Epithelial-mesenchymal transition（EMT） and mesenchymal-epithelial transition（MET） are essential for embryonic development and also important in cancer progression. In a conventional model, epithelial-like cancer c...Epithelial-mesenchymal transition（EMT） and mesenchymal-epithelial transition（MET） are essential for embryonic development and also important in cancer progression. In a conventional model, epithelial-like cancer cells transit to mesenchymal-like tumor cells with great motility via EMT transcription factors; these mesenchymallike cells migrate through the circulation system, relocate to a suitable site and then convert back to an epithelial-like phenotype to regenerate the tumor. However, recent findings challenge this conventional model and support the existence of a stable hybrid epithelial/mesenchymal（E/M） tumor population. Hybrid E/M tumor cells exhibit both epithelial and mesenchymal properties, possess great metastatic and tumorigenic capacity and are associated with poorer patient prognosis. The hybrid E/M model and associated regulatory networks represent a conceptual change regarding tumor metastasis and organ colonization. It may lead to the development of novel treatment strategies to ultimately stop cancer progression and improve disease-free survival.展开更多
At some point in the natural course of colorectal cancer up to 50% of patients will develop metastasis to the liver and it is one of the most critical effects for patient prognosis. The incidence of synchronous liver ...At some point in the natural course of colorectal cancer up to 50% of patients will develop metastasis to the liver and it is one of the most critical effects for patient prognosis. The incidence of synchronous liver metastasis has been detected at around 20% - 25%, but the optimal timing of surgical resection remains controversial. Neoadjuvant chemotherapy has also been found to be beneficial not only for initially unresectable but also resectable synchronous metastases. Then, traditional surgical strategies of hepatic resection in accordance with past chemotherapeutic regimens have been used decreasingly over the past several years. This review will primarily discuss treatments in association with the recent developed chemotherapeutic regimens and surgical procedure from the clinical data and the concept for epithetlial-mesenchymal transition, which has recently been studied to elucidate mechanisms of the liver metastatic process.展开更多
Objective： To investigate the effect of Rapamycin on epithelial-mesenchymal transition（EMT） of LoVo colonic adenocarcinoma cells in vitro. Methods：Cultured LoVo colonic adenocarcinoma cells were divided into three...Objective： To investigate the effect of Rapamycin on epithelial-mesenchymal transition（EMT） of LoVo colonic adenocarcinoma cells in vitro. Methods：Cultured LoVo colonic adenocarcinoma cells were divided into three groups： negative control group, EMT-inducing group（TGF-β1） and EMT-interfering group（TGF-β1 plus Rapamycin）. E-cadherin expression in LoVo cells was detected by Western Blot, while the expression of vimentin was evaluated through immunocytochemistry. The Snail mRNA in LoVo cells was examined by RT- PCR. Results：TGF-β1 induced LoVo cell switching from polygonal to spindle-shaped. TGF-β1 enhanced the expression of vimentin, but lowered the level of E-cadhefin. In contrast, Rapamycin impaired the transition induced by TGF-β1. Rapamycin dramatically abrogated TGF-β1-induced vimentin expression and restored E-cadherin expression in LoVo cells. Rapamycin significantly repressed the upregulation of Snail mRNA expression induced by TGF-β1. Conclusion：Rapamycin dramatically abrogated TGF-β1 induced Snail mRNA expression in LoVo cells, hence inhibiting EMT of these cells in vitro.展开更多
