目的观察银盏心脉滴丸对大鼠心肌细胞(H9C2)mTORC1/4EBP1信号通路的影响以探讨其对线粒体功能的机制。方法制备银盏心脉滴丸含药血清。将细胞分为对照组、模型组(缺氧/复氧)、空白血清组及银盏心脉滴丸含药血清组。制备缺氧/复氧细胞损...目的观察银盏心脉滴丸对大鼠心肌细胞(H9C2)mTORC1/4EBP1信号通路的影响以探讨其对线粒体功能的机制。方法制备银盏心脉滴丸含药血清。将细胞分为对照组、模型组(缺氧/复氧)、空白血清组及银盏心脉滴丸含药血清组。制备缺氧/复氧细胞损伤模型,利用激光共聚焦检测线粒体膜电位(ΔΨm),利用流式细胞仪检测活性氧(reactive oxygen species, ROS),运用Western Blot技术检测细胞雷帕霉素靶蛋白(mammalian target of rapamycin, mTOR)、真核翻译起始因子4E结合蛋白(eukaryotic translation initiation factor 4E-binding proteins,4E-BP)、mTOR复合体蛋白(regulatory-associated protein of mammalian target of rapamycin,Raptor)蛋白表达,运用q-PCR方法检测mTORC1、4EBP1、Raptor的mRNA含量。结果与对照组相比,模型组细胞内绿色荧光增强,ΔΨm显著高于对照组(P<0.05);而与模型组相比,银盏心脉滴丸组红色荧光增强(P<0.05),说明银盏心脉保护ΔΨm稳定,保护线粒体膜结构;与对照组相比,模型组的ROS合成较对照组升高(P<0.05);而与模型组相比,银盏心脉滴丸组细胞内ROS产生明显降低(P<0.05);与对照组相比,模型组mTOR、Raptor基因mRNA水平下调(P<0.05),4ebp1基因mRNA水平上调,差异有统计学意义(P<0.05)。与模型组比较,银盏心脉滴丸组mTOR、Raptor基因mRNA水平上调(P<0.05),4ebp1基因mRNA水平下调(P<0.05)。结论银盏心脉滴丸改善缺氧复氧损伤的机制可能是通过激活mTORC1/4EBP1信号通路,从而抑制线粒体膜电位,改善活性氧,保护线粒体功能。展开更多
Background: Intramuscular fat(IMF) content is a vital parameter for assessing pork quality. Increasing evidence has shown that microRNAs(miRNAs) play an important role in regulating porcine IMF deposition. Here, a nov...Background: Intramuscular fat(IMF) content is a vital parameter for assessing pork quality. Increasing evidence has shown that microRNAs(miRNAs) play an important role in regulating porcine IMF deposition. Here, a novel miRNA implicated in porcine IMF adipogenesis was found, and its effect and regulatory mechanism were further explored with respect to intramuscular preadipocyte proliferation and differentiation.Results: By porcine adipose tissue miRNA sequencing analysis, we found that miR-146a-5p is a potential regulator of porcine IMF adipogenesis. Further studies showed that miR-146a-5p mimics inhibited porcine intramuscular preadipocyte proliferation and differentiation, while the miR-146a-5p inhibitor promoted cell proliferation and adipogenic differentiation. Mechanistically, miR-146a-5p suppressed cell proliferation by directly targeting SMAD family member 4(SMAD4) to attenuate TGF-β signaling. Moreover, miR-146a-5p inhibited the differentiation of intramuscular preadipocytes by targeting TNF receptor-associated factor 6(TRAF6) to weaken the AKT/mTORC1 signaling downstream of the TRAF6 pathway.Conclusions: MiR-146a-5p targets SMAD4 and TRAF6 to inhibit porcine intramuscular adipogenesis by attenuating TGF-β and AKT/mTORC1 signaling, respectively. These findings provide a novel miRNA biomarker for regulating intramuscular adipogenesis to promote pork quality.展开更多
Bone defects and non-union are prevalent in clinical orthopedy,and the outcomes of current treatments are often suboptimal.Bone tissue engineering offers a promising approach to treating these conditions effectively.B...Bone defects and non-union are prevalent in clinical orthopedy,and the outcomes of current treatments are often suboptimal.Bone tissue engineering offers a promising approach to treating these conditions effectively.Bone morphogenetic protein 9(BMP9)can commit mesenchymal stem cells to osteogenic lineage,and a knowledge of the underlying mechanisms may help advance the field of bone tissue engineering.Leucine-rich repeats con-taining G protein-coupled receptor 4(LGR4),a member of G protein-coupled receptors,is essential for modulating bone development.This study is aimed at investigating the impact of LGR4 on BMP9-induced osteogenesis in mesenchymal stem cells as well as the underlying mechanisms.Bone marrow