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김승욱,Waraporn Malilas,Seong Woo Kang,김성봉,Hah Young Yoo,Warawut Chulalaksananukul 한국화학공학회 2013 Korean Journal of Chemical Engineering Vol.30 No.2
Lipase was produced by Penicillium camembertii KCCM 11268 under solid state fermentation (SSF), and the production process was optimized by using statistical experimental designs. The initial moisture content, cultivation time, inoculum size and concentration of basal medium were considered as the factors of optimum conditions for SSF. P. camembertii KCCM 11268 was cultivated in SSF using wheat bran as the substrate for lipase production. Under the optimized condition, lipase activity was reached around 7.8 U/ml after eight days fermentation. To partially purify the lipase, ammonium sulfate (80% saturation) was added to the crude lipase solution and concentrated using a diafiltration (VIVAFLOW 50). The concentrated lipase solution from P. camembertii KCCM 11268 (PCL) was immobilized on silica gel by cross-linking method. Also, PCL was mixed with a commercial lipase solution from Candida rugosa (CRL), and this mixture was co-immobilized on silica gel. The immobilized and co-immobilized lipase activities were 1150.1 and 7924.8 U/g matrix, respectively. Palm oil and methanol were used as substrates and 1mmol of methanol was added every 1.5 h and 2 times during biodiesel production. The reaction was carried out at temperatures of 30,40, 50, 60 and 70 oC. The maximum biodiesel conversion by co-immobilized lipase was 99% after 5 h at 50 oC.
KAEWPIBOON, CHUTIMA,SRISUTTEE, RATAKORN,MALILAS, WARAPORN,MOON, JEONG,OH, SANGTAEK,JEONG, HYE GWANG,JOHNSTON, RANDAL N.,ASSAVALAPSAKUL, WANCHAI,CHUNG, YOUNG-HWA SPANDIDOS PUBLICATIONS 2015 MOLECULAR MEDICINE REPORTS Vol.11 No.3
<P>Despite efforts to develop efficient chemotherapeutic drug strategies to treat cancer, acquired drug resistance is a commonly encountered problem. In the present study, to investigate this phenomenon, human A549 lung cancer cells resistant to the topoisomerase inhibitor etoposide (A549RT???eto) were used and compared with A549 parental cells. A549RT???eto cells demonstrated increased resistance to etoposide???induced apoptosis when compared with A549 parental cells. Notably, A549RT???eto cells were observed to exhibit greater levels of histone deacetylase 4 (HDAC4), phospho???Stat1 and P???glycoprotein [P???gp; encoded by the multidrug resistance 1 (MDR1) gene], compared with A549 cells. To address whether HDAC4 protein is involved in etoposide resistance in A549 cells, A549RT???eto cells were treated with trichostatin A (TSA; an HDAC inhibitor) during etoposide treatment. The combined treatment was demonstrated to enhance etoposide???induced apoptosis and reduce expression levels of HDAC4, P???gp and phospho???Stat1. In addition, the suppression of Stat1 with siRNA enhanced etoposide???induced apoptosis and reduced the expression levels of HDAC4 and P???gp, suggesting that Stat1 is essential in the regulation of resistance to etoposide, and in the upregulation of P???gp. Notably, TSA treatment reduced P???gp transcript levels but Stat1 siRNA treatment did not, suggesting that P???gp is regulated by HDAC at the transcriptional level and by Stat1 at the post???transcriptional level. These results suggest that the upregulation of Stat1 and HDAC4 determines etoposide resistance through P???gp expression in human A549 lung cancer cells.</P>