Objective: To investigate the correlation of SphK1, FAK, Musashi 1 and CA199 expression with angiogenesis and epithelial-mesenchymal transition in surgically removed colon cancer lesions. Methods: A total of 60 patien...Objective: To investigate the correlation of SphK1, FAK, Musashi 1 and CA199 expression with angiogenesis and epithelial-mesenchymal transition in surgically removed colon cancer lesions. Methods: A total of 60 patients with colon cancer who underwent radical operation in our hospital between August 2015 and August 2017 were selected, intraoperative colon cancer tissue samples were collected as colon cancer group, and normal tissue specimens adjacent to carcinoma were collected as adjacent tissue group. Fluorescence quantitative PCR was adopted to determine the expression levels of SphK1, FAK, Musashi 1, CA199 as well as the genes related to angiogenesis and epithelial-mesenchymal transition in colon tissues with different properties. Results: SphK1, FAK, Musashi 1 and CA199 mRNA expression in colon cancer group were higher than those in adjacent tissue group;angiogenesis-related genes ANGPTL4, Apelin-13, DLL1, VEGF and HIF-α mRNA expression were higher than those in adjacent tissue group whereas TSP-1 mRNA expression was lower than that in adjacent tissue group;epithelial-mesenchymal transition-related gene E-cadherin mRNA expression was lower than that in adjacent tissue group whereas Vimentin, N-cadherin, Twist and Snail mRNA expression were higher than those in adjacent tissue group. Correlation analysis showed that the SphK1, FAK, Musashi 1 and CA199 expression in colon cancer tissues were directly correlated with the angiogenesis genes and epithelial-mesenchymal transition genes. Conclusion: SphK1, FAK, Musashi 1 and CA199 genes are abnormally expressed in colon cancer tissues and their expression levels are directly correlated with tumor angiogenesis and epithelial-mesenchymal transition process.展开更多
Objective: To investigate the role and mechanism of autophagy in epithelial-mesenchymal transition (EMT) of oral squamous cell carcinoma cells induced by CQ (chloroquine) and rapamycin (RAPA). Methods: TGF-β (transfo...Objective: To investigate the role and mechanism of autophagy in epithelial-mesenchymal transition (EMT) of oral squamous cell carcinoma cells induced by CQ (chloroquine) and rapamycin (RAPA). Methods: TGF-β (transforming growth factor β) was used to induce EMT in Cal-27 cell line. At the same time, RAPA was used to enhance and CQ was used to inhibit autophagy. The ability of cell migration was detected by scratch distribution test and the ability of cell migration was detected by Transwell chamber test. Western blot was used to detect the changes of ZO-1, vimentin, FN1 and other EMT-related proteins after 3 d induction, and SPSS 22.0 statistical software was used to analyze the data. Results: After 3 d of induction with 5 ng/mL TGF-β, E-cadherin decreased significantly and Vimentin increased significantly. Compared with the control group, the wound healing rate increased significantly (P<0.05) and the number of penetrating cells increased significantly (P<0.05) after 3 d induction with 5 ng/mL TGF-β, and then the cells were co-induced with 100 ng/mL RAPA and 100 ng/mL CQ and 5 ng/mL TGF-β for 3 d. Compared with TGF-β group. The healing rate of the RAPA co-induced with 5 ng/mL TGF-β group decreased significantly (P<0.05) and the number of penetrating cells decreased significantly (P<0.05). Compared with TGF-β group. The healing rate of the CQ co-induced with 5 ng/mL TGF-β group increased significantly (P<0.05) and the number of penetrating cells increased significantly (P<0.05). Compared with the control group, FN1 and Vimentin expression increased and ZO-1 expression decreased 3 d after induction with 5 ng/mL TGF-β. And then induced Cal-27 cells with 100 ng/mL RAPA and 100 ng/mL CQ and 5 ng/mL TGF-β respectively for 3 d. Compared with TGF-β group, FN1 and Vimentin expression decreased in RAPA co-induction group. Compared with TGF-βgroup, the expression of FN1 and Vimentin increased and the expression of ZO-1 decreased in CQ co-induction group. Conclusion: TGF-β can induce Cal-27 cells to establish EMT model. In EMT model, promoting autophagy can inhibit EMT, inhibiting autophagy can promote EMT.展开更多
