目的探讨TAp63基因在儿童急性白血病骨髓单个核细胞中的表达及意义。方法收集2015年6月—2016年6月郑州大学第三附属医院和郑州儿童医院住院的初治或复发急性白血病患儿104例为急性白血病组,其中急性淋巴细胞白血病(ALL)80例[急性B淋巴...目的探讨TAp63基因在儿童急性白血病骨髓单个核细胞中的表达及意义。方法收集2015年6月—2016年6月郑州大学第三附属医院和郑州儿童医院住院的初治或复发急性白血病患儿104例为急性白血病组,其中急性淋巴细胞白血病(ALL)80例[急性B淋巴细胞白血病(B-ALL)61例,急性T淋巴细胞白血病(T-ALL)19例],急性非淋巴细胞白血病(ANLL)24例;初发患儿90例(高危型18例,低危型72例),复发患儿14例。选择同期郑州大学第三附属医院和郑州儿童医院住院的非恶性血液病患儿36例作为对照组。利用半定量反转录聚合酶链反应法检测各组患儿TAp63基因表达。结果急性白血病组104例患儿TAp63基因阳性表达86例,阳性表达率为82.7%,TAp63 m RNA相对表达量为(0.61±0.19);对照组患儿TAp63基因阳性表达0例。ALL与ANLL患儿TAp63基因阳性表达率比较,差异无统计学意义(P>0.05);ALL患儿TAp63 m RNA相对表达量较ANLL患儿升高(P<0.05)。初发与复发患儿TAp63基因阳性表达率比较,差异无统计学意义(P>0.05);复发患儿TAp63 m RNA相对表达量较初发患儿升高(P<0.05)。B-ALL患儿TAp63基因阳性表达率、TAp63 m RNA相对表达量较T-ALL患儿升高(P<0.05)。高危型与低危型初发患儿TAp63基因阳性表达率比较,差异无统计学意义(P>0.05);高危型初发患儿TAp63 m RNA相对表达量较低危型初发患儿升高(P<0.05)。完全缓解与未缓解患儿TAp63基因阳性表达率比较,差异无统计学意义(P>0.05);未缓解患儿TAp63 m RNA相对表达量较完全缓解患儿升高(P<0.05)。结论儿童急性白血病的发生、发展可能与TAp63基因的过度表达相关,可作为探讨化疗疗效的观察指标之一;TAp63高表达者易复发,可作为评估预后的指标之一。展开更多
Background: The hepatitis B virus X (HBx) protein plays a critical role in the initiation and progression of hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). In the early stage of the disease, HBx fa...Background: The hepatitis B virus X (HBx) protein plays a critical role in the initiation and progression of hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). In the early stage of the disease, HBx facilitates tumor onset by inactivating the tumor suppressor p53. The p53-encoding gene, however, is frequently mutated or deleted as the cancer progresses to the late stage and, under such circumstance, the p53 homolog TAp63 can harness HCC growth by transactivating several important p53-target genes.Methods: To determine whether HBx regulates TAp63, we performed co-immunoprecipitation assay, real-time quantitative polymerase chain reaction, immunoblotting, and flow cytometry analysis in p53-null cancer cell lines, Hep3B and H1299.Results: HBx interacts with the transactivation domain of TAp63, as HBx was co-immunoprecipitated with TAp63 but not with ΔNp63. The interaction between HBx and TAp63 abolished transcriptional activity of TAp63, as evidenced by the reduction of the levels of its target genesp21 andPUMA, consequently leading to restricted apoptosis and augmented proliferation of HCC cells.Conclusion: HBV induces progression of HCC that harbors defective p53 by inhibiting the tumor suppressor TAp63.展开更多
文摘目的探讨TAp63基因在儿童急性白血病骨髓单个核细胞中的表达及意义。方法收集2015年6月—2016年6月郑州大学第三附属医院和郑州儿童医院住院的初治或复发急性白血病患儿104例为急性白血病组,其中急性淋巴细胞白血病(ALL)80例[急性B淋巴细胞白血病(B-ALL)61例,急性T淋巴细胞白血病(T-ALL)19例],急性非淋巴细胞白血病(ANLL)24例;初发患儿90例(高危型18例,低危型72例),复发患儿14例。选择同期郑州大学第三附属医院和郑州儿童医院住院的非恶性血液病患儿36例作为对照组。利用半定量反转录聚合酶链反应法检测各组患儿TAp63基因表达。结果急性白血病组104例患儿TAp63基因阳性表达86例,阳性表达率为82.7%,TAp63 m RNA相对表达量为(0.61±0.19);对照组患儿TAp63基因阳性表达0例。ALL与ANLL患儿TAp63基因阳性表达率比较,差异无统计学意义(P>0.05);ALL患儿TAp63 m RNA相对表达量较ANLL患儿升高(P<0.05)。初发与复发患儿TAp63基因阳性表达率比较,差异无统计学意义(P>0.05);复发患儿TAp63 m RNA相对表达量较初发患儿升高(P<0.05)。B-ALL患儿TAp63基因阳性表达率、TAp63 m RNA相对表达量较T-ALL患儿升高(P<0.05)。高危型与低危型初发患儿TAp63基因阳性表达率比较,差异无统计学意义(P>0.05);高危型初发患儿TAp63 m RNA相对表达量较低危型初发患儿升高(P<0.05)。完全缓解与未缓解患儿TAp63基因阳性表达率比较,差异无统计学意义(P>0.05);未缓解患儿TAp63 m RNA相对表达量较完全缓解患儿升高(P<0.05)。结论儿童急性白血病的发生、发展可能与TAp63基因的过度表达相关,可作为探讨化疗疗效的观察指标之一;TAp63高表达者易复发,可作为评估预后的指标之一。
基金supported by grants from the Beijing Municipal Institute of Public Medical Research Development and Reform Pilot Project(jingyiyan2019-6,jingyiyan2021-10)China Primary Health Care Foundation-YouAn Foundation of Liver Disease and AIDS(Scientific Research Project of Beijing YouAn Hospital,CCMU,2018)the National Natural Science Foundation of China(No.82072879).
文摘Background: The hepatitis B virus X (HBx) protein plays a critical role in the initiation and progression of hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). In the early stage of the disease, HBx facilitates tumor onset by inactivating the tumor suppressor p53. The p53-encoding gene, however, is frequently mutated or deleted as the cancer progresses to the late stage and, under such circumstance, the p53 homolog TAp63 can harness HCC growth by transactivating several important p53-target genes.Methods: To determine whether HBx regulates TAp63, we performed co-immunoprecipitation assay, real-time quantitative polymerase chain reaction, immunoblotting, and flow cytometry analysis in p53-null cancer cell lines, Hep3B and H1299.Results: HBx interacts with the transactivation domain of TAp63, as HBx was co-immunoprecipitated with TAp63 but not with ΔNp63. The interaction between HBx and TAp63 abolished transcriptional activity of TAp63, as evidenced by the reduction of the levels of its target genesp21 andPUMA, consequently leading to restricted apoptosis and augmented proliferation of HCC cells.Conclusion: HBV induces progression of HCC that harbors defective p53 by inhibiting the tumor suppressor TAp63.
