Liang Gai, Li Shuang, Du Wei, Ke Qinghua, Cai Jun, Yang Jiyuan
Department of Oncology, First Affiliated Hospital of Yangtze University, Jingzhou, Hubei 434000, P.R. China.
Oncol Lett. 2017 Feb;13(2):967-972. doi: 10.3892/ol.2016.5473. Epub 2016 Dec 8.
Hypoxia induces proliferation and invasion in cancer cells via hypoxia-inducible factor (HIF)-1α. The cell adhesion molecule cluster of differentiation (CD) 44 has been associated with increased cell invasion and metastasis. Whether hypoxia regulates the expression of CD44 in gastric cancer cells remains to be established. In the current study, the effects of hypoxia on HIF-1α and CD44 expression levels in human gastric cell lines SGC-7901 and BGC-823 were evaluated. The cells were cultured in 1% O for 1 week and then treated with 20 nM rapamycin for 72 h. Cell viability was evaluated using the Cell Counting kit-8 assay, and cell invasion was detected by the Transwell invasion assay. The protein and messenger (m) RNA expression levels of HIF-1α and CD44 were detected using western blotting and reverse transcription-quantitative polymerase chain reaction, respectively. The results revealed that cell viability and invasion increased under hypoxic conditions, but decreased following rapamycin treatment in SGC-7901 and BGC-823 cells. Hypoxia also increased the protein and mRNA expression levels of HIF-1α and CD44 in these two cell lines. However, this hypoxia-induced increase in HIF-1α and CD44 protein and mRNA expression levels was inhibited by rapamycin. These findings suggest that hypoxia induced the proliferation and invasion of SGC-7901 and BGC-823 cells. Furthermore, CD44 expression levels were potentially associated with HIF-1α expression levels. Therefore, in gastric cancer cells, hypoxia may regulate CD44 expression via HIF-1α in order to promote cell proliferation and invasion.
缺氧通过缺氧诱导因子（HIF）-1α诱导癌细胞增殖和侵袭。细胞黏附分子分化簇（CD）44与细胞侵袭和转移增加有关。缺氧是否调节胃癌细胞中CD44的表达仍有待确定。在本研究中，评估了缺氧对人胃癌细胞系SGC-7901和BGC-823中HIF-1α和CD44表达水平的影响。将细胞在1%氧气中培养1周，然后用20 nM雷帕霉素处理72小时。使用细胞计数试剂盒-8检测法评估细胞活力，并通过Transwell侵袭试验检测细胞侵袭。分别使用蛋白质印迹法和逆转录定量聚合酶链反应检测HIF-1α和CD44的蛋白质和信使（m）RNA表达水平。结果显示，在缺氧条件下，SGC-7901和BGC-823细胞的细胞活力和侵袭增加，但雷帕霉素处理后降低。缺氧还增加了这两种细胞系中HIF-1α和CD44的蛋白质和mRNA表达水平。然而，雷帕霉素抑制了这种缺氧诱导的HIF-1α和CD44蛋白质及mRNA表达水平的增加。这些发现表明，缺氧诱导了SGC-7901和BGC-823细胞的增殖和侵袭。此外，CD44表达水平可能与HIF-1α表达水平相关。因此，在胃癌细胞中，缺氧可能通过HIF-1α调节CD44表达，以促进细胞增殖和侵袭。