Metastasis is the main cause of cancer mortality. One of the initiating events of cancer metastasis of epithelial tumors is epithelial-to-mesenchymal transition(EMT), during which cells dedifferentiate from a relative...Metastasis is the main cause of cancer mortality. One of the initiating events of cancer metastasis of epithelial tumors is epithelial-to-mesenchymal transition(EMT), during which cells dedifferentiate from a relatively rigid cell structure/morphology to a flexible and changeable structure/morphology often associated with mesenchymal cells. The presence of EMT in human epithelial tumors is reflected by the increased expression of genes and levels of proteins that are preferentially present in mesenchymal cells. The combined presence of these genes forms the basis of mesenchymal gene signatures, which are the foundation for classifying a mesenchymal subtype of tumors. Indeed, tumor classification schemes that use clustering analysis of large genomic characterizations, like The Cancer Genome Atlas(TCGA), have defined mesenchymal subtype in a number of cancer types, such as high-grade serous ovarian cancer and glioblastoma. However, recent analyses have shown that gene expression-based classifications of mesenchymal subtypes often do not associate with poor survival. This "paradox" can be ameliorated using integrated analysis that combines multiple data types. We recently found that integrating m RNA and micro RNA(mi RNA) data revealed an integrated mesenchymal subtype that is consistently associated with poor survival in multiple cohorts of patients with serous ovarian cancer. This network consists of 8 major mi RNAs and 214 m RNAs. Among the 8 mi RNAs, 4 are known to be regulators of EMT. This review provides a summary of these 8 mi RNAs, which were associated with the integrated mesenchymal subtype of serous ovarian cancer.展开更多
目的:探讨抑制素β亚基A反义RNA1(INHBA-AS1)对宫颈癌HeLa细胞EMT和鸟氨酸代谢途径的影响及其机制。方法:体外常规培养HeLa细胞,实验分为10组:对照组、阴性对照(NC)组、sh-INHBA-AS1组、PluriSIn 1[硬脂酰辅酶A去饱和酶(stearyl CoA des...目的:探讨抑制素β亚基A反义RNA1(INHBA-AS1)对宫颈癌HeLa细胞EMT和鸟氨酸代谢途径的影响及其机制。方法:体外常规培养HeLa细胞,实验分为10组:对照组、阴性对照(NC)组、sh-INHBA-AS1组、PluriSIn 1[硬脂酰辅酶A去饱和酶(stearyl CoA desaturase,SCD)抑制剂]组、NC+PluriSIn 1组、sh-INHBA-AS1+PluriSIn 1组、10058-F4(c-Myc抑制剂)组、NC+10058-F4组、sh-INHBA-AS1+10058-F4组、sh-INHBA-AS1+OE-c-Myc组。平板克隆实验检测各组细胞的增殖能力,FCM检测各组细胞的凋亡情况,Transwell小室实验检测各组细胞的侵袭、迁移能力,qPCR法检测各组细胞中INHBA-AS1、c-Myc、SCD和EMT相关基因(N-cadherin、TGF-β、ZEB1)mRNA的表达,WB法检测各组细胞中c-Myc、SCD、EMT相关(N-cadherin、TGF-β、ZEB1)、S-腺苷-甲硫氨酸脱羧酶(SAMDC)和亚精胺/精胺N1-乙酰转移酶(SSAT)蛋白的表达,ELISA检测各组细胞上清液中鸟氨酸脱羧酶(ODC)的含量。结果:敲减INHBA-AS1表达使HeLa细胞的增殖、侵袭和迁移能力显著降低(均P<0.05)而细胞凋亡率显著升高(P<0.05),q PCR、WB法检测结果显示,敲减INHBA-AS1均可显著抑制HeLa细胞中c-Myc、SCD、N-cadherin、TGF-β、ZEB1和SAMDC的表达(均P<0.05),而促进SSAT的表达(P<0.05),并降低HeLa细胞上清液中ODC的含量(P<0.05)。与c-Myc抑制剂和SCD抑制剂单独处理相比,其联合敲减INHBA-AS1后上述作用更加显著(均P<0.05);与sh-INHBA-AS1组相比,进一步过表达c-Myc后HeLa细胞的增殖能力显著升高(P<0.05)、SCD和N-cadherin蛋白表达水平显著升高(P<0.05)、细胞上清液中ODC含量显著升高(P<0.05)。结论:INHBA-AS1可通过c-Myc调控SCD的表达,从而影响HeLa细胞鸟氨酸代谢和EMT进程,进而促进HeLa细胞的增殖、侵袭和迁移能力。展开更多
Background：Core fucosylation （CF）,catalyzed by α-1,6 fucosyltransferase （Fut8） in mammals,plays an important role in pathological processes through posttranslational modification of key signaling receptor protei...Background：Core fucosylation （CF）,catalyzed by α-1,6 fucosyltransferase （Fut8） in mammals,plays an important role in pathological processes through posttranslational modification of key signaling receptor proteins,including transforming growth factor （TGF）-β receptors and platelet-derived growth factor （PDGF） receptors.However,its effect on peritoneal fibrosis is unknown.Here,we investigated its influence on epithelial-mesenchymal transition （EMT） of rat peritoneal mesothelial cells （PMCs） in vitro induced by a high-glucose （HG） culture solution.Methods：Rat PMCs were first cultured in a HG （2.5%） culture solution to observe the CF expression level （fluorescein isothiocyanate-lens culinaris agglutinin）,we next established a knockdown model of rat PMCs in vitro with Fut8 small interfering RNA （siRNA） to observe whether inhibiting CF decreases the messenger RNA （mRNA） expression and protein expression of Fut8 and reverses EMT status.Rat PMCs were randomly divided into control group,mock group （transfected with scrambled siRNA）,Fut8 siRNA group,HG group,HG ＋ mock group,and HG ＋ Fut8 siRNA group.Finally,we examined the activation of TGF-β/Smad2/3 signaling and PDGF/extracellular signal-regulated kinase （ERK） signaling to observe the influence of CF on them.Results：CF,Fut8 mRNA,and protein expression were all significantly upregulated in HG-induced EMT model than those in the control rat PMCs （P 〈 0.05）.Fut8 siRNA successfully blocked CF of TGF-β receptors and PDGF receptors and