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( You Jin Chang ),( Seon Ye Kim ),( Yun Jung Choi ),( Kwang Sup So ),( Jin Kyung Rho ),( Woo Sung Kim ),( Jae Cheol Lee ),( Jin Haeng Chung ),( Chang Min Choi ) 대한결핵 및 호흡기학회 2013 Tuberculosis and Respiratory Diseases Vol.75 No.3
Background:Smallcelllungcancer(SCLC)transformationduringepidermalgrowthfactorreceptortyrosinekinaseinhibitor(EGFR-TKI)treatmentinlungcancerhasbeensuggestedasoneofpossibleresistancemechanisms.Methods:WeevaluatedwhetherSCLCtransformationorneuroendocrine(NE)differentiationcanbefoundinthecelllinemodel.Inaddition,wealsoinvestigateditseffectonresponsestoconventionalchemotherapeuticdrugsoftheSCLCtreatment.Results:ResistantcelllinestovariouskindsofEGFR-TKIssuchasgefitinib,erlotinib,CL-387,785andZD6474withA549,PC-9andHCC827lungadenocarcinomacelllineswereestablished.Amongthem,tworesistantcelllines,A549/GR(resistanttogefitinib)andPC-9/ZDR(resistanttoZD6474)showedincreasedexpressionsofCD56whileincreasedsynaptophysin,Rb,p16andpoly(ADP-ribose)polymerasewerefoundonlyinA549/GRinwesternblotting,suggestingthatNEdifferentiationoccurredinA549/GR.A549/GRcellsweremoresensitivetoetoposideandcisplatin,chemotherapeuticdrugsforSCLC,comparedtoparentalcells.TreatmentwithcAMPandIBMXinducedsynaptophysinandchromograninAexpressioninA549cells,whichalsomadethemmoresensitivetoetoposideandcisplatinthanparentalcells.Furthermore,wefoundatissuesamplefromapatientwhichshowedincreasedexpressionsofCD56andsynaptophysinafterdevelopmentofresistancetoerlotinib.Conclusion:NEdifferentiationcanoccurduringacquisitionofresistancetoEGFR-TKI,leadingtoincreasedchemosensitivity.
So, Kwang Sup,Rho, Jin Kyung,Choi, Yun Jung,Kim, Seon Ye,Choi, Chang Min,Chun, Young Jin,Lee, Jae Cheol Potamitis Press 2015 Anticancer research Vol.35 No.3
<P>The response to chemotherapeutic drugs in non-small cell lung cancer (NSCLC) is unsatisfactory, leading to poor outcomes. This study the aimed to investigates anticancer effects of CX-4945, a potent casein kinase II (CK2) inhibitor, in chemorefractory NSCLC cells.</P>
Chang, Youjin,Kim, Seon Ye,Choi, Yun Jung,So, Kwang Sup,Rho, Jin Kyung,Kim, Woo Sung,Lee, Jae Cheol,Chung, Jin-Haeng,Choi, Chang-Min The Korean Academy of Tuberculosis and Respiratory 2013 Tuberculosis and Respiratory Diseases Vol.75 No.3
Background: Small cell lung cancer (SCLC) transformation during epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) treatment in lung cancer has been suggested as one of possible resistance mechanisms. Methods: We evaluated whether SCLC transformation or neuroendocrine (NE) differentiation can be found in the cell line model. In addition, we also investigated its effect on responses to conventional chemotherapeutic drugs of the SCLC treatment. Results: Resistant cell lines to various kinds of EGFR-TKIs such as gefitinib, erlotinib, CL-387,785 and ZD6474 with A549, PC-9 and HCC827 lung adenocarcinoma cell lines were established. Among them, two resistant cell lines, A549/GR (resistant to gefitinib) and PC-9/ZDR (resistant to ZD6474) showed increased expressions of CD56 while increased synaptophysin, Rb, p16 and poly(ADP-ribose) polymerase were found only in A549/GR in western blotting, suggesting that NE differentiation occurred in A549/GR. A549/GR cells were more sensitive to etoposide and cisplatin, chemotherapeutic drugs for SCLC, compared to parental cells. Treatment with cAMP and IBMX induced synaptophysin and chromogranin A expression in A549 cells, which also made them more sensitive to etoposide and cisplatin than parental cells. Furthermore, we found a tissue sample from a patient which showed increased expressions of CD56 and synaptophysin after development of resistance to erlotinib. Conclusion: NE differentiation can occur during acquisition of resistance to EGFR-TKI, leading to increased chemosensitivity.
