Zhong Yun-Hua, Cheng Hong-Zhong, Peng Hao, Tang Shi-Cong, Wang Ping
Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, Yunnan 650500, P.R. China; Cadres Treatment Section, The First People's Hospital of Yunnan Province, Kunming, Yunnan 510032, P.R. China.
Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, Yunnan 650500, P.R. China; Thoracic Surgery, The First People's Hospital of Yunnan Province, Kunming, Yunnan 510032, P.R. China.
Oncol Lett. 2016 Dec;12(6):5106-5112. doi: 10.3892/ol.2016.5368. Epub 2016 Nov 8.
Cancer is the leading cause of morbidity and mortality worldwide, particularly lung cancer. Heat shock proteins and their upstream heat shock factors are involved in the occurrence of cancer and have been widely researched. However, the role of heat shock factor 2 (HSF2) in lung cancer remains unclear. In the present study, expression levels of HSF2 in lung cancer tissues from 50 lung cancer patients were detected by reverse transcription quantitative polymerase chain reaction, and 76% (38/50) were upregulated compared with the matched normal tissues. This suggested possible involvement of HSF2 in lung cancer. To additionally investigate the role of HSF2 in lung cancer occurrence, a plasmid encoding HSF2 was constructed. HSF2 was over expressed in normal lung epithelial BEAS-2B cells and lung cancer A549 cells. The results showed that HSF2 overexpression promoted cell proliferation and cell migration in BEAS-2B and A549 cells. Additional experiments showed that the HSF2-induced cell proliferation and cell migration were dependent on induction of HSPs, particularly HSP27 and HSP90, as co-transfection of HSP27 small interfering RNA (siRNA) or HSP90 siRNA attenuated HSF2-induced cell growth and migration. In conclusion, the present study showed that HSF2 is aberrantly expressed in lung cancer, and it may be an upstream regulator of HSPs, which may strongly affect cell growth and cell migration. Additional studies are required to explain the detailed mechanism between lung cancer, HSF2, HSPs and other possible signaling pathways.
癌症是全球发病和死亡的主要原因，尤其是肺癌。热休克蛋白及其上游热休克因子参与癌症的发生，并且已经得到广泛研究。然而，热休克因子2（HSF2）在肺癌中的作用仍不清楚。在本研究中，通过逆转录定量聚合酶链反应检测了50例肺癌患者肺癌组织中HSF2的表达水平，与配对的正常组织相比，76%（38/50）的患者表达上调。这表明HSF2可能参与肺癌的发生。为了进一步研究HSF2在肺癌发生中的作用，构建了编码HSF2的质粒。HSF2在正常肺上皮BEAS-2B细胞和肺癌A549细胞中过表达。结果表明，HSF2过表达促进了BEAS-2B和A549细胞的增殖和迁移。进一步的实验表明，HSF2诱导的细胞增殖和迁移依赖于热休克蛋白的诱导，特别是HSP27和HSP90，因为共转染HSP27小干扰RNA（siRNA）或HSP90 siRNA可减弱HSF2诱导的细胞生长和迁移。总之，本研究表明HSF2在肺癌中异常表达，它可能是热休克蛋白的上游调节因子，可能强烈影响细胞生长和细胞迁移。需要进一步的研究来解释肺癌、HSF2、热休克蛋白和其他可能信号通路之间的详细机制。