attenuated the EMT status （E-cadherin and α-SMA and phenotypic changes） in HG-induced rat PMCs.In TGF-β/Smad2/3 signaling,Fut8 siRNA did not suppress the protein expression of TGF-3 receptors and Smad2/3;however,it significantly suppressed the phosphowlation of Smad2/3 （relative expression folds of HG ＋ Fut8 group vs.HG group：7.6 ± 0.4 vs.15.1 ± 0.6,respectively,P 〈 0.05）.In PDGF/ERK signaling,Fut8 siRNA did not suppress the protein expression of PDGF receptors and ERK,but it significantly suppressed the phosphorylation of ERK （relative expression folds of HG ＋ Fut8 group vs.HG group：8.7 ± 0.9 vs.15.6 ± 1.2,respectively,P 〈 0.05）.Blocking CF inactivated the activities of TGF-β and PDGF signaling pathways,and subsequently blocked EMT.Conclusions：These results demonstrate that CF contributes to rat PMC EMT.and that blocking it attenuates EMT.CF regulation is a potential therapeutic target of peritoneal fibrosis.展开更多
基金supported by operating grants from Canadian Breast Cancer Foundation-Ontario Regionthe Canadian Institutes of Health Research MOP111224 to LW
文摘Epithelial-mesenchymal transition（EMT） and mesenchymal-epithelial transition（MET） are essential for embryonic development and also important in cancer progression. In a conventional model, epithelial-like cancer cells transit to mesenchymal-like tumor cells with great motility via EMT transcription factors; these mesenchymallike cells migrate through the circulation system, relocate to a suitable site and then convert back to an epithelial-like phenotype to regenerate the tumor. However, recent findings challenge this conventional model and support the existence of a stable hybrid epithelial/mesenchymal（E/M） tumor population. Hybrid E/M tumor cells exhibit both epithelial and mesenchymal properties, possess great metastatic and tumorigenic capacity and are associated with poorer patient prognosis. The hybrid E/M model and associated regulatory networks represent a conceptual change regarding tumor metastasis and organ colonization. It may lead to the development of novel treatment strategies to ultimately stop cancer progression and improve disease-free survival.
文摘At some point in the natural course of colorectal cancer up to 50% of patients will develop metastasis to the liver and it is one of the most critical effects for patient prognosis. The incidence of synchronous liver metastasis has been detected at around 20% - 25%, but the optimal timing of surgical resection remains controversial. Neoadjuvant chemotherapy has also been found to be beneficial not only for initially unresectable but also resectable synchronous metastases. Then, traditional surgical strategies of hepatic resection in accordance with past chemotherapeutic regimens have been used decreasingly over the past several years. This review will primarily discuss treatments in association with the recent developed chemotherapeutic regimens and surgical procedure from the clinical data and the concept for epithetlial-mesenchymal transition, which has recently been studied to elucidate mechanisms of the liver metastatic process.
基金supported by National Natural science foundation of China (No.30772128)
文摘Objective： To investigate the effect of Rapamycin on epithelial-mesenchymal transition（EMT） of LoVo colonic adenocarcinoma cells in vitro. Methods：Cultured LoVo colonic adenocarcinoma cells were divided into three groups： negative control group, EMT-inducing group（TGF-β1） and EMT-interfering group（TGF-β1 plus Rapamycin）. E-cadherin expression in LoVo cells was detected by Western Blot, while the expression of vimentin was evaluated through immunocytochemistry. The Snail mRNA in LoVo cells was examined by RT- PCR. Results：TGF-β1 induced LoVo cell switching from polygonal to spindle-shaped. TGF-β1 enhanced the expression of vimentin, but lowered the level of E-cadhefin. In contrast, Rapamycin impaired the transition induced by TGF-β1. Rapamycin dramatically abrogated TGF-β1-induced vimentin expression and restored E-cadherin expression in LoVo cells. Rapamycin significantly repressed the upregulation of Snail mRNA expression induced by TGF-β1. Conclusion：Rapamycin dramatically abrogated TGF-β1 induced Snail mRNA expression in LoVo cells, hence inhibiting EMT of these cells in vitro.
