Fluorodeoxyglucose positron emission tomography/conlputed tomography （FDG PET/CT） is widely applied in non-small cell lung cancer （NSCLC）. The standardized uptake value （SUV）, a semi-quantitative index, plays an...Fluorodeoxyglucose positron emission tomography/conlputed tomography （FDG PET/CT） is widely applied in non-small cell lung cancer （NSCLC）. The standardized uptake value （SUV）, a semi-quantitative index, plays an essential role in NSCLC tbr diagnosis, staging, and efficacy evaklation. It has been px3posed that the SUV of tumors may correlate with the presence or absence of chemotherapy resistance-associated biomarkers based on studies that have displayed a close correlation between SUV and the expression levels of excision repair cross-complementary Group 1 （ERCC 1 ）1~1 and Tp53-induced glycolysis and apoptosis regulator.121 FDG avidity of NSCLC and ERCC 1 and ribonucleotide reductase subunit M 1 （RRM 1 ） levels have not been as extensively investigated. Based on these findings, we looked tbr correlations among metabolic parameters （SUVm,,. metabolic tumor volume [MTV], and total lesion glycolysis [TLG]） and ERCC1 and RRM1 expression in patients with NSCLC, to investigate whether FDG uptake reflects the presence or absence ofchemoresistance proteins （ERCC1 and RRM 1 ） within tumor cells.展开更多
AIM:To elucidate the effects of melatonin on cisplatininduced hepatocellular carcinoma(HepG2) cell death and to identify potential cross-talk pathways.METHODS:Hepatocellular carcinoma HepG2 cells were treated with mel...AIM:To elucidate the effects of melatonin on cisplatininduced hepatocellular carcinoma(HepG2) cell death and to identify potential cross-talk pathways.METHODS:Hepatocellular carcinoma HepG2 cells were treated with melatonin and/or cisplatin for 24 to 48 h.Cell viability and the 50% cytotoxic concentration(CC50) were calculated by MTT assays.The effects and intracellular events induced by the selected concentrations of melatonin(1 mmol/L) and cisplatin(20 μmol/L) were investigated.Cell death and survival detection were primarily evaluated using a fluorescence microscope to assess 4',6 diamideno-2-phenylindol DNA staining and acridine orange lysosome staining and then further analyzed with immunocytochemistry using an anti-LC3 antibody.The potential molecularresponses mediated by melatonin against cisplatin after the combined treatment were investigated by reverse transcription-polymerase chains reaction and Western blot analyses of the genes and proteins associated with cell survival and death.A cell cycle analysis was performed using a flow cytometry assay.RESULTS:Melatonin had a concentration-dependent effect on HepG2 cell viability.At 1 mmol/L,melatonin significantly increased the cell viability percentage and decreased reactive oxygen species production due to cisplatin.Melatonin reduced cisplatin-induced cell death,decreasing phosphorylated p53 apoptotic protein,cleaved caspase 3 and Bax levels but increasing anti-apoptotic Bcl-2 gene and protein expression.When combined with cisplatin,melatonin induced S phase(DNA synthesis) cell cycle arrest and promoted autophagic events in HepG2 cells.Melatonin also had a concentration-dependent effect on Beclin-1 and its autophagic regulator mammalian target of rapamycin(mTOR) as well as the DNA excision repair cross complementary 1(ERCC1) protein.The expression levels of these proteins were altered in HepG2 cells during cisplatin or melatonin treatment alone.In the combination treatment,melatonin reversed the effects of cisplatin by suppressing the over-expression of m展开更多
文摘Fluorodeoxyglucose positron emission tomography/conlputed tomography （FDG PET/CT） is widely applied in non-small cell lung cancer （NSCLC）. The standardized uptake value （SUV）, a semi-quantitative index, plays an essential role in NSCLC tbr diagnosis, staging, and efficacy evaklation. It has been px3posed that the SUV of tumors may correlate with the presence or absence of chemotherapy resistance-associated biomarkers based on studies that have displayed a close correlation between SUV and the expression levels of excision repair cross-complementary Group 1 （ERCC 1 ）1~1 and Tp53-induced glycolysis and apoptosis regulator.121 FDG avidity of NSCLC and ERCC 1 and ribonucleotide reductase subunit M 1 （RRM 1 ） levels have not been as extensively investigated. Based on these findings, we looked tbr correlations among metabolic parameters （SUVm,,. metabolic tumor volume [MTV], and total lesion glycolysis [TLG]） and ERCC1 and RRM1 expression in patients with NSCLC, to investigate whether FDG uptake reflects the presence or absence ofchemoresistance proteins （ERCC1 and RRM 1 ） within tumor cells.
基金Supported by Center of Excellence on Environmental Health and Toxicology,Science and Technology Postgraduate Education and Research Development Office,Thailand Ministry of Education
文摘AIM:To elucidate the effects of melatonin on cisplatininduced hepatocellular carcinoma(HepG2) cell death and to identify potential cross-talk pathways.METHODS:Hepatocellular carcinoma HepG2 cells were treated with melatonin and/or cisplatin for 24 to 48 h.Cell viability and the 50% cytotoxic concentration(CC50) were calculated by MTT assays.The effects and intracellular events induced by the selected concentrations of melatonin(1 mmol/L) and cisplatin(20 μmol/L) were investigated.Cell death and survival detection were primarily evaluated using a fluorescence microscope to assess 4',6 diamideno-2-phenylindol DNA staining and acridine orange lysosome staining and then further analyzed with immunocytochemistry using an anti-LC3 antibody.The potential molecularresponses mediated by melatonin against cisplatin after the combined treatment were investigated by reverse transcription-polymerase chains reaction and Western blot analyses of the genes and proteins associated with cell survival and death.A cell cycle analysis was performed using a flow cytometry assay.RESULTS:Melatonin had a concentration-dependent effect on HepG2 cell viability.At 1 mmol/L,melatonin significantly increased the cell viability percentage and decreased reactive oxygen species production due to cisplatin.Melatonin reduced cisplatin-induced cell death,decreasing phosphorylated p53 apoptotic protein,cleaved caspase 3 and Bax levels but increasing anti-apoptotic Bcl-2 gene and protein expression.When combined with cisplatin,melatonin induced S phase(DNA synthesis) cell cycle arrest and promoted autophagic events in HepG2 cells.Melatonin also had a concentration-dependent effect on Beclin-1 and its autophagic regulator mammalian target of rapamycin(mTOR) as well as the DNA excision repair cross complementary 1(ERCC1) protein.The expression levels of these proteins were altered in HepG2 cells during cisplatin or melatonin treatment alone.In the combination treatment,melatonin reversed the effects of cisplatin by suppressing the over-expression of m
