AIM: To evaluate the expression of special AT-rich sequence-binding protein 1 (SATB1 ) gene in colorectal cancer and its role in colorectal cancer cell proliferation and invasion.METHODS: Immunohistochemistry was used...AIM: To evaluate the expression of special AT-rich sequence-binding protein 1 (SATB1 ) gene in colorectal cancer and its role in colorectal cancer cell proliferation and invasion.METHODS: Immunohistochemistry was used to detect the protein expression of SATB1 in 30 colorectal cancer (CRC) tissue samples and pair-matched adjacent nontumor samples. Cell growth was investigated after enhancing expression of SATB1. Wound-healing assay and Transwell assay were used to investigate the impact of SATB1 on migratory and invasive abilities of SW480 cells in vitro . Nude mice that received subcutaneous implantation or lateral tail vein were used to study the effects of SATB1 on tumor growth or metastasis in vivo . RESULTS: SATB1 was over-expressed in CRC tissues and CRC cell lines. SATB1 promotes cell proliferation and cell cycle progression in CRC SW480 cells. SATB1 over-expression could promote cell growth in vivo . In addition, SATB1 could significantly raise the ability of cell migration and invasion in vitro and promote the ability of tumor metastasis in vivo . SATB1 could up-regulate matrix metalloproteases 2, 9, cyclin D1 and vimentin, meanwhile SATB1 could down-regulate E-cadherin in CRC. CONCLUSION: SATB1 acts as a potential growth and metastasis promoter in CRC. SATB1 may be useful as a therapeutic target for CRC.展开更多
目的探讨核基质结合区结合蛋白,富含A-T序列特异性结合蛋白1(special A-T rich sequencebinding protein 1,SATB1)对乳腺癌干细胞表型CD44+/CD24-的影响及机制。方法用SATB1相关小干扰RNA(SATB1related small interfering RNA,SATB1-siR...目的探讨核基质结合区结合蛋白,富含A-T序列特异性结合蛋白1(special A-T rich sequencebinding protein 1,SATB1)对乳腺癌干细胞表型CD44+/CD24-的影响及机制。方法用SATB1相关小干扰RNA(SATB1related small interfering RNA,SATB1-siRNA)双链寡核糖核酸干扰MDA-MB-231细胞;pEGFP-N1-SATB1-GFP真核表达质粒瞬时转染MCF7细胞后,流式细胞术检测SATB1对乳腺癌干细胞表型CD44+/CD24-表达的影响。结果 MCF7细胞转染SATB1后,表达CD44+/CD24-的细胞比例明显升高;MDA-MB-231细胞在SATB1-siRNA干扰后,表达CD44+/CD24-的细胞比例明显降低(P<0.05)。结论 SATB1可能在形成并维持乳腺癌肿瘤干细胞特性中起重要作用。展开更多
目的:检测特别富含AT序列结合蛋白1(Special AT rich sequence binding protein 1,SATB1)在原发性肝癌(Hepato-cellular carcinoma,HCC)中的表达情况,并研究SATB1对LM3高转移人肝癌细胞株促进增殖及侵袭转移能力的影响。方法:运用实时定...目的:检测特别富含AT序列结合蛋白1(Special AT rich sequence binding protein 1,SATB1)在原发性肝癌(Hepato-cellular carcinoma,HCC)中的表达情况,并研究SATB1对LM3高转移人肝癌细胞株促进增殖及侵袭转移能力的影响。方法:运用实时定量PCR方法检测正常肝组织及HCC组织中SATB1的表达情况,并通过实时定量PCR及Western blot检测LM3高转移人肝癌细胞株中SATB1的表达。运用RNA干扰技术对LM3细胞株中的SATB1进行干扰并验证,对干扰前后的细胞株进行MTT、划痕实验及Transwell实验,观察SATB1对LM3高转移人肝癌细胞株增殖及侵袭转移能力的影响。结果:HCC组织中的SATB1的mRNA水平明显高于正常肝脏组织,且LM3高转移人肝癌细胞株中的SATB1表达水平显著高于正常肝脏细胞株HL-7702;在LM3细胞株中成功干扰SATB1,干扰后细胞株的增殖及侵袭转移能力均明显降低。结论:SATB1在HCC中显著表达,并有促进HCC细胞株的增殖及转移的作用。展开更多
目的检测组织特异性核基质结合蛋白1(special AT-rich binding protein 1,SATB1)及上皮钙粘蛋白(E-Cadher-in,E-Cad)在胆囊癌中的表达,探讨其可能的临床病理意义。方法应用免疫组织化学SP法检测SATB1、E-Cad在39例胆囊癌组织和23例对照...目的检测组织特异性核基质结合蛋白1(special AT-rich binding protein 1,SATB1)及上皮钙粘蛋白(E-Cadher-in,E-Cad)在胆囊癌中的表达,探讨其可能的临床病理意义。方法应用免疫组织化学SP法检测SATB1、E-Cad在39例胆囊癌组织和23例对照患者的胆囊组织中的表达。结果 SATB1在胆囊癌中的阳性表达率高于对照组阳性表达率(P<0.05);E-Cad在胆囊癌中的阳性表达率低于对照组中的阳性表达率(P<0.05);胆囊癌组织中SATB1、E-Cad的表达呈负相关(r=-0.374,P<0.05);E-Cad、SATB1均为影响胆囊癌患者预后的独立因素(P<0.05)。结论胆囊癌中SATB1、E-Cad的异常表达与肿瘤发生及侵袭转移有关,可望成为胆囊癌早期诊断及判断预后的参考指标。展开更多
