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ABSTRACT: The present study aimed to evaluate the role of melanoma antigen family A (MAGEA) in gastric and colorectal cancer cell lines and clinical tissue samples. we used 10 gastric and 9 colorectal cancer cell lines, 20 early-stage and 21 advanced-stage gastric cancer tissues, 20 colon adenomas and 19 colorectal cancer tissues. Real-time RT-PCR assay was used for the determination of MAGEA mRNA levels. Western blot analysis and immunohistochemistry were used for the determination of MAGEA protein levels in cell lines and tissues, respectively. Gastric and colorectal cancer cell lines showed variable mRNA expression levels of MAGEA. The MAGEA protein was detected in 30% of gastric cancer cell lines and in 22.2% of colorectal cancer cell lines. There was a high correlation between mRNA and protein expression. Regarding the clinical samples, MAGEA expression was noted in 25, 28.6 and 31.6%, respectively in early-stage, advanced-stage gastric cancer tissues and colon adenocarcinoma, but was negative in the adjacent normal tissues of the stomach and colon as well as colon adenoma. These results indicate that MAGEA is involved in the carcinogenesis of gastric and colorectal cancer and, therefore, can be used as a diagnostic marker to predict these cancers.
Oncology Reports 05/2013; · 1.84 Impact Factor
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Cheol-Hee Choi,
Hyang-Sook Kim,
Oh-Seong Kweon, Tae-Bum Lee,
Ho-Jin You,
Han-Sik Rha,
Jae-Hwan Jeong,
Dong-Yoon Lim,
Young-Don Min,
Myung-Suk Kim,
Myung-Hee Chung
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ABSTRACT: Reactive oxygen species (ROS)-specific mechanisms of drug resistance were explored in paraquat (PQ)-resistant acute myelogenous
leukemia cell (OCI/AML-2) sublines. For this, PQ-resistant AML sublines, AML-2/PQ100 and AML-2/PQ400, were selected in the
presence of PQ concentrations of 100 μg/ml and 400 μg/ml, respectively. They showed a moderate level of cross resistance to
cisplatin and doxorubicin. They were also slightly more resistant than the parental cell (AML-2/WT) to etoposide, camptothecin
and daunorubicin. The resistance of PQ-resistant AML-2 sublines to cisplatin seemed to be due to increased amounts of metallothionein,
which was not only supported by reversal of resistance to cisplatin by propargylglycin (an inhibitor of metallothionein synthesis)
but also confirmed by Western blot analysis and reverse transcription-PCR assay. In addition, both AML-PQ100 and /PQ400 sublines
showed increased activities of Cu-, Zn-containing superoxide dismutase (Cu,Zn-SOD) and Mn-containing superoxide dismutase
(Mn-SOD), whereas AML-2/PQ400, but not AML-2/PQ100, showed increased glutathione S-transferase activity as compared to that
of AML-2/WT. However, there was no difference in other ROS-related cellular antioxidants between AML-2/WT and its PQ-resistant
sublines. Taken together, these results strongly suggest that increases in levels of metallothionein, glutathione S-transferase,
Cu,Zn-SOD and Mn-SOD play important roles in protective mechanisms against toxicity of PQ or ROS in AML cells.
KeywordsAcute Myelogenous Leukemia-Glutathione
Molecules and Cells 04/2012; 10(1):38-46. · 2.18 Impact Factor
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ABSTRACT: We explored if epigenetic mechanisms could be involved in the down-regulated expression of catalase gene (CAT) in the doxorubicin-resistant acute myelogenous leukemia (AML)-2/DX100 cells. Down-regulated CAT expression in AML-2/DX100 cells was completely recovered after treatment of hydrogen peroxide (H(2)O(2)) and histone deacetylase inhibitor, trichostatin A (TSA) but was increased slightly by the treatment of DNA methylation inhibitor, 5-aza-2'-deoxycytidine (5-AdC). Bisulfite-sequencing PCR revealed that a CpG island of CAT was not methylated in AML-2/DX100 cells. Chromatin immunoprecipitation assay confirmed that acetylation of histone H4 in AML-2/DX100 cells significantly decreased as compared with that in AML-2/WT cells, which was significantly increased by TSA more than 5-AdC. Meanwhile, overexpression of other up-regulated peroxidase genes appears to make compensation for decreased H(2)O(2)-scavenging activity for the down-regulated CAT expression in AML-2/DX100 cells. These results suggest that histone H4 deacetylation is responsible for the down-regulated CAT expression in AML-2/DX100 cells, which are well adapted to oxidative stress.
