目的观察Aurora A在人前列腺癌中的表达情况,探讨Aurora A是否在前列腺癌发生发展中起一定作用。方法采用RT-PCR、免疫组织化学和Western blot,检测在前列腺癌组织及其细胞系中Aurora A mRNA和蛋白表达。同时,在前列腺癌细胞系PC3中导...目的观察Aurora A在人前列腺癌中的表达情况,探讨Aurora A是否在前列腺癌发生发展中起一定作用。方法采用RT-PCR、免疫组织化学和Western blot,检测在前列腺癌组织及其细胞系中Aurora A mRNA和蛋白表达。同时,在前列腺癌细胞系PC3中导入靶向Aurora A mRNA的DNA核酶,观察抑制Aurora A对前列腺癌细胞生长的影响。结果91%的前列腺癌组织和三种前列腺癌细胞系(PC3、LNCaP和Du145)中Aurora A表达阳性,而且,靶向Aurora A mRNA的DNA核酶导入PC3细胞后抑制了Aurora A表达,使PC3细胞停滞在G2/M期,并促进细胞凋亡。结论Aurora A可能在前列腺癌形成中起一定作用,Aurora A可望成为前列腺癌治疗中有价值的靶点。展开更多
Objective： Aurora A kinase representing a family of evolutionadly conserved mitotic serine/threonine kinases has been found elevated in human lung adenocarcinoma cell line A549. It is suggested that the overexpressio...Objective： Aurora A kinase representing a family of evolutionadly conserved mitotic serine/threonine kinases has been found elevated in human lung adenocarcinoma cell line A549. It is suggested that the overexpression of Aurora A contributes to the carcinogenesis, chromosomal instability （CIN）, and de-differentiation of lung cancers. To address its possibility as a therapeutic target for lung cancer, we employed the antisense oligodeoxynucleotide （ASODN） technique to inhibit Aurora A expression and investigate its effects on tumor growth and cell cycle of A549, as well as the chemosensitivity to paclitaxel. Methods： Aurora AASODN was synthesized and transfected into A549 cells by lipofectAMINE 2000. Aurora A mRNA and protein expression were examined by reverse transcription-polymerase chain reaction （RT-PCR） and Western blot respectively. Cell cycle distribution was observed by flow cytometer. MTT assay was used to evaluate cell inhibition ratio before and after transfection. Results： The proliferation of the A549 cells was inhibited by Aurora A ASODN dose and time dependently. It was also observed that the IC50 of A549 cells after 48 hours＇ treatment of ASODN was about 300 nmol/L and under such circumstances, the Aurora A mRNA and protein expression significantly decreased （P 〈 0.05）, along with the induction of accumulation of cells in S phase and the G2-M transition. Furthermore, cell inhibition ratio of the combination of Aurora AASODN and paclitaxel was higher significantly than paclitaxel （P 〈 0.05） or Aurora AASODN alone （P 〈 0.05）. Conclusion： Inhibition of Aurora A expression can result in the suppression of cell growth and chemosensitizing activity to paclitaxel in human lung cancer cell line A549.展开更多
文摘目的观察Aurora A在人前列腺癌中的表达情况,探讨Aurora A是否在前列腺癌发生发展中起一定作用。方法采用RT-PCR、免疫组织化学和Western blot,检测在前列腺癌组织及其细胞系中Aurora A mRNA和蛋白表达。同时,在前列腺癌细胞系PC3中导入靶向Aurora A mRNA的DNA核酶,观察抑制Aurora A对前列腺癌细胞生长的影响。结果91%的前列腺癌组织和三种前列腺癌细胞系(PC3、LNCaP和Du145)中Aurora A表达阳性,而且,靶向Aurora A mRNA的DNA核酶导入PC3细胞后抑制了Aurora A表达,使PC3细胞停滞在G2/M期,并促进细胞凋亡。结论Aurora A可能在前列腺癌形成中起一定作用,Aurora A可望成为前列腺癌治疗中有价值的靶点。
基金Hubei Provincial Science and Technology Key Program Foundation (No. 2004AA304B08)
文摘Objective： Aurora A kinase representing a family of evolutionadly conserved mitotic serine/threonine kinases has been found elevated in human lung adenocarcinoma cell line A549. It is suggested that the overexpression of Aurora A contributes to the carcinogenesis, chromosomal instability （CIN）, and de-differentiation of lung cancers. To address its possibility as a therapeutic target for lung cancer, we employed the antisense oligodeoxynucleotide （ASODN） technique to inhibit Aurora A expression and investigate its effects on tumor growth and cell cycle of A549, as well as the chemosensitivity to paclitaxel. Methods： Aurora AASODN was synthesized and transfected into A549 cells by lipofectAMINE 2000. Aurora A mRNA and protein expression were examined by reverse transcription-polymerase chain reaction （RT-PCR） and Western blot respectively. Cell cycle distribution was observed by flow cytometer. MTT assay was used to evaluate cell inhibition ratio before and after transfection. Results： The proliferation of the A549 cells was inhibited by Aurora A ASODN dose and time dependently. It was also observed that the IC50 of A549 cells after 48 hours＇ treatment of ASODN was about 300 nmol/L and under such circumstances, the Aurora A mRNA and protein expression significantly decreased （P 〈 0.05）, along with the induction of accumulation of cells in S phase and the G2-M transition. Furthermore, cell inhibition ratio of the combination of Aurora AASODN and paclitaxel was higher significantly than paclitaxel （P 〈 0.05） or Aurora AASODN alone （P 〈 0.05）. Conclusion： Inhibition of Aurora A expression can result in the suppression of cell growth and chemosensitizing activity to paclitaxel in human lung cancer cell line A549.