特异性核基质结合区结合蛋白1(special AT rich sequence binding protein 1,SATB1)又称AT富集序列特异性结合蛋白1,是一种独特的全局调节因子,通过基因表达调控结合染色质高级结构,对染色质进行表观遗传修饰和动态改变,直接调节促癌基...特异性核基质结合区结合蛋白1(special AT rich sequence binding protein 1,SATB1)又称AT富集序列特异性结合蛋白1,是一种独特的全局调节因子,通过基因表达调控结合染色质高级结构,对染色质进行表观遗传修饰和动态改变,直接调节促癌基因的表达.自2008年在乳腺癌细胞中发现他对肿瘤细胞的发生和转移有促进作用后,近年来又发现其高表达对消化系肿瘤(包括口腔癌、胃癌、肝癌、胆囊癌、结直肠癌)的肿瘤细胞增殖、侵袭、转移关系密切.我国以消化系肿瘤多见,如何控制恶性肿瘤的转移,一直是国内外研究的重点.随着对SATB1作用机制的深入研究必将为恶性肿瘤的诊断、治疗以及预后评估提供新的思路和方法.本文就近年来SATB1在消化系肿瘤中的相关研究进展作一综述.展开更多
BCL2 is a key regulator of apoptosis.Our previous work has demonstrated that special AT-rich sequence-binding protein 1 （SATB1） is positively correlated with BCL2 expression.In the present study,we report a new SATB...BCL2 is a key regulator of apoptosis.Our previous work has demonstrated that special AT-rich sequence-binding protein 1 （SATB1） is positively correlated with BCL2 expression.In the present study,we report a new SATB1 binding site located between P1 and P2 promoters of the BCL2 gene.The candidate SATB1 binding sequence predicted by bioinformatic analysis was investigated in vitro and in vivo by electrophoretic gel mobility shift assays （EMSA） and chromatin immunoprecipitation （ChIP）.One 25-bp sequence,named SB1,was confirmed to be SATB1 binding site.The regulatory function of SB1 and its relevance to SATB1 were further examed with dual-luciferase reporter assay system in Jurkat cells.We found that SB1 could negatively regulate reporter gene activity.Mutation of SATB1 binding site further repressed the activity.Knockdown of SATB1 also enhanced this negative effect of SB1.Our data indicate that the SB1 sequence possesses negative transcriptional regulatory function and this function can be antagonized by SATB1.展开更多
基金Supported by The National Natural Science Foundation of China, No. 81101580
文摘AIM: To evaluate the expression of special AT-rich sequence-binding protein 1 (SATB1 ) gene in colorectal cancer and its role in colorectal cancer cell proliferation and invasion.METHODS: Immunohistochemistry was used to detect the protein expression of SATB1 in 30 colorectal cancer (CRC) tissue samples and pair-matched adjacent nontumor samples. Cell growth was investigated after enhancing expression of SATB1. Wound-healing assay and Transwell assay were used to investigate the impact of SATB1 on migratory and invasive abilities of SW480 cells in vitro . Nude mice that received subcutaneous implantation or lateral tail vein were used to study the effects of SATB1 on tumor growth or metastasis in vivo . RESULTS: SATB1 was over-expressed in CRC tissues and CRC cell lines. SATB1 promotes cell proliferation and cell cycle progression in CRC SW480 cells. SATB1 over-expression could promote cell growth in vivo . In addition, SATB1 could significantly raise the ability of cell migration and invasion in vitro and promote the ability of tumor metastasis in vivo . SATB1 could up-regulate matrix metalloproteases 2, 9, cyclin D1 and vimentin, meanwhile SATB1 could down-regulate E-cadherin in CRC. CONCLUSION: SATB1 acts as a potential growth and metastasis promoter in CRC. SATB1 may be useful as a therapeutic target for CRC.