stromal cells from BMp9-knockout mice exhibited diminished LGR4 expression,and exogenous LGR4 clearly restored the impaired osteogenic potency of the bone marrow stromal cells.Furthermore,LGR4 expression was increased by BMP9 in C3H10T1/2 cells.LGR4 augmented the benefits of BMP9-induced osteogenic markers and bone formation,whereas LGR4 inhibition restricted these effects.Meanwhile,the BMP9-induced li-pogenic markers were increased by LGR4 inhibition.The protein levels of Raptor and p-Stat3 were elevated by BMP9.Raptor knockdown or p-Stat3 suppression attenuated the osteoblastic markers and LGR4 expression brought on by BMP9.LGR4 significantly reversed the blocking ef-fect of Raptor knockdown or p-Stat3 suppression on the BMP9-induced osteoblastic markers.Raptor interacts with p-Stat3,and p-Stat3 activates the LGR4 promoter activity.In conclusion,LGR4 boosts BMP9 osteoblastic potency in mesenchymal stem cells,and BMP9 may up-regulate LGR4 via the mTORC1/Stat3 signal activation.展开更多
Objective:To investigate the mechanism of MiR-34a-mediated mTOR/4E-BP1 signaling pathway on apoptosis of esophageal cancer cells.Methods:Esophageal cancer cell lines were purchased from the ATCC cell bank and randomly...Objective:To investigate the mechanism of MiR-34a-mediated mTOR/4E-BP1 signaling pathway on apoptosis of esophageal cancer cells.Methods:Esophageal cancer cell lines were purchased from the ATCC cell bank and randomly divided into three groups. The first group, miR-34a group (miR-34a group): transfected miR-34a mimics into esophageal cancer cells by transfection;The second group, esophageal cancer group (EC group): simple esophageal cancer cell line without other treatment, normal culture;third group, idling group (ID group): transfected miR-34a negative control into esophageal cancer cell line . To explore MiR by qRT-PCR, TUNEL, cck-8 and Westernblot in the detection of miR-34a mRNA expression, apoptosis, proliferation, and protein content of mTOR/4E-BP1 in esophageal cancer cells. -34a mediates the mechanism of mTOR/4E-BP1 signaling pathway on apoptosis of esophageal cancer cells.Results:The results of qRT-PCR showed that the expression of miR-34a mRNA was the lowest in esophageal cancer cells in EC group, and the highest in miR-34a group in miR-34a group, miR-34a group and ID group, EC Compared with the group, the miR-34a mRNA content increased significantly, indicating successful transfection (allP<0.05). The results of TUNEL showed that the number of apoptosis of esophageal cancer cells in EC group was the least, and the apoptosis of esophageal carcinoma cells in miR-34a group was significantly increased. The apoptosis rate of miR-34a group was significantly higher than that of EC group and ID group (P<0.05). There was no significant difference in apoptosis between EC group and ID group. The OD value of cell proliferation in ID group and EC group was higher than that in miR-34a group, and there was significant difference between groups (P<0.05). The proliferation of esophageal cancer cells in EC group was the highest, and the number of esophageal cancer cells in miR-34a group was the least. There was no significant difference in the proliferation of esophageal cancer cells in the ID group compared with the EC group (P>0.05). The mTOR/4E-BP1 protein in esophageal cancer cells of EC group, ID group and miR-34a group was immunoblotted by Western blot. The gray scale showed that the mTOR/4E-BP1 protein content of EC group was the highest, EC group and Compared with the ID group, the protein content was similar, no significant (P>0.05), and the miR-34a group had the lowest protein content. Compared with the EC group and the ID group, the miR-34a group had lower protein content in esophageal cancer cells (allP< 0.05).Conclusions:MiR-34a may promote the apoptosis of esophageal cancer cells by inhibiting the expression of mTOR/4E-BP1 signaling pathway.展开更多
