S100 calcium binding protein A6 (S100A6) has been reported to involve in many kinds of cancers through regulating intracellular calcium homeostasis. Previous studies found that S100A6 increased in lung cancer patients' plasma and pleural effusion. This study focused on its function in Calu-6 lung cancer cells. S100A6 gene was transferred into Calu-6 lung cancer cell line by lentivirus vector, the empty vector transfected cells and the blank cells were set as control groups. MTT was evaluating cell proliferation. The transwell assay was reflecting cell migration and cell invasion. The flow cytometric analysis was detecting cell apoptosis and cell cycle of three groups (Calu-6, Calu-6/neo, Calu-6/S100A6). Nude mouse tumorigenicity was then applied to evaluate S100A6's effect on cellular tumorigenicity. Compared with control groups, Calu-6/S100A6 cells showed a weakening trend in the cell behaviours of proliferation, migration and invasiveness, while had an enhancement of cell apoptosis, with all P < .05. The cell cycle of Calu-6/S100A6 cells had a reduction of S phase and an increase of G1 phase (P < .05). In animal study, after 5 weeks of cell injection, the tumour bulk of Calu-6/S100A6 group was smaller than controls, with P < .05. Our results demonstrate S100A6 inhibits the growth of Calu-6 lung cancer cells, as well as impairs Calu-6's ability in tumorigenesis. At cellular level, S100A6 is supposed to act as a tumour suppressor gene in lung cancer.

中文翻译：

---

S100A6通过抑制细胞增殖、迁移、侵袭和增强细胞凋亡抑制Calu-6肺癌细胞生长

据报道，S100 钙结合蛋白 A6（S100A6）通过调节细胞内钙稳态参与多种癌症。以前的研究发现肺癌患者血浆和胸腔积液中 S100A6 增加。本研究侧重于其在 Calu-6 肺癌细胞中的功能。慢病毒载体将S100A6基因转入Calu-6肺癌细胞系，以空载体转染细胞和空白细胞为对照组。MTT 正在评估细胞增殖。Transwell 测定反映细胞迁移和细胞侵袭。流式细胞术检测三组（Calu-6、Calu-6/neo、Calu-6/S100A6）的细胞凋亡和细胞周期。然后应用裸鼠致瘤性来评估 S100A6 对细胞致瘤性的影响。与对照组相比，P  < .05。Calu-6/S100A6细胞的细胞周期S期减少，G1期增加（P  < .05）。在动物研究中，细胞注射5周后，Calu-6/S100A6组的肿瘤体积小于对照组，P  < .05。我们的结果表明 S100A6 抑制 Calu-6 肺癌细胞的生长，并削弱 Calu-6 在肿瘤发生中的能力。在细胞水平上，S100A6 被认为是肺癌的抑癌基因。