Cell Biology and Toxicology 02/2012; 28(1):11-8. · 2.51 Impact Factor
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ABSTRACT: It has been suggested that constitutive up-regulation of cyclooxygenase (COX)-2 is associated with resistance to apoptosis, increased angiogenesis, and increased tumor invasiveness in various cancers including colon cancer. There are many factors involved in the resistance to 5-fluorouracil (5-FU) in colon cancer. However, little is known about the role of COX-2 in acquired resistance to 5-FU in colon cancer.
Hence we investigated whether COX-2 contribute to acquired resistance to 5-FU in colon cancer cells, using cytotoxicity assay for cell survival, reverse transcription-polymerase chain reaction (RT-PCR) for vascular endothelial growth factor (VEGF), quantitative RT-PCR for COX-1 and COX-2, and enzyme-linked immunosorbent assay for PGE(2).
The 5-FU resistant colon cancer cells, SNU-C5/5FUR, showed increased expression of COX-2, prostaglandin E(2) (PGE(2)), and VEGF, compared to its parental cell (SNU-C5). By treatment with meloxicam, the expression of PGE(2) and VEGF was reduced significantly in the resistant cells, but not in the parent cells.
These results demonstrate that COX-2 derived PGE(2) is up-regulated and COX-2 inhibitor may have an anti-angiogenic effect in the colon cancer cells resistant to 5-FU.
Journal of the Korean Surgical Society. 08/2011; 81(2):115-21.
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ABSTRACT: Ursodeoxycholic acid (UDCA) is known as a suppressor of cholestatic liver diseases and colorectal cancer development. Here, we demonstrate that UDCA induces apoptosis without necrotic features in SNU601, SNU638, SNU1 and SNU216 human gastric cancer cells, implying its possible use as an effective chemotherapeutic agent in treatment of gastric cancer. UDCA-induced apoptosis was dominantly mediated by an extrinsic pathway dependent on caspase-8, -6 and -3. UDCA increased expression of death receptor 5 [(DR5), also known as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2], and this DR appeared to be responsible for UDCA-induced apoptosis, as evidenced by DR5 knockdown. UDCA triggered formation of lipid rafts that played crucial roles in UDCA-induced apoptotic actions. Lipid rafts were required not only for provision of a proper site for DR5 action but also for mediation of DR5 expression. In addition, reactive oxygen species (ROS) and protein kinase C (PKC) δ appeared to be implicated in UDCA-induced raft-dependent DR5 expression. Our results indicate that UDCA-induced apoptosis is mediated by DR5 expression, which is regulated by the raft formation/ROS production/PKCδ activation pathway and DR5 localization into lipid rafts in gastric cancer cells. Tumor-suppressive activity of UDCA was confirmed in an in vivo system: UDCA (120 mg/kg/day) significantly decreased tumor growth in gastric cancer xenograft mice. Taken together, our results demonstrate that UDCA can be used as a potent chemotherapeutic agent for treatment of gastric cancer.
Carcinogenesis 02/2011; 32(5):723-31. · 5.70 Impact Factor
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ABSTRACT: In addition to cyclooxygenase-2 (COX-2) which is related to prostaglandin E2 synthesis, other enzymes such as cytosolic phospholipase A2 (cPLA2), microsomal prostaglandin E2 synthase-1 (mPGES-1), and 15-prostaglandin dehydrogenase (15-PGDH) have been suggested to be related to carcinogenesis of colorectal cancer (CRC). The aim of this study was to investigate the roles of cPLA2, COX-2, mPGES-1, and 15-PGDH in tumor progression.
cPLA2, COX-2, mPGES-1, 15-PGDH, and vascular endothelial growth factor (VEGF) expressions were immunohistochemically examined in 89 CRC, and their expressions were compared with each other or clinicopathologic parameters as well as VEGF as tumor progression parameters.
cPLA2 was expressed in 54.5%, COX-2 in 80.5%, mPGES-1 in 96.4%, 15-PGDH in 46.1%, and VEGF in 65.9%. The expression of cPLA2 correlated with VEGF expression. COX-2 expression was correlated with the depth of invasion, tumor stage, cPLA2, and VEGF expressions. Moreover, VEGF revealed the highest expression in the tissues positive for both cPLA2 and COX-2. Furthermore, 15-PGDH expression was inversely correlated with VEGF expression.