Kim, Ji Hye,Nam, Boas,Choi, Yun Jung,Kim, Seon Ye,Lee, Jung-Eun,Sung, Ki Jung,Kim, Woo Sung,Choi, Chang-Min,Chang, Eun-Ju,Koh, Jae Soo,Song, Joon Seon,Yoon, Shinkyo,Lee, Jae Cheol,Rho, Jin Kyung,Son, American Association for Cancer Research 2018 Cancer Research Vol.78 No.16
<P>Enhanced glycolysis by EGFR mutation is required for maintaining EGFR levels via inhibition of JNK-induced autophagy. This provides a promising rationale for use of JNK activators in patients with EGFR-mutated NSCLC.</P><P>Oncogenic EGFR is essential for the development and growth of non–small cell lung cancer (NSCLC), but the precise roles of EGFR in lung cancer metabolism remain unclear. Here, we show that EGFR mutation-mediated enhancement of glycolysis is critical for EGFR stability. EGFR knockdown significantly decreased levels of glycolytic pathway intermediates via transcriptional regulation of glycolytic genes. EGFR mutation-enhanced glycolysis was required for fueling the tricarboxylic acid cycle, a critical component of EGFR stability. Nonsustained ATP production enhanced reactive oxygen species accumulation and subsequent JNK-mediated activation of autophagy, which in turn induced EGFR degradation. Our data show that EGFR-mutant NSCLCs require EGFR mutation-enhanced glycolysis to maintain EGFR stability. This pathway may serve as an attractive therapeutic target for EGFR-mutant NSCLCs.</P><P><B>Significance:</B> Enhanced glycolysis by EGFR mutation is required for maintaining EGFR levels via inhibition of JNK-induced autophagy. This provides a promising rationale for use of JNK activators in patients with EGFR-mutated NSCLC. <I>Cancer Res; 78(16); 4482–96. ©2018 AACR</I>.</P>
Yoon, Jin-Hwan,Kim, Kwang-Woo,Kim, Je-Han,Heo, Kyu-Young,Jin, Kyeong-Sik,Jin, Sang-Woo,Shin, Tae-Joo,Lee, Byeong-Du,Rho, Ye-Cheol,Ahn, Byung-Cheol,Ree, Moon-Hor The Polymer Society of Korea 2008 Macromolecular Research Vol.16 No.7
There are two beamlines (BLs), 4C1 and 4C2, at the Pohang Accelerator Laboratory that are dedicated to small angle X-ray scattering (SAXS). The 4C1 BL was constructed in early 2000 and is open to public users, including both domestic and foreign researchers. In 2003, construction of the second SAXS BL, 4C2, was complete and commissioning and user support were started. The 4C2 BL uses the same bending magnet as its light source as the 4C1 BL. The 4C1 BL uses a synthetic double multilayer monochromator, whereas the 4C2 BL uses a Si(111) double crystal monochromator for both small angle and wide angle X-ray scattering. In the 4C2 BL, the collimating mirror is positioned behind the monochromator in order to enhance the beam flux and energy resolution. A toroidal focusing mirror is positioned in front of the monochromator to increase the beam flux and eliminate higher harmonics. The 4C2 BL also contains a digital cooled charge coupled detector, which has a wide dynamic range and good sensitivity to weak scattering, thereby making it suitable for a range of SAXS and wide angle X-ray scattering experiments. The general performance of the 4C2 BL was initially tested using standard samples and further confirmed by the experience of users during three years of operation. In addition, several grazing incidence X-ray scattering measurements were carried out at the 4C2 BL.