然而, 越来越多的证据表明miR-297在肿瘤的发展和进展中起到一定作用, 但在肝细胞癌（HCC）中, miR-297及其潜在的分子作用机制仍不清楚。在这里, 我们报道了在人羊膜上皮细胞（hAECs）的培养基处理之后, miR-297在HepG2细胞中的表达显著增加, 而此处理可抑制HepG2的增殖和迁移。此外, 过量表达的miR-297能够抑制体外HCC细胞系的细胞增殖、迁移和侵袭，并且在体内抑制HCC的肿瘤形成。在HCC细胞系中, 明确鉴定了多嘧嘌核苷酸结合蛋白3（PTBP3）是miR-297的直接靶基因, 并调节了miR-297在HCC细胞中的功能。在临床样本中, miR-297水平有下降趋势, 但差异无统计学意义。此外, 体外细胞实验证实, miR-297的过量表达通过下调PTBP3表达来抑制PI3K/AKT信号通路, 进而抑制HCC细胞的增殖、迁移和侵袭。总之, 我们的结果揭示了miR-297能够下调PTBP3的表达并抑制PI3K/AKT信号通路的激活, 从而阻止HCC的生长、迁移和侵袭。© 2023. 作者.

Whereas increasing evidences demonstrate that miR-297 contributes to the tumour development and progression, the role of miR-297 and its underlying molecular mechanisms in hepatocellular carcinoma (HCC) was still unclear. Here, we reported that the expression of miR-297 increased significantly in hepG2 cells after the treatment of the conditioned medium of human amniotic epithelial cells(hAECs) which can inhibit the proliferation and migration of hepG2. And the overexpression of miR-297 inhibits the cell proliferation, migration and invasion of HCC cell lines in vitro and suppressed the tumorigenesis of HCC in vivo. Polypyrimidine tract-binding protein 3 (PTBP3) was identified as a direct target gene of miR-297 in HCC cell lines, and mediated the function of miR-297 in HCC cells. In clinical samples, miR-297 levels have a tendency to decrease, but there are no statistically significant differences. Furthermore, in vitro cell experiments confirmed that overexpression of miR-297 could inhibit the PI3K/AKT signaling pathway by down-regulating PTBP3 expression, thereby inhibiting the proliferation, migration and invasion of HCC cells. In conclusion, our results revealed that miR-297 could down-regulate the expression of PTBP3 and inhibit the activation of PI3K/AKT signaling pathway, thereby preventing HCC growth, migration and invasion.© 2023. The Author(s).