The present study demonstrates that cPLA2 and mPGES-1, in addition to COX-2, are constitutively overexpressed, and that 15-PGDH might be attenuated in colorectal cancer. Furthermore, cPLA2 and 15-PGDH as well as COX-2 could have an important role in tumor progression.
Yonsei medical journal 09/2010; 51(5):692-9. · 0.77 Impact Factor
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ABSTRACT: Membrane transporters play important roles in mediating chemoresistance and chemosensitivity of tumor cells. Five sets of 5 genes were designed to simultaneously detect drug transporter expression in a single reaction tube using multiplex RT-PCR for 25 genes, including 17 ABC transporters, one non-ABC transporter, 4 SLC transporters, 2 copper transporters and one housekeeping gene. We optimized the multiplex RT-PCR conditions using chemosensitive cancer cells and then validated the system using chemoresistant cancer cells. This reliable multiplex RT-PCR assay can be utilized not only to investigate anticancer drug-resistance mechanisms but also to estimate the efficacy of anticancer chemotherapy in the clinic.
Biotechnology Letters 07/2009; 31(10):1485-92. · 1.68 Impact Factor
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ABSTRACT: To examine the relationship between p-STAT3 and the clinicopathological parameters of colorectal adenocarcinoma (CRA), we initially conducted immunohistochemical (IHC) analyses on formalin-fixed tissues. A total of 127 invasive CRA, 20 colorectal adenomas and 20 normal mucosae were obtained. To clarify the validity of p-STAT3 as determined by the IHC analysis, quantitative real-time PCR was performed on fresh samples from 51 CRA-4 carcinomas in situ, 47 invasive CRA and on 51 normal mucosae. IHC analyses were conducted after formalin fixation from 51 CRA for comparison. The statistically significant difference of immunoreactivity for p-STAT3 between the CRA and adenoma, and between the CRA and normal mucosae was identified. Among the 174 CRA, p-STAT3 immunoreactivity significantly correlated with the T- and clinical stage. Among the 47 invasive CRA, the expression of STAT3 as determined by real-time PCR significantly correlated with tumor size, M stage and clinical stage. The overall findings of the real-time PCR analyses correlated with the findings of the IHC analyses. These findings suggest that p-STAT3 expression has an important role related to the tumorigenesis and tumor progression of CRAs. Moreover, IHC analysis is a reliable and useful modality of assessing the status of p-STAT3 expression in formalin-fixed samples.
Oncology Reports 10/2008; 20(3):597-604. · 1.84 Impact Factor
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ABSTRACT: Both cellular and clinical studies have shown that hyperthermia is one of the most potent sensitizers for the action of ionizing radiation. Although hyperthermic improvement in clinical outcome is suggested to be linked to its ability to induce cell cycle arrest and apoptosis, and to activate the immune system and to cause increases in blood flow and tumor oxygenation, the mechanism behind this is still unclear. Previously, we demonstrated that glucose deprivation (GD), a common characteristic of the tumor microenvironment, induced necrosis, which is implicated in tumor progression and aggressiveness, through the production of reactive oxygen species (ROS) in A549 lung carcinoma cells. We examined the effects of heat shock on ROS production and necrosis in response to GD. Here we show that mild, but not harsh, heat shock prevented GD-induced necrosis and switched the cell death mode to apoptosis in A549 cells through the ERK1/2 pathway that could suppress GD-induced CuZnSOD release and ROS production. These results demonstrate that contrary to severe heat shock, mild heat shock has the ability to decrease oxidative stress in cells, thereby causing the cell death mode switch from tumor promoting necrosis to tumor suppressive apoptosis, which may contribute to its anti-neoplastic activities.
International Journal of Oncology 05/2008; 32(4):851-60. · 2.40 Impact Factor
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ABSTRACT: The membrane transporters such as P-glycoprotein (Pgp), the MDR1 gene product, are one of causes of treatment failure in cancer patients. In this study, the epigenetic mechanisms involved in differential MDR1 mRNA expression were compared between 10 gastric and 9 colon cancer cell lines.
