin significantly blocked the stimulatory effect of TGF-β observed at low concentrations. In addition, effect of TGF-β appeared to be time-dependent rather than a generalized one during the whole culture period. TGF-β effectively inhibited PGE₂-induced OC-like cell formation only when it was present at particular period of cultures. These findings suggest that TGF-β modulates various steps in cascade of osteoclast development and activation in different ways involving PG-mediated or PG-insensitive pathways.
Wonhee Kim,Choong Woo Lee,Jong-Shik Baek,Chung Choo Chung,Tomizuka, Masayoshi IEEE 2014 IEEE/ASME transactions on mechatronics Vol.19 No.4
<P>In this paper, a nonlinear controller with dead-zone and saturation is proposed in order to improve the antishock performance. Since using dead-zone and saturation improves the stability margin, we can use a higher gain for the dead-zone than in the previous methods. In addition, we find that the overall controller with a linear lead-lag controller has an improved stability margin over controllers with the PID linear control in this application. The experimental results confirmed that the proposed method provides improved protection against external shock.</P>