Department of Pathology, The Second Hospital of Longyan, Longyan, China.
Department of Pathology, Ganzhou People's Hospital, the Affiliated Ganzhou Hospital of Nanchang University, Ganzhou, China.
Bioengineered. 2022 Apr;13(4):8503-8514. doi: 10.1080/21655979.2022.2051827.
Cervical squamous cell carcinoma (CSCC), the most common cervical malignancy, is more likely to invade and metastasize than other cervical cancers. miR-125a, a tumor suppressor gene, has been confirmed to be associated with cancer metastasis. However, the role of miR-125a in CSCC and the underlying mechanism are unknown. miR-125a expression was confirmed by real-time quantitative PCR (RT-qPCR), and the Rad51 expression level was measured by western blotting analysis. CSCC cell proliferation, migration and invasion were assessed with functional assays, including CCK-8, colony formation, wound healing and Transwell assays. Our data confirmed that miR-125a is expressed at low levels in CSCC tissues and cells. Functionally, the overexpression of miR-125a greatly prevented the proliferation, migration and invasion of CSCC cells, and the inhibition of miR-125a expression strongly enhanced these behaviors in CSCC cells. Moreover, the expression of Rad51, a miR-125a target gene, greatly reversed the miR-125-mediated inhibition of CSCC cell proliferation, migration and invasion. In addition, we discovered that miR-125a downregulated the levels of phosphorylated PI3K, AKT and mTOR through Rad51 in CSCC cells. miR-125a, a tumor suppressor, can attenuate the malignant behaviors of CSCC cells by targeting Rad51. Therefore, the miR-125a/Rad51 axis might be a target for CSCC therapy.
宫颈鳞状细胞癌（CSCC）是最常见的宫颈癌，比其他宫颈癌更容易侵袭和转移。miR-125a 是一种肿瘤抑制基因，已被证实与癌症转移有关。然而，miR-125a 在 CSCC 中的作用及其潜在机制尚不清楚。通过实时定量 PCR（RT-qPCR）证实了 miR-125a 的表达，通过 Western blot 分析测量了 Rad51 的表达水平。通过 CCK-8、集落形成、划痕愈合和 Transwell 测定等功能测定评估了 CSCC 细胞的增殖、迁移和侵袭。我们的数据证实 miR-125a 在 CSCC 组织和细胞中的表达水平较低。功能上，miR-125a 的过表达极大地阻止了 CSCC 细胞的增殖、迁移和侵袭，而 miR-125a 表达的抑制则强烈增强了 CSCC 细胞的这些行为。此外，miR-125a 靶基因 Rad51 的表达极大地逆转了 miR-125a 介导的 CSCC 细胞增殖、迁移和侵袭的抑制。此外，我们发现 miR-125a 通过 Rad51 在 CSCC 细胞中下调了磷酸化 PI3K、AKT 和 mTOR 的水平。miR-125a 作为一种肿瘤抑制因子，可以通过靶向 Rad51 来减弱 CSCC 细胞的恶性行为。因此，miR-125a/Rad51 轴可能是 CSCC 治疗的一个靶点。
