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.

中文翻译：

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LINC00662通过调节miR-497-5p和CDC25A促进宫颈癌的进展和放射抵抗。

据报道，长的基因间非编码RNA 00662（LINC00662）在肿瘤中起致癌作用。但是，LINC00662在调节宫颈癌（CC）的进程和放射敏感性中的机制尚不清楚。在这项研究中，采用定量实时聚合酶链反应（qRT-PCR）检测CC组织和细胞中LINC00662和miR-497-5p的表达。通过Western印迹检查CC细胞中细胞分裂周期25A（CDC25A）的表达。CC细胞增殖是通过细胞计数试剂盒‐8（CCK‐8）和BrdU分析确定的。在不同剂量的X射线照射下，通过菌落形成试验评估CC细胞的存活率。通过Transwell测定探查CC细胞的迁移和侵袭。此外，miR-497-5p与LINC00662之间的相互作用 CDC25A的miR-497-5p和3'UTR已通过双荧光素酶报告基因检测，RIP检测和RNA下拉实验进行了验证。我们证明，LINC00662表达在CC组织和细胞系中显着升高。LINC00662的过表达促进CC细胞的增殖，迁移，侵袭和放射抗性，而LINC00662的抑制则抑制了CC细胞的上述恶性表型。就机理而言，LINC00662通过吸附miR-497-5p并间接上调CDC25A表达来促进CC进程和放射抵抗。总之，LINC00662 / miR-497-5p / CDC25A轴可促进CC细胞的增殖和转移，并增强癌细胞的抗辐射性。LINC00662表达在CC组织和细胞系中显着升高。LINC00662的过表达促进CC细胞的增殖，迁移，侵袭和放射抗性，而LINC00662的抑制则抑制了CC细胞的上述恶性表型。就机理而言，LINC00662通过吸附miR-497-5p并间接上调CDC25A表达来促进CC进程和放射抵抗。总之，LINC00662 / miR-497-5p / CDC25A轴可促进CC细胞的增殖和转移，并增强癌细胞的抗辐射性。LINC00662表达在CC组织和细胞系中显着升高。LINC00662的过表达促进CC细胞的增殖，迁移，侵袭和放射抗性，而LINC00662的抑制则抑制了CC细胞的上述恶性表型。就机理而言，LINC00662通过吸附miR-497-5p并间接上调CDC25A表达来促进CC进程和放射抵抗。总之，LINC00662 / miR-497-5p / CDC25A轴可促进CC细胞的增殖和转移，并增强癌细胞的抗辐射性。LINC00662通过吸附miR-497-5p并间接上调CDC25A表达来促进CC进程和放射抵抗。总之，LINC00662 / miR-497-5p / CDC25A轴可促进CC细胞的增殖和转移，并增强癌细胞的抗辐射性。LINC00662通过吸附miR-497-5p并间接上调CDC25A表达来促进CC进程和放射抵抗。总之，LINC00662 / miR-497-5p / CDC25A轴可促进CC细胞的增殖和转移，并增强癌细胞的抗辐射性。