Overexpression of constitutive signal transducer and activator of transcription 3 mRNA in cisplatin-resistant human non-small cell lung cancer cells.
Overexpression of constitutive signal transducer and activator of transcription 3 mRNA in cisplatin-resistant human non-small cell lung cancer cells.
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DOI：
10.3892/or.13.2.217
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发表时间：
2005-02
期刊：
影响因子：
4.2
通讯作者：
K. Ikuta;K. Takemura;M. Kihara;M. Nishimura;N. Ueda;S. Naito;Eibai Lee;E. Shimizu;A. Yamauchi
中科院分区：
文献类型：
--
作者：
K. Ikuta;K. Takemura;M. Kihara;M. Nishimura;N. Ueda;S. Naito;Eibai Lee;E. Shimizu;A. Yamauchi
非小细胞肺癌（NSCLC）往往表现出内在的多药耐药，这是顺铂辅助化疗中最严重的问题之一。近年来，在多种人类癌症中发现了信号换能器和转录激活因子（STAT）的本构激活。本研究采用实时定量逆转录聚合酶链反应（RT-PCR）技术，研究了STATs mRNA在不同NSCLC细胞系中的表达，以确定STATs是否与顺铂耐药和细胞凋亡诱导有关。根据生化和形态学结果，顺铂可触发Ma-46细胞的凋亡，但对Ma-31细胞无影响。STAT3 mRNA在顺铂耐药Ma-31中表达最高，在顺铂敏感Ma-46中表达最低。将癌细胞暴露于顺铂6小时后，无法刺激stat3mrna的表达。因此，本构性STAT3转录水平的升高可能与内在耐药NSCLC细胞凋亡通路的抑制调控有关。
Non-small cell lung cancer (NSCLC) often shows intrinsic multidrug resistance, which is one of the most serious problems in cisplatin-based adjuvant chemotherapy. Recently, the constitutive activation of signal transducer and activator of transcription (STAT) factors has been found in a variety of human cancers. In the present study, the mRNA expression of STATs in various human NSCLC cell lines was investigated by quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) to determine whether STATs can be implicated in cisplatin resistance and apoptosis inducibility. Cisplatin triggered apoptosis in Ma-46 based on biochemical and morphological findings, but not in Ma-31. The mRNA expression of STAT3 was highest in cisplatin-resistant Ma-31 and lowest in cisplatin-sensitive Ma-46. A 6-hour exposure of cancer cells to cisplatin failed to stimulate STAT3 mRNA expression. Therefore, an increased transcriptional level of constitutive STAT3 may be related to the suppressive regulation of the apoptotic pathway in intrinsically chemo-resistant NSCLC cells.