The MDR1 mRNA levels were determined using PCR and real-time PCR assays after reverse transcription. Cytotoxicity was performed using the MTT assay. Methylation status was explored by quantification PCR-based methylation and bisulfite DNA sequencing analyses.
The MDR1 mRNA levels obtained by 35 cycles of RT-PCR in gastric cancer cells were just comparable to those obtained by 22 cycles of RT-PCR in colon cancer cells. Real-time RT-PCR analysis revealed that MDR1 mRNA was not detected in the 10 gastric cancer cell lines but variable MDR1 mRNA levels in 7 of 9 colon cancer cell lines except the SNU-C5 and HT-29 cells. MTT assay showed that Pgp inhibitors such as cyclosporine A, verapamil and PSC833 sensitized Colo320HSR (colon, highest MDR1 expression) but not SNU-668 (gastric, highest) and SNU-C5 (gastric, no expression) to paclitaxel. Quantification PCR-based methylation analysis revealed that 90% of gastric cancer cells, and 33% of colon cancer cells were methylated, which were completely matched with the results obtained by bisulfite DNA sequencing analysis. 5-aza-2'-deoxcytidine (5AC, a DNA methyltransferase inhibitor) increased the MDR1 mRNA levels in 60% of gastric cells, and in 11% of colon cancer cells. Trichostatin A (TSA, histone deacetylase inhibitor) increased the MDR1 mRNA levels in 70% of gastric cancer cells and 55% of colon cancer cells. The combined treatment of 5AC with TSA increased the MDR1 mRNA levels additively in 20% of gastric cancer cells, but synergistically in 40% of gastric and 11% of colon cancer cells.
These results indicate that the MDR1 mRNA levels in gastric cancer cells are significantly lower than those in colon cancer cells, which is at least in part due to different epigenetic regulations such as DNA methylation and/or histone deacetylation. These results can provide a better understanding of the efficacy of combined chemotherapy as well as their oral bioavailability.
BMC Gastroenterology 02/2008; 8:33. · 2.42 Impact Factor
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ABSTRACT: Cyclooxygenase (COX)-2 is believed to be an important enzyme related to the pathogenesis of colorectal cancer (CRC). p53 has been reported to be a negative regulator of COX-2 expression in in vitro studies. The aim of this study was to investigate COX-2 expression and its relationship with nuclear p53 accumulation and their prognostic significance in CRC.
COX-2 expression and nuclear p53 accumulation were examined by immunohistochemistry in 231 sporadic CRCs. Their prognostic significance and interrelationship were statistically evaluated.
We found 42.4% of the 231 cases of CRCs with positive COX-2 expression. Nuclear p53 accumulation was observed in 46.8% of cases. There was no significant correlation between COX-2 expression and nuclear p53 accumulation. COX-2 expression had no correlation with patient survival, whereas nuclear p53 accumulation was significantly correlated with poor patient survival on univariate and multivariate analysis.
These results suggest that COX-2 expression does not play a role in the prognosis of CRC and COX-2 expression is not affected by the status of nuclear p53 accumulation in CRC. In addition, our findings support that nuclear p53 accumulation may be a useful prognostic marker for patients with CRC.
Journal of Surgical Oncology 02/2008; 97(1):51-6. · 2.10 Impact Factor
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ABSTRACT: This study investigated radioresistance mechanisms in the doxorubicin-resistant acute myelogenous leukemia (AML)-2/DX100. AML-2/DX100 also showed resistance to radiation. AML-2/DX100 characterized by down-regulated catalase expression was supersensitive to exogenous hydrogen peroxide whereas they increased defense mechanisms against endogenous reactive oxygen species (ROS) as compared with AML-2/WT. In AML-2/WT, radiation increased Bax expression and its translocation to mitochondria but had little effect on translocation of Bcl-2 and consequently induced the release of cytochrome c from the mitochondria with the subsequent caspase-3 activation. On the contrary, in AML-2/DX100, radiation neither increased Bax expression nor its translocation to mitochondria while it increased Bcl-2 translocation to mitochondria. A specific p38 MAPK inhibitor SB203580 increased radioresistance in AML-2/WT but little in AML-2/DX100. It inhibited radiation-induced Bax translocation in AML-2/WT but not in AML-2/DX100, indicating that p38 MAPK is working after irradiation in AML-2/WT but not in AML-2/DX100. Electrophoretic mobility shift assay and Western blot analysis revealed that NF-kappaB in AML-2/DX100 was more activated with degradation of cytosolic IkappaBalpha than was that of AML-2/WT. cDNA microarray showed that Bfl-1/A1 and granzyme H in AML-2/DX100 were highly up-regulated (6.21-fold) and down-regulated (6.49-fold), respectively, as compared with each of AML-2/WT, which were confirmed by RT-PCR assay. Taken together, these results indicate that radioresistance mechanisms of AML-2/DX100 could be related to alterations in ROS-scavenging activity, in mitochondrial translocation of Bax and Bcl-2, and in expression of pro-apoptotic (granzyme H) and anti-apoptotic (Bfl-1/A1) genes. It has been shown that balance of p38 MAPK and NF-kappaB signals is a determinant in radiosensitivity of AML-2/WT and AML-2/DX100.