文摘目的:检测特别富含AT序列结合蛋白1(Special AT rich sequence binding protein 1,SATB1)在原发性肝癌(Hepato-cellular carcinoma,HCC)中的表达情况,并研究SATB1对LM3高转移人肝癌细胞株促进增殖及侵袭转移能力的影响。方法:运用实时定量PCR方法检测正常肝组织及HCC组织中SATB1的表达情况,并通过实时定量PCR及Western blot检测LM3高转移人肝癌细胞株中SATB1的表达。运用RNA干扰技术对LM3细胞株中的SATB1进行干扰并验证,对干扰前后的细胞株进行MTT、划痕实验及Transwell实验,观察SATB1对LM3高转移人肝癌细胞株增殖及侵袭转移能力的影响。结果:HCC组织中的SATB1的mRNA水平明显高于正常肝脏组织,且LM3高转移人肝癌细胞株中的SATB1表达水平显著高于正常肝脏细胞株HL-7702;在LM3细胞株中成功干扰SATB1,干扰后细胞株的增殖及侵袭转移能力均明显降低。结论:SATB1在HCC中显著表达,并有促进HCC细胞株的增殖及转移的作用。
文摘特异性核基质结合区结合蛋白1(special AT rich sequence binding protein 1,SATB1)又称AT富集序列特异性结合蛋白1,是一种独特的全局调节因子,通过基因表达调控结合染色质高级结构,对染色质进行表观遗传修饰和动态改变,直接调节促癌基因的表达.自2008年在乳腺癌细胞中发现他对肿瘤细胞的发生和转移有促进作用后,近年来又发现其高表达对消化系肿瘤(包括口腔癌、胃癌、肝癌、胆囊癌、结直肠癌)的肿瘤细胞增殖、侵袭、转移关系密切.我国以消化系肿瘤多见,如何控制恶性肿瘤的转移,一直是国内外研究的重点.随着对SATB1作用机制的深入研究必将为恶性肿瘤的诊断、治疗以及预后评估提供新的思路和方法.本文就近年来SATB1在消化系肿瘤中的相关研究进展作一综述.
基金supported by grants from the National Natural Science Foundation of China (No. 30772490)and Special Major National Natural Science Foundation of China (No. 90919051)
文摘BCL2 is a key regulator of apoptosis.Our previous work has demonstrated that special AT-rich sequence-binding protein 1 （SATB1） is positively correlated with BCL2 expression.In the present study,we report a new SATB1 binding site located between P1 and P2 promoters of the BCL2 gene.The candidate SATB1 binding sequence predicted by bioinformatic analysis was investigated in vitro and in vivo by electrophoretic gel mobility shift assays （EMSA） and chromatin immunoprecipitation （ChIP）.One 25-bp sequence,named SB1,was confirmed to be SATB1 binding site.The regulatory function of SB1 and its relevance to SATB1 were further examed with dual-luciferase reporter assay system in Jurkat cells.We found that SB1 could negatively regulate reporter gene activity.Mutation of SATB1 binding site further repressed the activity.Knockdown of SATB1 also enhanced this negative effect of SB1.Our data indicate that the SB1 sequence possesses negative transcriptional regulatory function and this function can be antagonized by SATB1.
