Department of Human Anatomy, Medical College of Qinghai University, Xining, China.
Eur Rev Med Pharmacol Sci. 2021 Nov;25(22):6853-6861. doi: 10.26355/eurrev_202111_27233.
To reveal the role of LINC00958 in the progression of endometrial cancer (EC) and the underlying molecular mechanism.
Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was conducted to detect relative level of LINC00958 in EC specimens and cell lines. Its prognostic potential in EC was analyzed by Kaplan-Meier method. After in vitro knockdown of LINC00958, cell proliferative, migratory and invasive abilities in KLE and Ishikawa cells were evaluated by Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) and transwell assay. Dual-Luciferase reporter assay was carried out to identify the LINC00958/miR-3174/PHF6 axis, and their expression interaction was determined by Pearson correlation test. The role of miR-3174 in influencing LINC00958-induced phenotype changes of EC cells was determined through rescue experiments.
LINC00958 was abnormally upregulated in EC specimens and cell lines, which was unfavorable to the prognosis of EC. Knockdown of LINC00958 reduced proliferative, migratory and invasive rates in KLE and Ishikawa cells. MiR-3174 shared a binding site in the 3'-untranslated region (3'-UTR) to that of LINC00958, which was lowly expressed in EC specimens and negatively linked to LINC00958 level. Overexpression of miR-3174 partially abolished the role of LINC00958 in accelerating the malignant phenotypes of EC cells. PHF6 was the downstream target of miR-3174 and it was upregulated in EC specimens.
LINC00958 is upregulated in EC specimens, which is a prognostic factor of EC. It stimulates EC to proliferate, migrate and invade through the miR-3174/PHF6 axis.
揭示 LINC00958 在子宫内膜癌（EC）进展中的作用及其潜在的分子机制。
采用实时定量聚合酶链反应（qRT-PCR）检测 EC 标本和细胞系中 LINC00958 的相对水平。采用 Kaplan-Meier 法分析其在 EC 中的预后潜力。体外敲低 LINC00958 后，通过细胞计数试剂盒-8（CCK-8）、5-乙炔基-2'-脱氧尿苷（EdU）和 Transwell 分析评估 KLE 和 Ishikawa 细胞的增殖、迁移和侵袭能力。通过双荧光素酶报告实验鉴定 LINC00958/miR-3174/PHF6 轴，通过 Pearson 相关检验确定它们的表达相互作用。通过挽救实验确定 miR-3174 在影响 EC 细胞中 LINC00958 诱导的表型变化中的作用。
LINC00958 在 EC 标本和细胞系中异常上调，不利于 EC 的预后。敲低 LINC00958 降低了 KLE 和 Ishikawa 细胞的增殖、迁移和侵袭率。miR-3174 与 LINC00958 的 3'-非翻译区（3'-UTR）共享一个结合位点，在 EC 标本中表达水平较低，与 LINC00958 水平呈负相关。miR-3174 的过表达部分消除了 LINC00958 对加速 EC 细胞恶性表型的作用。PHF6 是 miR-3174 的下游靶标，在 EC 标本中上调。
LINC00958 在 EC 标本中上调，是 EC 的预后因素。它通过 miR-3174/PHF6 轴刺激 EC 增殖、迁移和侵袭。
