a Department of Oral and Maxillofacial Surgery, Binzhou Medical University Hospital , Binzhou , China.
b Department of Orthodontics, Binzhou Medical University Hospital , Binzhou , China.
Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):3153-3162. doi: 10.1080/21691401.2019.1642206.
Alkannin (ALK) has anti-inflammatory and anti-tumour activities. We tried to probe the underlying functions of ALK in oral squamous carcinoma (OSCC) cells growth, migration and invasion. OSCC cells viability was investigated after treatment with ALK. Then, BrdU, flow cytometry, Western blot and Transwell assays were executed to appraise proliferation, apoptosis, migration and invasion in OSCC cells with ALK stimulation. The biological functions of miR-9 were explored after miR-9 mimic/inhibitor transfection. The relevance of RECK and miR-9 was predicated by dual luciferase activity assay. JAK1/STAT3 and PI3K/AKT pathways were estimated by Western blot. Tumour formation was executed by xenograft tumours assay. We found that ALK restrained cell proliferation, facilitated apoptosis, repressed migration and invasion also interdicted JAK1/STAT3 and PI3K/AKT pathways in CAL-27 and SCC-9 cells. miR-9 expression was upgraded in OSCC tissues but decreased in OSCC cells along with ALK administration; meanwhile, overexpressed miR-9 inverted the influences of ALK in OSCC cells growth, migration and invasion. RECK was predicated as a novel target gene of miR-9, and overexpressed RECK hindered JAK1/STAT3 and PI3K/AKT pathways in OSCC cells. ALK prohibited tumour formation . In conclusion, ALK restrained OSCC cells growth, migration and invasion via adjusting miR-9/RECK axis. Highlights ALK restrains cell growth, migration and invasion in OSCC cells; miR-9 is enhanced in OSCC tissues but is repressed by ALK in OSCC cells; miR-9 inverts the repressive effect of ALK on CAL-27 and SCC-9 cells; RECK is a novel target of miR-9; ALK or RECK hinders JAK1/STAT3 and PI3K/AKT pathways in CAL-27 and SCC-9 cells; ALK prohibits tumour formation .
白花丹素（ALK）具有抗炎和抗肿瘤作用。我们试图探讨 ALK 在口腔鳞状细胞癌（OSCC）细胞生长、迁移和侵袭中的潜在功能。用 ALK 处理后，检测 OSCC 细胞活力。然后，进行 BrdU、流式细胞术、Western blot 和 Transwell 测定，以评估 ALK 刺激下 OSCC 细胞的增殖、凋亡、迁移和侵袭。转染 miR-9 模拟物/抑制剂后，研究了 miR-9 的生物学功能。通过双荧光素酶活性测定预测 RECK 和 miR-9 的相关性。通过 Western blot 评估 JAK1/STAT3 和 PI3K/AKT 通路。通过异种移植肿瘤实验进行肿瘤形成实验。结果发现，ALK 抑制 CAL-27 和 SCC-9 细胞增殖，促进凋亡，抑制迁移和侵袭，同时抑制 JAK1/STAT3 和 PI3K/AKT 通路。OSCC 组织中 miR-9 表达上调，而 ALK 处理后 OSCC 细胞中 miR-9 表达下调；同时，过表达 miR-9 逆转了 ALK 对 OSCC 细胞生长、迁移和侵袭的影响。RECK 被预测为 miR-9 的一个新的靶基因，过表达 RECK 抑制 OSCC 细胞中 JAK1/STAT3 和 PI3K/AKT 通路。ALK 抑制肿瘤形成。总之，ALK 通过调节 miR-9/RECK 轴抑制 OSCC 细胞的生长、迁移和侵袭。