Leukemia Research 10/2007; 31(9):1267-76. · 2.92 Impact Factor
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ABSTRACT: The purpose of this study was to investigate the adaptive mechanisms of hydrogen peroxide-supersensitive AML cells against the reactive oxygen species (ROS). Their scavenging capacity against ROS was determined using a fluorometric probe in the doxorubicin-resistant AML-2/DX100 cell characterized by the down-regulation of catalase. AML-2/DX100 cells had more scavenging capacity against endogenous pro-oxidants than did the parental cells AML-2/WT, suggesting that an anti-oxidant adaptation against ROS occurred. cDNA microarrays for 8000 human genes revealed that among 21 anti-oxidant genes, each four gene was up- and down-regulated more than 1.5-fold in AML-2/DX100 compared with AML-2/WT. The mRNA expression of glutathione S-transferase Pi, peroxiredoxin 2, thioredoxin 2, and glutaredoxin was elevated whereas that of peroxiredoxin 3, metallothionein-1F, superoxide dismutase 2, and thioredoxin reductase 1 was depressed. The result indicates that the down-regulation of certain anti-oxidant mechanisms can be compensated for by the up- and down-regulation of the other anti-oxidant mechanisms.
Biochemical and Biophysical Research Communications 07/2004; 319(1):41-5. · 2.48 Impact Factor
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ABSTRACT: Reactive oxygen species (ROS) cause macromolecular damage and may play an important role in tumor development. Superoxide dismutase (SOD) and metallothionein (MT) serve as initial and final defense mechanisms, respectively, against ROS. We hypothesized that the inducibility of Mn-SOD and MT mRNA by paraquat, an intracellular superoxide generator, might be altered in lymphocytes of gastric cancer patients. The inducibility of Mn-SOD mRNA by paraquat in lymphocytes of 19 normal subjects and the 14 gastric cancer patients was 162.4 +/- 16.7% and 87.9 +/- 9.5%, respectively (P = 0.001). The inducibility of MT mRNA by paraquat in the normal subjects and the gastric cancer patients was 126.7 +/- 15.8% and 115.4 +/- 12.9%, respectively. This suggests that the failure of Mn-SOD mRNA induction by oxidative stress in peripheral lymphocytes may be involved in the development of gastric cancer and may be of value in predicting the future occurrence of gastric cancer. In addition, the wide variation in Mn-SOD and MT mRNA levels among normal subjects may reflect different susceptibilities to diseases including cancer.
Molecules and Cells 09/2003; 16(1):13-8. · 2.18 Impact Factor
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ABSTRACT: Vitamin H (biotin) was incorporated into a hydrophobically modified polysaccharide, pullulan acetate (PA), in order to improve the cancer-targeting activity and internalization of self-assembled nanoparticles. The biotinylated pullulan acetate (BPA) nanoparticles were prepared by a diafiltration method and the mean diameter was approximately 100 nm. Three samples of biotinylated pullulan acetate (BPA), comprising 7 (BPA 1), 20 (BPA 2), and 39 (BPA 3) vitamin H groups per 100 anhydroglucose units of PA, were synthesized. The critical aggregation concentrations (CAC) of the BPA nanoparticles in distilled water were 3.1 x 10(-3), 4.3 x 10(-3) and 6.8 x 10(-3) mg/ml for BPA 1, BPA 2, and BPA 3, respectively. Adriamycin (ADR) was loaded into the BPA nanoparticles as a model drug. The loading efficiencies and ADR content in the BPA nanoparticles decreased with increasing vitamin H content due to a lower hydrophobicity. The RITC-labeled BPA nanoparticles exhibited very strong adsorption to the HepG2 cells, while the RITC-labeled PA nanoparticles did not show any significant interaction. The degree of the interaction increased with increasing vitamin H content. Confocal laser microscopy also revealed that internalization of the BPA nanoparticles into the cancer cells depended on the vitamin H content.