Although the mTOR-4E-BP1 signaling pathway is implicated in aging and aging-related disorders,the role of 4E-BP1 in regulating human stem cell homeostasis remains largely unknown.Here,we report that the expression of ...Although the mTOR-4E-BP1 signaling pathway is implicated in aging and aging-related disorders,the role of 4E-BP1 in regulating human stem cell homeostasis remains largely unknown.Here,we report that the expression of 4E-BP1 decreases along with the senescence of human mesenchymal stem celis(hMSCs).Genetic inactivation of 4E-BP1 in hMSCs compromises mitochondrial respiration,increases mitochondrial reactive oxygen species(Ros)production,and accelerates cellular senescence.Mechanistically,the absence of 4E-BP1 destabilizes proteins in mitochondrial respiration complexes,especially several key subunits of complex III including UQCRC2.Ectopic expression of 4E-BP1 attenuates mitochondrial abnormalities and alleviates cellular senescence in 4E-BP1-deficient hMSCs as well as in physiologically aged hMSCs.These findings together demonstrate that 4E-BP1 functions as a geroprotector to mitigate human stem cell senescence and maintain mitochondrial homeostasis,particularly for the mitochondrial respiration complex Il,thus providing a new potential target to counteract human stem cell senescence.展开更多
Introduction: The consensus report issued jointly by the American Diabetes Association and the American Cancer Society stated that “type 2 diabetes and cancer share many risk factors, but potential biologic links bet...Introduction: The consensus report issued jointly by the American Diabetes Association and the American Cancer Society stated that “type 2 diabetes and cancer share many risk factors, but potential biologic links between the two diseases are incompletely understood”. Interestingly, however, a recent report suggested that the expression of p27(Kip1), a cell cycle repressor protein, in the rodent liver was inversely associated with potential carcinogenic risk in the genetic rodent models of diabetic obesity. p27 is a cyclin-dependent kinase inhibitor that, when down-regulated, allows the progression of the cell cycle from G1 to S phase, thereby increasing the risk of developing cancer. Objective: The objective of the study described below was to extend the results of the recent report on the expression of p27 in the livers of obese, diabetic rodents to the humans and investigate whether the expression of p27 in the human peripheral blood mononuclear cells (PBMCs) might also be inversely associated with potential carcinogenic risk in obese type 2 diabetic individuals relative to the lean normal controls. Methods: Western immunoblot analysis was performed to evaluate the expression of p27 and the two most relevant upstream molecular signaling pathways of the expression of p27, namely 4E-BP1 and MNK1, in human PBMCs obtained from obese type 2 diabetic individuals relative to the lean normal controls. Results: First, expression of p27 in human PBMCs was significantly down-regulated in obese type 2 diabetic individuals relative to the lean normal controls. Secondly, expression of p27 in human PBMCs was also significantly down-regulated in obese type 2 diabetic African Americans relative even to the obese type 2 diabetic Caucasian Americans. Conclusions: Expression of p27 in human PBMCs was inversely associated with potential carcinogenic risk in obese type 2 diabetes relative to the lean normal controls.展开更多