文摘Objective: To investigate the correlation of SphK1, FAK, Musashi 1 and CA199 expression with angiogenesis and epithelial-mesenchymal transition in surgically removed colon cancer lesions. Methods: A total of 60 patients with colon cancer who underwent radical operation in our hospital between August 2015 and August 2017 were selected, intraoperative colon cancer tissue samples were collected as colon cancer group, and normal tissue specimens adjacent to carcinoma were collected as adjacent tissue group. Fluorescence quantitative PCR was adopted to determine the expression levels of SphK1, FAK, Musashi 1, CA199 as well as the genes related to angiogenesis and epithelial-mesenchymal transition in colon tissues with different properties. Results: SphK1, FAK, Musashi 1 and CA199 mRNA expression in colon cancer group were higher than those in adjacent tissue group;angiogenesis-related genes ANGPTL4, Apelin-13, DLL1, VEGF and HIF-α mRNA expression were higher than those in adjacent tissue group whereas TSP-1 mRNA expression was lower than that in adjacent tissue group;epithelial-mesenchymal transition-related gene E-cadherin mRNA expression was lower than that in adjacent tissue group whereas Vimentin, N-cadherin, Twist and Snail mRNA expression were higher than those in adjacent tissue group. Correlation analysis showed that the SphK1, FAK, Musashi 1 and CA199 expression in colon cancer tissues were directly correlated with the angiogenesis genes and epithelial-mesenchymal transition genes. Conclusion: SphK1, FAK, Musashi 1 and CA199 genes are abnormally expressed in colon cancer tissues and their expression levels are directly correlated with tumor angiogenesis and epithelial-mesenchymal transition process.
文摘Objective: To investigate the role and mechanism of autophagy in epithelial-mesenchymal transition (EMT) of oral squamous cell carcinoma cells induced by CQ (chloroquine) and rapamycin (RAPA). Methods: TGF-β (transforming growth factor β) was used to induce EMT in Cal-27 cell line. At the same time, RAPA was used to enhance and CQ was used to inhibit autophagy. The ability of cell migration was detected by scratch distribution test and the ability of cell migration was detected by Transwell chamber test. Western blot was used to detect the changes of ZO-1, vimentin, FN1 and other EMT-related proteins after 3 d induction, and SPSS 22.0 statistical software was used to analyze the data. Results: After 3 d of induction with 5 ng/mL TGF-β, E-cadherin decreased significantly and Vimentin increased significantly. Compared with the control group, the wound healing rate increased significantly (P<0.05) and the number of penetrating cells increased significantly (P<0.05) after 3 d induction with 5 ng/mL TGF-β, and then the cells were co-induced with 100 ng/mL RAPA and 100 ng/mL CQ and 5 ng/mL TGF-β for 3 d. Compared with TGF-β group. The healing rate of the RAPA co-induced with 5 ng/mL TGF-β group decreased significantly (P<0.05) and the number of penetrating cells decreased significantly (P<0.05). Compared with TGF-β group. The healing rate of the CQ co-induced with 5 ng/mL TGF-β group increased significantly (P<0.05) and the number of penetrating cells increased significantly (P<0.05). Compared with the control group, FN1 and Vimentin expression increased and ZO-1 expression decreased 3 d after induction with 5 ng/mL TGF-β. And then induced Cal-27 cells with 100 ng/mL RAPA and 100 ng/mL CQ and 5 ng/mL TGF-β respectively for 3 d. Compared with TGF-β group, FN1 and Vimentin expression decreased in RAPA co-induction group. Compared with TGF-βgroup, the expression of FN1 and Vimentin increased and the expression of ZO-1 decreased in CQ co-induction group. Conclusion: TGF-β can induce Cal-27 cells to establish EMT model. In EMT model, promoting autophagy can inhibit EMT, inhibiting autophagy can promote EMT.
