目的评价 r Hu TNF和阿霉素抗人结肠癌细胞株的序贯作用。方法采用克隆生成试验 ( Hamburger- Salmon法 ) ,研究 r Hu TNF和 DOX序贯作用于 SW4 80细胞株后的抗增殖效果。结果对结肠癌细胞系 SW4 80 ,存在 DOX至 r Hu TNF序贯抗增殖作...目的评价 r Hu TNF和阿霉素抗人结肠癌细胞株的序贯作用。方法采用克隆生成试验 ( Hamburger- Salmon法 ) ,研究 r Hu TNF和 DOX序贯作用于 SW4 80细胞株后的抗增殖效果。结果对结肠癌细胞系 SW4 80 ,存在 DOX至 r Hu TNF序贯抗增殖作用 ;除反序贯给药情况外 ,出现显著的协同作用。结论在 DOX存在情况下 ,TNF的抗瘤作用增强 ,从而支持DOX可干扰细胞保护机制以使瘤细胞对 TNF细胞毒作用更为敏感的理论。展开更多
The prostate secretory protein of 94 amino acids （PSP94） has been shown to interact with cysteine-rich secretory protein 3 （CRISP-3） in human seminal plasma. Interestingly, PSP94 expression is redaced or lost in t...The prostate secretory protein of 94 amino acids （PSP94） has been shown to interact with cysteine-rich secretory protein 3 （CRISP-3） in human seminal plasma. Interestingly, PSP94 expression is redaced or lost in the majority of the prostate tumours, whereas CRISP-3 expression is upregulated in prostate cancer compared with normal prostate tissue. To obtain a better understanding of the individual roles these proteins have in prostate tumourigenesis and the functional relevance of their interaction, we ectopically expressed either PSP94 or CRISP-3 alone or PSP94 along with CRISP-3 in three prostate cell lines （PC3, WPE1-NB26 and LNCaP） and performed growth inhibition assays. Reverse transcription-polymerase chain reaction and Western blot analysis were used to screen prostate cell lines for PSP94 and CRISP-3 expression. Mammalian expression constructs for human PSP94 and CRISP-3 were also generated and the expression, localization and secretion of recombinant protein were assayed by transfection followed by Western blot analysis and immunofluorescence assay. The effect that ectopic expression of PSP94 or CRISP-3 had on cell growth was studied by clonogenic survival assay follokving transfection. To evaluate the effects of coexpression of the two proteins, stable clones of PC3 that expressed PSP94 were generated. They were subsequently transfected with a CRISP-3 expression construct and subjected to clonogenic survival assay. Our results showed that PSP94 and CRISP-3 could each induce growth inhibition in a cell line specific manner. Although the growth of CRISP-3-positive cell lines was inhibited by PSP94, growth inhibition mediated by CRISP-3 was not affected by the presence or absence of PSP94. This suggests that CRISP-3 may participate in PSP94-independent activities during prostate tumourigenesis.展开更多
基金grants CA- 2 1893 CA- 170 94 and contract NO1- CM- 5 7662 from NIH
文摘目的评价 r Hu TNF和阿霉素抗人结肠癌细胞株的序贯作用。方法采用克隆生成试验 ( Hamburger- Salmon法 ) ,研究 r Hu TNF和 DOX序贯作用于 SW4 80细胞株后的抗增殖效果。结果对结肠癌细胞系 SW4 80 ,存在 DOX至 r Hu TNF序贯抗增殖作用 ;除反序贯给药情况外 ,出现显著的协同作用。结论在 DOX存在情况下 ,TNF的抗瘤作用增强 ,从而支持DOX可干扰细胞保护机制以使瘤细胞对 TNF细胞毒作用更为敏感的理论。
文摘The prostate secretory protein of 94 amino acids （PSP94） has been shown to interact with cysteine-rich secretory protein 3 （CRISP-3） in human seminal plasma. Interestingly, PSP94 expression is redaced or lost in the majority of the prostate tumours, whereas CRISP-3 expression is upregulated in prostate cancer compared with normal prostate tissue. To obtain a better understanding of the individual roles these proteins have in prostate tumourigenesis and the functional relevance of their interaction, we ectopically expressed either PSP94 or CRISP-3 alone or PSP94 along with CRISP-3 in three prostate cell lines （PC3, WPE1-NB26 and LNCaP） and performed growth inhibition assays. Reverse transcription-polymerase chain reaction and Western blot analysis were used to screen prostate cell lines for PSP94 and CRISP-3 expression. Mammalian expression constructs for human PSP94 and CRISP-3 were also generated and the expression, localization and secretion of recombinant protein were assayed by transfection followed by Western blot analysis and immunofluorescence assay. The effect that ectopic expression of PSP94 or CRISP-3 had on cell growth was studied by clonogenic survival assay follokving transfection. To evaluate the effects of coexpression of the two proteins, stable clones of PC3 that expressed PSP94 were generated. They were subsequently transfected with a CRISP-3 expression construct and subjected to clonogenic survival assay. Our results showed that PSP94 and CRISP-3 could each induce growth inhibition in a cell line specific manner. Although the growth of CRISP-3-positive cell lines was inhibited by PSP94, growth inhibition mediated by CRISP-3 was not affected by the presence or absence of PSP94. This suggests that CRISP-3 may participate in PSP94-independent activities during prostate tumourigenesis.