European Journal of Pharmaceutical Sciences 03/2003; 18(2):165-73. · 3.21 Impact Factor
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ABSTRACT: Background and aims: It has been proposed that the expression of Fas ligand (Fas L) in tumors may play an important role in immune escape. This study was undertaken to test a ‘counterattack’ theory as a mechanism of immune escape in gastric carcinoma.Methods: Expression of Fas and Fas L was examined in the human gastric cancer cell lines using reverse transcription–polymerase chain reaction. Cytotoxicity was determined by the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay. Apoptosis of target Jurkat cells was examined after coculture with the effector gastric cancer cells in vitro. Immunohistochemical staining was performed for the detection of Fas and FasL in tumor-infiltrating lymphocytes (TIL) and gastric cancer cells in vivo. Apoptosis was detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) method in vitro and in vivo.Results: Fas and FasL mRNA were found to be differentially expressed in gastric cancer cell lines. The coculture experiment showed that apoptosis of Jurkat was induced by a FasL-overexpressing effector gastric cell SNU-484. In a Fas-expressing gastric cell SNU-638, Fas expression was upregulated by the treatment of gamma-interferon in a time- and concentration-dependent manner. SNU-638 treated with gamma-interferon was more sensitive to anti-Fas antibody-mediated cytotoxicity than was the control cell line, suggesting an increase of functional Fas in gastric cancer cells. The expression of FasL in gastric cancer cells and of Fas in apoptotic TIL was also detected in vivo.Conclusion: The data indicate that the FasL expression of gastric cancer cells supports a ‘counterattack theory’ in gastric cancer cells and that the upregulation of Fas by IFN-γ in SNU-638 may accelerate the apoptosis pathway through the Fas and FasL interaction between gastric cancer cells and immune cells. This result is supported by the expression of FasL in gastric cancer cells and apoptotic TIL in vivo. It is implicated that the different biological behaviors of gastric cancer cells could be at least in part explained by Fas and FasL interaction with immune cells.
Journal of Gastroenterology and Hepatology 03/2002; 17(1):32 - 38. · 2.87 Impact Factor
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ABSTRACT: It has been proposed that the expression of Fas ligand (Fas L) in tumors may play an important role in immune escape. This study was undertaken to test a 'counterattack' theory as a mechanism of immune escape in gastric carcinoma.
Expression of Fas and Fas L was examined in the human gastric cancer cell lines using reverse transcription-polymerase chain reaction. Cytotoxicity was determined by the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay. Apoptosis of target Jurkat cells was examined after coculture with the effector gastric cancer cells in vitro. Immunohistochemical staining was performed for the detection of Fas and FasL in tumor-infiltrating lymphocytes (TIL) and gastric cancer cells in vivo. Apoptosis was detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) method in vitro and in vivo.
Fas and FasL mRNA were found to be differentially expressed in gastric cancer cell lines. The coculture experiment showed that apoptosis of Jurkat was induced by a FasL-overexpressing effector gastric cell SNU-484. In a Fas-expressing gastric cell SNU-638, Fas expression was upregulated by the treatment of gamma-interferon in a time- and concentration-dependent manner. SNU-638 treated with gamma-interferon was more sensitive to anti-Fas antibody-mediated cytotoxicity than was the control cell line, suggesting an increase of functional Fas in gastric cancer cells. The expression of FasL in gastric cancer cells and of Fas in apoptotic TIL was also detected in vivo.
The data indicate that the FasL expression of gastric cancer cells supports a 'counterattack theory' in gastric cancer cells and that the upregulation of Fas by IFN-gamma in SNU-638 may accelerate the apoptosis pathway through the Fas and FasL interaction between gastric cancer cells and immune cells. This result is supported by the expression of FasL in gastric cancer cells and apoptotic TIL in vivo. It is implicated that the different biological behaviors of gastric cancer cells could be at least in part explained by Fas and FasL interaction with immune cells.
Journal of Gastroenterology and Hepatology 02/2002; 17(1):32-8. · 2.87 Impact Factor
