Ovarian cancer (OC) is the most lethal gynecologic malignancy and long non-coding RNAs (lncRNAs) have been acknowledged as important regulators in human OC. This study aimed to investigate the function and underlying mechanisms of LINC00504 in OC. The expression levels of LINC00504 in human OC tissues and cell lines were investigated by qRT-PCR analysis. The OC cell proliferation, and apoptosis were evaluated by MTT assay, colony-formation assay, Caspase-3 activity assay, and nucleosome ELISA assay, respectively. The metabolic shift in OC cells was examined by aerobic glycolysis analysis. Dual-luciferase activity reporter assay and mRNA-miRNA pull-down assay were conducted to validate the interaction between LINC00504 and miR-1244. LINC00504 was upregulated in OC cell lines and specimens. Knockdown of LINC00504 inhibited cell proliferation, enhanced apoptosis, decreased glycolysis-related gene (PKM2, HK2, and PDK1) expression, and altered aerobic glycolysis in OC cells and vice versa. LINC00504 downregulated miR-1244 expression levels by acting as an endogenous sponge of miR-1244. Inhibition of miR-1244 diminished the effects of LINC00504 on OC cells. Our study shows that LINC00504 promotes OC cell progression and stimulates aerobic glycolysis by interacting with miR-1244, which indicates that LINC00504 might act as a promising therapeutic target for OC treatment.

中文翻译：

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长的非编码RNA LINC00504通过抑制miR-1244调节卵巢癌的Warburg效应。

卵巢癌（OC）是最致命的妇科恶性肿瘤，长期的非编码RNA（lncRNA）被认为是人类OC中的重要调节剂。这项研究旨在调查LINC00504在OC中的功能和潜在机制。通过qRT-PCR分析研究LINC00504在人OC组织和细胞系中的表达水平。分别通过MTT测定，集落形成测定，Caspase-3活性测定和核小体ELISA测定来评估OC细胞的增殖和凋亡。通过有氧糖酵解分析检查OC细胞中的代谢变化。进行了双重荧光素酶活性报告基因测定和mRNA-miRNA下拉测定，以验证LINC00504和miR-1244之间的相互作用。LINC00504在OC细胞系和标本中上调。敲低LINC00504抑制细胞增殖，增强细胞凋亡，降低糖酵解相关基因（PKM2，HK2和PDK1）的表达，并改变OC细胞中的有氧糖酵解，反之亦然。LINC00504通过充当miR-1244的内源海绵来下调miR-1244的表达水平。抑制miR-1244可减少LINC00504对OC细胞的影响。我们的研究表明，LINC00504通过与miR-1244相互作用来促进OC细胞进程并刺激有氧糖酵解，这表明LINC00504可能成为有前景的OC治疗靶标。