目的:筛选不同转移潜能人大肠癌细胞株的差异信号通路,探讨大肠癌转移的分子机制。方法:利用Full Moon抗体芯片(Phospho Explorer Array PEX100)对31条信号通路、432个信号蛋白的679个磷酸化位点进行高通量检测,分析来自同一病人的原位...目的:筛选不同转移潜能人大肠癌细胞株的差异信号通路,探讨大肠癌转移的分子机制。方法:利用Full Moon抗体芯片(Phospho Explorer Array PEX100)对31条信号通路、432个信号蛋白的679个磷酸化位点进行高通量检测,分析来自同一病人的原位和转移大肠癌细胞株SW480和SW620信号通路蛋白磷酸化水平的变化谱。通过生物信息学分析,了解大肠癌转移相关信号通路并进行Western-blot检测。结果:SW480和SW620两个细胞株存在169个差异磷酸化蛋白(31个上调,138个下调)。差异表达的蛋白质中,大部分与基因转录、信号转导、细胞凋亡等通路相关。Western-blot证实PI3K-AKT-mTOR信号通路分子在原位和转移性大肠癌中存在明显差异表达。结论:蛋白质芯片方法有助于鉴定大肠癌转移相关的差异蛋白,PI3K-AKT-mTOR细胞信号通路活性的变化可能与大肠癌转移有关。展开更多
文摘目的观察银盏心脉滴丸对大鼠心肌细胞(H9C2)mTORC1/4EBP1信号通路的影响以探讨其对线粒体功能的机制。方法制备银盏心脉滴丸含药血清。将细胞分为对照组、模型组(缺氧/复氧)、空白血清组及银盏心脉滴丸含药血清组。制备缺氧/复氧细胞损伤模型,利用激光共聚焦检测线粒体膜电位(ΔΨm),利用流式细胞仪检测活性氧(reactive oxygen species, ROS),运用Western Blot技术检测细胞雷帕霉素靶蛋白(mammalian target of rapamycin, mTOR)、真核翻译起始因子4E结合蛋白(eukaryotic translation initiation factor 4E-binding proteins,4E-BP)、mTOR复合体蛋白(regulatory-associated protein of mammalian target of rapamycin,Raptor)蛋白表达,运用q-PCR方法检测mTORC1、4EBP1、Raptor的mRNA含量。结果与对照组相比,模型组细胞内绿色荧光增强,ΔΨm显著高于对照组(P<0.05);而与模型组相比,银盏心脉滴丸组红色荧光增强(P<0.05),说明银盏心脉保护ΔΨm稳定,保护线粒体膜结构;与对照组相比,模型组的ROS合成较对照组升高(P<0.05);而与模型组相比,银盏心脉滴丸组细胞内ROS产生明显降低(P<0.05);与对照组相比,模型组mTOR、Raptor基因mRNA水平下调(P<0.05),4ebp1基因mRNA水平上调,差异有统计学意义(P<0.05)。与模型组比较,银盏心脉滴丸组mTOR、Raptor基因mRNA水平上调(P<0.05),4ebp1基因mRNA水平下调(P<0.05)。结论银盏心脉滴丸改善缺氧复氧损伤的机制可能是通过激活mTORC1/4EBP1信号通路,从而抑制线粒体膜电位,改善活性氧,保护线粒体功能。
基金supported by grants from the National Natural Science Foundation (31872979, 31572366)the National Key Research and Development Program of China (2017YFD0502002)the National Basic Research Programs of China (2015CB943102)。
文摘Background: Intramuscular fat(IMF) content is a vital parameter for assessing pork quality. Increasing evidence has shown that microRNAs(miRNAs) play an important role in regulating porcine IMF deposition. Here, a novel miRNA implicated in porcine IMF adipogenesis was found, and its effect and regulatory mechanism were further explored with respect to intramuscular preadipocyte proliferation and differentiation.Results: By porcine adipose tissue miRNA sequencing analysis, we found that miR-146a-5p is a potential regulator of porcine IMF adipogenesis. Further studies showed that miR-146a-5p mimics inhibited porcine intramuscular preadipocyte proliferation and differentiation, while the miR-146a-5p inhibitor promoted cell proliferation and adipogenic differentiation. Mechanistically, miR-146a-5p suppressed cell proliferation by directly targeting SMAD family member 4(SMAD4) to attenuate TGF-β signaling. Moreover, miR-146a-5p inhibited the differentiation of intramuscular preadipocytes by targeting TNF receptor-associated factor 6(TRAF6) to weaken the AKT/mTORC1 signaling downstream of the TRAF6 pathway.Conclusions: MiR-146a-5p targets SMAD4 and TRAF6 to inhibit porcine intramuscular adipogenesis by attenuating TGF-β and AKT/mTORC1 signaling, respectively. These findings provide a novel miRNA biomarker for regulating intramuscular adipogenesis to promote pork quality.
基金All animal experiments were approved by The Ethics Committee of Chongqing Medical University(No.2022030).