基金supported by the U.S. National Institutes of Health grants (U24 CA143835 to IS and WZ, P50 CA083639 and P50 CA098258 to AKS)MD Anderson support grant (CA016672) to WZ+6 种基金a grant from the Blanton-Davis Ovarian Cancer Research Program to WZgrants from the Program for Changjiang Scholars, Innovative Research Team in University (PCSIRT) in Chinathe National Key Scientifi c and Technological Project (2011ZX0 9307-001-04)Tianjin Science and Technology Committee Foundation (09ZCZDSF04700) to KCa grant from National Nature Science Foundation of China (#81201651) to YSa grant from Fondazione CARIPLO (2013-0865) to DMthe A. Lavoy Moore Endowment Fund to YS and DY
文摘Metastasis is the main cause of cancer mortality. One of the initiating events of cancer metastasis of epithelial tumors is epithelial-to-mesenchymal transition(EMT), during which cells dedifferentiate from a relatively rigid cell structure/morphology to a flexible and changeable structure/morphology often associated with mesenchymal cells. The presence of EMT in human epithelial tumors is reflected by the increased expression of genes and levels of proteins that are preferentially present in mesenchymal cells. The combined presence of these genes forms the basis of mesenchymal gene signatures, which are the foundation for classifying a mesenchymal subtype of tumors. Indeed, tumor classification schemes that use clustering analysis of large genomic characterizations, like The Cancer Genome Atlas(TCGA), have defined mesenchymal subtype in a number of cancer types, such as high-grade serous ovarian cancer and glioblastoma. However, recent analyses have shown that gene expression-based classifications of mesenchymal subtypes often do not associate with poor survival. This "paradox" can be ameliorated using integrated analysis that combines multiple data types. We recently found that integrating m RNA and micro RNA(mi RNA) data revealed an integrated mesenchymal subtype that is consistently associated with poor survival in multiple cohorts of patients with serous ovarian cancer. This network consists of 8 major mi RNAs and 214 m RNAs. Among the 8 mi RNAs, 4 are known to be regulators of EMT. This review provides a summary of these 8 mi RNAs, which were associated with the integrated mesenchymal subtype of serous ovarian cancer.
基金This work was supported by a grant from the National Natural Science Foundation of China （No. 81530021）.
文摘Background：Core fucosylation （CF）,catalyzed by α-1,6 fucosyltransferase （Fut8） in mammals,plays an important role in pathological processes through posttranslational modification of key signaling receptor proteins,including transforming growth factor （TGF）-β receptors and platelet-derived growth factor （PDGF） receptors.However,its effect on peritoneal fibrosis is unknown.Here,we investigated its influence on epithelial-mesenchymal transition （EMT） of rat peritoneal mesothelial cells （PMCs） in vitro induced by a high-glucose （HG） culture solution.Methods：Rat PMCs were first cultured in a HG （2.5%） culture solution to observe the CF expression level （fluorescein isothiocyanate-lens culinaris agglutinin）,we next established a knockdown model of rat PMCs in vitro with Fut8 small interfering RNA （siRNA） to observe whether inhibiting CF decreases the messenger RNA （mRNA） expression and protein expression of Fut8 and reverses EMT status.Rat PMCs were randomly divided into control group,mock group （transfected with scrambled siRNA）,Fut8 siRNA group,HG group,HG ＋ mock group,and HG ＋ Fut8 siRNA group.Finally,we examined the activation of TGF-β/Smad2/3 signaling and PDGF/extracellular signal-regulated kinase （ERK） signaling to observe the influence of CF on them.Results：CF,Fut8 mRNA,and protein expression were all significantly upregulated in HG-induced EMT model than those in the control rat PMCs （P 〈 0.05）.Fut8 siRNA successfully blocked CF of TGF-β receptors and PDGF receptors and attenuated the EMT status （E-cadherin and α-SMA and phenotypic changes） in HG-induced rat PMCs.In TGF-β/Smad2/3 signaling,Fut8 siRNA did not suppress the protein expression of TGF-3 receptors and Smad2/3;however,it significantly suppressed the phosphowlation of Smad2/3 （relative expression folds of HG ＋ Fut8 group vs.HG group：7.6 ± 0.4 vs.15.1 ± 0.6,respectively,P 〈 0.05）.In PDGF/ERK signaling,Fut8 siRNA did not suppress the protein expression of PDGF receptors and ERK,but it significantly suppressed the phosphorylation of ERK （relative expression folds of HG ＋ Fut8 group vs.HG group：8.7 ± 0.9 vs.15.6 ± 1.2,respectively,P 〈 0.05）.Blocking CF inactivated the activities of TGF-β and PDGF signaling pathways,and subsequently blocked EMT.Conclusions：These results demonstrate that CF contributes to rat PMC EMT.and that blocking it attenuates EMT.CF regulation is a potential therapeutic target of peritoneal fibrosis.
