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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>
Alu Methylation in Serum from Patients with Nasopharyngeal Carcinoma
Tiwawech, Danai,Srisuttee, Ratakorn,Rattanatanyong, Prakasit,Puttipanyalears, Charoenchai,Kitkumthorn, Nakarin,Mutirangura, Apiwat Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.22
Background: Nasopharyngeal carcinoma (NPC) is a common cancer in Southern China and Southeast Asia. Alu elements are among the most prevalent repetitive sequences and constitute 11% of the human genome. Although Alu methylation has been evaluated in many types of cancer, few studies have examined the levels of this modification in serum from NPC patients. Objective: To compare the Alu methylation levels and patterns between serum from NPC patients and normal controls. Materials and Methods: Sera from 50 NPC patients and 140 controls were examined. Quantitative combined bisulfite restriction analysis-Alu (qCOBRA-Alu) was applied to measure Alu methylation levels and characterize Alu methylation patterns. Amplified products were classified into four patterns according to the methylation status of 2 CpG sites: hypermethylated (methylation at both loci), partially methylated (methylation of either of the two loci), and hypomethylated (unmethylated at both loci). Results: A comparison of normal control sera with NPC sera revealed that the latter presented a significantly lower methylation level (p=0.0002) and a significantly higher percentage of hypomethylated loci (p=0.0002). The sensitivity of the higher percentage of Alu hypomethyted loci for distinguishing NPC patients from normal controls was 96%. Conclusions: Alu elements in the circulating DNA of NPC patients are hypomethylated. Moreover, Alu hypomethylated loci may represent a potential biomarker for NPC screening.
Down-regulation of HIF-1α by oncolytic reovirus infection independently of VHL and p53
Cho, I-R,Koh, S S,Min, H-J,Park, E-H,Ratakorn, S,Jhun, B H,Jeong, S H,Yoo, Y H,Youn, H D,Johnston, R N,Chung, Y-H Nature Publishing Group 2010 Cancer gene therapy Vol.17 No.5
<P>Many oncolytic viruses are currently being tested as potential cancer therapeutic agents. To be effective, these viruses must replicate and propagate efficiently through the tumor mass. However, it is possible that the hypoxia that characterizes many tumors may be an obstacle to viral therapy because of its inhibition of viral replication and propagation. We, therefore, decided to test how oncolytic reovirus and its target cells respond to hypoxia. We found that reovirus infection suppresses hypoxia inducible factor (HIF)-1 alpha protein levels (but not transcript abundance) in colon cancer HCT116 cells under CoCl(2) or hypoxia. Reovirus infection was able to reduce HIF-1 alpha levels in both von Hippel Lindau (VHL)-/- renal carcinoma A498 and p53-/- HCT116 cells, indicating that the decrease of HIF-1 alpha mediated by reovirus requires neither VHL nor p53 proteins. However, treatment with the inhibitor MG132 restored HIF-1 alpha levels, suggesting that reovirus-induced HIF-1 alpha decrease needs proteosomal activity. A498 VHL-/- cells with constitutive expression of HIF-1 alpha were relatively resistant to reovirus-induced apoptosis when compared with A498 VHL+/+ cells. However, we found that the use of YC-1 to target HIF-1 alpha promoted reovirus-induced apoptosis in A498 VHL-/- cells. Accordingly, we propose that reovirus may be used together with YC-1 as a potential therapeutic agent against chemoresistant or radioresistant tumors that are hypoxic and show increased levels of HIF-1 alpha. Cancer Gene Therapy (2010) 17, 365-372; doi:10.1038/cgt.2009.84; published online 15 January 2010</P>
Identification of Pancreatic Cancer in Biliary Obstruction Patients by FRY Site-specific Methylation
Angsuwatcharakon, Phonthep,Rerknimitr, Rungsun,Kongkam, Pradermchai,Ridtitid, Wiriyaporn,Ponauthai, Yuwadee,Srisuttee, Ratakorn,Kitkumthorn, Nakarin,Mutirangura, Apiwat Asian Pacific Journal of Cancer Prevention 2016 Asian Pacific journal of cancer prevention Vol.17 No.9
Background: Methylation at cg 16941656 of FRY is exclusively found in normal pancreatic tissue and has been proven to be specific for pancreatic-in-origin among several adenocarcinomas. Here, we investigated methylated DNA in the bile as a biomarker to differentiate the cause of obstruction between pancreatic cancer and benign causes. Materials and Methods: Bile samples of 45 patients with obstructive jaundice who underwent ERCP were collected and classified into pancreatic cancer (group 1) and benign causes (group 2) in 24 and 21 patients, respectively. DNA was extracted from bile and bisulfite modification was performed. After, methylation in cg 16941656 of FRY was identified by real-time PCR, with beta-actin used as a positive control. Results: Methylated DNA was identified in 10/24 (41.67%) and 1/21 (4.8%) of cases in groups 1 and 2, respectively (P= 0.012). The sensitivity, specificity, positive predictive value and negative predictive value to differentiate pancreatic cancer from benign causes were 42%, 95%, 91%, and 59%, respectively. Conclusions: Detecting a methylation at cg 16941656 of FRY in bile has high specificity, with an acceptable positive likelihood rate, and may therefore be helpful in distinguish pancreatic cancer from benign strictures.