文摘Bone defects and non-union are prevalent in clinical orthopedy,and the outcomes of current treatments are often suboptimal.Bone tissue engineering offers a promising approach to treating these conditions effectively.Bone morphogenetic protein 9(BMP9)can commit mesenchymal stem cells to osteogenic lineage,and a knowledge of the underlying mechanisms may help advance the field of bone tissue engineering.Leucine-rich repeats con-taining G protein-coupled receptor 4(LGR4),a member of G protein-coupled receptors,is essential for modulating bone development.This study is aimed at investigating the impact of LGR4 on BMP9-induced osteogenesis in mesenchymal stem cells as well as the underlying mechanisms.Bone marrow stromal cells from BMp9-knockout mice exhibited diminished LGR4 expression,and exogenous LGR4 clearly restored the impaired osteogenic potency of the bone marrow stromal cells.Furthermore,LGR4 expression was increased by BMP9 in C3H10T1/2 cells.LGR4 augmented the benefits of BMP9-induced osteogenic markers and bone formation,whereas LGR4 inhibition restricted these effects.Meanwhile,the BMP9-induced li-pogenic markers were increased by LGR4 inhibition.The protein levels of Raptor and p-Stat3 were elevated by BMP9.Raptor knockdown or p-Stat3 suppression attenuated the osteoblastic markers and LGR4 expression brought on by BMP9.LGR4 significantly reversed the blocking ef-fect of Raptor knockdown or p-Stat3 suppression on the BMP9-induced osteoblastic markers.Raptor interacts with p-Stat3,and p-Stat3 activates the LGR4 promoter activity.In conclusion,LGR4 boosts BMP9 osteoblastic potency in mesenchymal stem cells,and BMP9 may up-regulate LGR4 via the mTORC1/Stat3 signal activation.
基金National Youth Science Fund Project(No.8180140119).
文摘Objective:To investigate the mechanism of MiR-34a-mediated mTOR/4E-BP1 signaling pathway on apoptosis of esophageal cancer cells.Methods:Esophageal cancer cell lines were purchased from the ATCC cell bank and randomly divided into three groups. The first group, miR-34a group (miR-34a group): transfected miR-34a mimics into esophageal cancer cells by transfection;The second group, esophageal cancer group (EC group): simple esophageal cancer cell line without other treatment, normal culture;third group, idling group (ID group): transfected miR-34a negative control into esophageal cancer cell line . To explore MiR by qRT-PCR, TUNEL, cck-8 and Westernblot in the detection of miR-34a mRNA expression, apoptosis, proliferation, and protein content of mTOR/4E-BP1 in esophageal cancer cells. -34a mediates the mechanism of mTOR/4E-BP1 signaling pathway on apoptosis of esophageal cancer cells.Results:The results of qRT-PCR showed that the expression of miR-34a mRNA was the lowest in esophageal cancer cells in EC group, and the highest in miR-34a group in miR-34a group, miR-34a group and ID group, EC Compared with the group, the miR-34a mRNA content increased significantly, indicating successful transfection (allP<0.05). The results of TUNEL showed that the number of apoptosis of esophageal cancer cells in EC group was the least, and the apoptosis of esophageal carcinoma cells in miR-34a group was significantly increased. The apoptosis rate of miR-34a group was significantly higher than that of EC group and ID group (P<0.05). There was no significant difference in apoptosis between EC group and ID group. The OD value of cell proliferation in ID group and EC group was higher than that in miR-34a group, and there was significant difference between groups (P<0.05). The proliferation of esophageal cancer cells in EC group was the highest, and the number of esophageal cancer cells in miR-34a group was the least. There was no significant difference in the proliferation of esophageal cancer cells in the ID group compared with the EC group (P>0.05). The mTOR/4E-BP1 protein in esophageal cancer cells of EC group, ID group and miR-34a group was immunoblotted by Western blot. The gray scale showed that the mTOR/4E-BP1 protein content of EC group was the highest, EC group and Compared with the ID group, the protein content was similar, no significant (P>0.05), and the miR-34a group had the lowest protein content. Compared with the EC group and the ID group, the miR-34a group had lower protein content in esophageal cancer cells (allP< 0.05).Conclusions:MiR-34a may promote the apoptosis of esophageal cancer cells by inhibiting the expression of mTOR/4E-BP1 signaling pathway.
基金supported by the National Key Research and Development Program of China(2018YFC2000100)the Strategic Priority Research Program of the Chinese Academy of Sciences(XDA16000000)+9 种基金the National Natural Science Foundation of China(8190143281921006,82125011,92149301,92168201,91949209,92049304,92049116,32121001,82192863,82122024,82071588,81861168034,81922027,81870228,32100937,31900524,82201727)the National Key Research and Development Program of China(2020YFA0804000,2020YFA0113400,2020YFA0112200,2018YFA0107203,the STI2030-Major Projects-2021ZD0202400,2021YFF1201005,2022YFA1103700,2022YFA1103800)CAS Project for Young Scientists in Basic Research(YSBR-076,YSBR-012)the Program of the Beijing Natural Science Foundation(Z190019,JQ20031)K.C.Wong Education Foundation(GJTD-2019-06,GJTD-2019-08)Young Elite Scientists Sponsorship Program by CAST(YESS20200012)Youth Innovation Promotion Association of CAS(EiCAZW0401)the Pilot Project for Public Welfare Development and Reform of Beijing-affliated Medical Research Institutes(11000022T000000461062)the Informatization Plan of Chinese Academy of Sciences(CAS-WX2021SF-0301,CASWX2022SDC-XK14)CAS Special Research Assistant(SRA)Program,and the Tencent Foundation(2021-1045).
