Long intergenic non-protein coding RNA00665 (LINC00665) plays a crucial tumorigenic role in many cancers, such as gastric cancer and lung adenocarcinoma. However, its role and mechanism of action in the progression of breast cancer (BC) are unknown. LINC00665 expression levels were determined using quantitative polymerase chain reaction analysis with BC tissues and cell lines. BC cell proliferation was tested by performing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, whereas BC cell migration and invasion capabilities were analyzed by performing transwell migration assays. Percentages of apoptotic cells were measured by flow cytometry. Interactions between LINC00665 and miR-3169-5p were examined by performing luciferase reporter assays, and the expression levels of proteins, such as β-catenin, were examined by western blot analysis. LINC00665 was expressed at high levels in BC tissues and cells. Upregulated LINC00665 expression correlated with tumor size and tumor, node, and metastasis stages, but not with the age of patients. LINC00665 knockdown inhibited BC cell proliferation, migration, and invasion, whereas it promoted apoptosis. Moreover, bioinformatics analysis and the luciferase reporter assay revealed that LINC00665 bound the microRNA (miR) miR-3619-5p. miR-3619-5p expression correlated negatively with LINC00665 expression in BC tissues. miR-3619-5p overexpression inhibited BC cell proliferation, migration, and invasion, but promoted apoptosis. Simultaneous knockdown of LINC00665 and miR-3619-5p led to increased cell proliferation, migration, and invasion, and inhibited apoptosis. Additionally, catenin beta 1, which encodes the β-catenin protein, was the target gene of miR-3619-5p. β-catenin expression clearly decreased after LINC00665 knockdown and miR-3619-5p overexpression, but increased after simultaneous knockdown of LINC00665 and miR-3619-5p. LINC00665 knockdown inhibited BC cell proliferation and invasion by binding miR-3619-5p and inhibiting β-catenin expression.

中文翻译：

---

敲低 LINC00665 通过竞争性结合 miR-3619-5p 和抑制连环蛋白 1 来抑制乳腺癌的增殖和侵袭

长基因间非蛋白编码 RNA00665 (LINC00665) 在许多癌症（如胃癌和肺腺癌）中起着至关重要的致瘤作用。然而，其在乳腺癌（BC）进展中的作用和作用机制尚不清楚。LINC00665 表达水平使用 BC 组织和细胞系的定量聚合酶链反应分析来确定。通过进行 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide 测定来测试 BC 细胞增殖，而通过进行 transwell 迁移测定来分析 BC 细胞迁移和侵袭能力。通过流式细胞术测量凋亡细胞的百分比。LINC00665 和 miR-3169-5p 之间的相互作用通过执行荧光素酶报告基因检测，以及蛋白质的表达水平，如 β-连环蛋白，通过蛋白质印迹分析检查。LINC00665 在 BC 组织和细胞中高水平表达。上调的 LINC00665 表达与肿瘤大小和肿瘤、淋巴结和转移阶段相关，但与患者的年龄无关。LINC00665 敲低抑制 BC 细胞增殖、迁移和侵袭，而促进细胞凋亡。此外，生物信息学分析和荧光素酶报告基因分析显示 LINC00665 与 microRNA (miR) miR-3619-5p 结合。miR-3619-5p 表达与 BC 组织中的 LINC00665 表达负相关。miR-3619-5p 过表达抑制 BC 细胞增殖、迁移和侵袭，但促进细胞凋亡。同时敲低 LINC00665 和 miR-3619-5p 导致细胞增殖、迁移和侵袭增加，并抑制细胞凋亡。此外，连环蛋白 beta 1，编码β-catenin蛋白的基因是miR-3619-5p的靶基因。β-catenin 表达在 LINC00665 敲低和 miR-3619-5p 过表达后明显降低，但在 LINC00665 和 miR-3619-5p 同时敲低后增加。LINC00665 敲低通过结合 miR-3619-5p 和抑制 β-catenin 表达来抑制 BC 细胞增殖和侵袭。