Department of Internal Medicine, Central Hospital of Linyi, Linyi, China.
Department of Laboratory, The Third People's Hospital of Linyi, Linyi, China.
Cell Biochem Funct. 2020 Dec;38(8):1139-1151. doi: 10.1002/cbf.3580. Epub 2020 Sep 1.
It is reported that long intergenic non-coding RNA 00662 (LINC00662) plays an oncogenic role in tumours. However, the mechanism of LINC00662 in regulating the progression and radiosensitivity of cervical cancer (CC) is not clear. In this study, quantitative real-time polymerase chain reaction (qRT-PCR) was adopted to detect LINC00662 and miR-497-5p expressions in CC tissues and cells. The expression of cell division cycle 25 A (CDC25A) in CC cells was examined by Western blot. CC cell proliferation was determined by cell counting kit-8 (CCK-8) and BrdU assays. The survival rate of CC cells was evaluated by colony formation assay under different doses of X-ray irradiation. CC cell migration and invasion were probed by Transwell assay. Besides, the interactions between miR-497-5p and LINC00662, and miR-497-5p and the 3'UTR of CDC25A were verified by dual-luciferase reporter assay, RIP assay, and RNA pull-down experiments. We demonstrated that, LINC00662 expression was remarkably raised in CC tissues and cell lines. LINC00662 overexpression promoted proliferation, migration, invasion and radioresistance of CC cells, and LINC00662 knockdown inhibited the above malignant phenotypes of CC cells. In terms of mechanism, LINC00662 facilitated CC progression and radioresistance by adsorbing miR-497-5p and indirectly up-regulating CDC25A expression. In a word, the LINC00662/miR-497-5p/CDC25A axis boosts proliferation and metastasis of CC cells and enhances the radioresistance of cancer cells. SIGNIFICANCE OF THE STUDY: CC poses a threat to the health of women all over the world. In this study, we demonstrated for the first time that LINC00662 expression was remarkably raised in CC tissues and cells. Cellular experiments confirmed that LINC00662 facilitated cell proliferation, migration, invasion and radiation resistance through the miR-497-5p/CDC25A axis, which might be a promising target for CC treatments.
据报道，长链非编码 RNA 00662（LINC00662）在肿瘤中发挥致癌作用。然而，LINC00662 调节宫颈癌（CC）进展和放射敏感性的机制尚不清楚。在本研究中，采用实时定量聚合酶链反应（qRT-PCR）检测 CC 组织和细胞中 LINC00662 和 miR-497-5p 的表达。Western blot 检测 CC 细胞中细胞分裂周期蛋白 25A（CDC25A）的表达。通过细胞计数试剂盒-8（CCK-8）和 BrdU 测定法检测 CC 细胞的增殖。在不同剂量 X 射线照射下，通过集落形成实验评估 CC 细胞的存活率。通过 Transwell 测定法探测 CC 细胞的迁移和侵袭。此外，通过双荧光素酶报告基因测定、RIP 测定和 RNA 下拉实验验证了 miR-497-5p 与 LINC00662 以及 miR-497-5p 与 CDC25A 的 3'UTR 之间的相互作用。我们证明，LINC00662 在 CC 组织和细胞系中表达明显上调。LINC00662 的过表达促进了 CC 细胞的增殖、迁移、侵袭和放射抵抗，而 LINC00662 的敲低抑制了 CC 细胞的上述恶性表型。就机制而言，LINC00662 通过吸附 miR-497-5p 并间接上调 CDC25A 的表达促进 CC 的进展和放射抵抗。总之，LINC00662/miR-497-5p/CDC25A 轴促进 CC 细胞的增殖和转移，并增强癌细胞的放射抵抗能力。研究的意义：CC 对全世界妇女的健康构成威胁。在这项研究中，我们首次证明，LINC00662 在 CC 组织和细胞中表达明显上调。细胞实验证实，LINC00662 通过 miR-497-5p/CDC25A 轴促进细胞增殖、迁移、侵袭和辐射抵抗，这可能是 CC 治疗的一个有前途的靶点。