文摘Although the mTOR-4E-BP1 signaling pathway is implicated in aging and aging-related disorders,the role of 4E-BP1 in regulating human stem cell homeostasis remains largely unknown.Here,we report that the expression of 4E-BP1 decreases along with the senescence of human mesenchymal stem celis(hMSCs).Genetic inactivation of 4E-BP1 in hMSCs compromises mitochondrial respiration,increases mitochondrial reactive oxygen species(Ros)production,and accelerates cellular senescence.Mechanistically,the absence of 4E-BP1 destabilizes proteins in mitochondrial respiration complexes,especially several key subunits of complex III including UQCRC2.Ectopic expression of 4E-BP1 attenuates mitochondrial abnormalities and alleviates cellular senescence in 4E-BP1-deficient hMSCs as well as in physiologically aged hMSCs.These findings together demonstrate that 4E-BP1 functions as a geroprotector to mitigate human stem cell senescence and maintain mitochondrial homeostasis,particularly for the mitochondrial respiration complex Il,thus providing a new potential target to counteract human stem cell senescence.
文摘Introduction: The consensus report issued jointly by the American Diabetes Association and the American Cancer Society stated that “type 2 diabetes and cancer share many risk factors, but potential biologic links between the two diseases are incompletely understood”. Interestingly, however, a recent report suggested that the expression of p27(Kip1), a cell cycle repressor protein, in the rodent liver was inversely associated with potential carcinogenic risk in the genetic rodent models of diabetic obesity. p27 is a cyclin-dependent kinase inhibitor that, when down-regulated, allows the progression of the cell cycle from G1 to S phase, thereby increasing the risk of developing cancer. Objective: The objective of the study described below was to extend the results of the recent report on the expression of p27 in the livers of obese, diabetic rodents to the humans and investigate whether the expression of p27 in the human peripheral blood mononuclear cells (PBMCs) might also be inversely associated with potential carcinogenic risk in obese type 2 diabetic individuals relative to the lean normal controls. Methods: Western immunoblot analysis was performed to evaluate the expression of p27 and the two most relevant upstream molecular signaling pathways of the expression of p27, namely 4E-BP1 and MNK1, in human PBMCs obtained from obese type 2 diabetic individuals relative to the lean normal controls. Results: First, expression of p27 in human PBMCs was significantly down-regulated in obese type 2 diabetic individuals relative to the lean normal controls. Secondly, expression of p27 in human PBMCs was also significantly down-regulated in obese type 2 diabetic African Americans relative even to the obese type 2 diabetic Caucasian Americans. Conclusions: Expression of p27 in human PBMCs was inversely associated with potential carcinogenic risk in obese type 2 diabetes relative to the lean normal controls.
文摘目的:筛选不同转移潜能人大肠癌细胞株的差异信号通路,探讨大肠癌转移的分子机制。方法:利用Full Moon抗体芯片(Phospho Explorer Array PEX100)对31条信号通路、432个信号蛋白的679个磷酸化位点进行高通量检测,分析来自同一病人的原位和转移大肠癌细胞株SW480和SW620信号通路蛋白磷酸化水平的变化谱。通过生物信息学分析,了解大肠癌转移相关信号通路并进行Western-blot检测。结果:SW480和SW620两个细胞株存在169个差异磷酸化蛋白(31个上调,138个下调)。差异表达的蛋白质中,大部分与基因转录、信号转导、细胞凋亡等通路相关。Western-blot证实PI3K-AKT-mTOR信号通路分子在原位和转移性大肠癌中存在明显差异表达。结论:蛋白质芯片方法有助于鉴定大肠癌转移相关的差异蛋白,PI3K-AKT-mTOR细胞信号通路活性的变化可能与大肠癌转移有关。
