Human ovarian cancer specific transcript 2 (HOST2) is a long non-coding RNA (lncRNA) reported to be specifically high expressed in human ovarian cancer. However, the mechanism that how HOST2 regulates triple negative breast cancer (TNBC) need to be explored. In this study, expression of HOST2 was determined in 40 TNBC patients and matched non-cancerous tissues by qRT-PCR and in situ hybridization (ISH) assay. The biological functions of HOST2 was measured by losing features. The effect of HOST2 on viability, proliferation and migration was evaluated by MTT, colony formation assay, EDU analysis, transwell invasion assay and nude mouse xenograft model. Fluorescence in situ hybridization (FISH), Luciferase report assay, RNA immunoprecipitation (RIP) assay and Western blot were fulfilled to measure molecular mechanisms. The results showed that HOST2 was up-regulated in BC tissues and cell lines. Clinical outcome analysis demonstrated that high expression of HOST2 was associated with poor prognosis of TNBC patients. Functional experiments illustrated that knockdown of HOST2 significantly suppressed TNBC cell proliferation and migration. Western blot assays, qRT-PCR assays, RIP assays and luciferase reporter assays revealed that HOST2 regulated STAT3 via crosstalk with let-7b. Depression of HOST2 suppressed STAT3-mediated proliferation and migration in TNBC cells. HOST2 could function as a decoy of let-7b to depress expression of STAT3. HOST2 could function as a oncogene and promoted STAT3-mediated proliferation and migration through acting as a competing endogenous RNA, which might act as a potential biomarker for TNBC patients.

中文翻译：

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长的非编码RNA HOST2，作为竞争性内源RNA，通过三联阴性乳腺癌中let-7b的诱变来促进STAT3介导的细胞增殖和迁移。

人卵巢癌特异性转录本2（HOST2）是一种长的非编码RNA（lncRNA），据报道在人卵巢癌中特异性高表达。然而，HOST2如何调节三阴性乳腺癌（TNBC）的机制需要探索。在这项研究中，通过qRT-PCR和原位杂交（ISH）测定了40例TNBC患者和匹配的非癌组织中HOST2的表达。HOST2的生物学功能通过丢失特征来测量。通过MTT，集落形成测定，EDU分析，穿孔侵袭测定和裸鼠异种移植模型评价了HOST2对生存力，增殖和迁移的影响。完成了荧光原位杂交（FISH），荧光素酶报告测定，RNA免疫沉淀（RIP）测定和蛋白质印迹法以测量分子机制。结果表明，HOST2在BC组织和细胞系中上调。临床结果分析表明，HOST2的高表达与TNBC患者的预后不良有关。功能实验表明，敲除HOST2可以显着抑制TNBC细胞的增殖和迁移。Western印迹测定，qRT-PCR测定，RIP测定和荧光素酶报告基因测定显示，HOST2通过与let-7b的串扰来调节STAT3。HOST2的抑制抑制了TNBC细胞中STAT3介导的增殖和迁移。HOST2可以充当let-7b的诱饵来抑制STAT3的表达。HOST2可以充当癌基因，并通过充当竞争性内源RNA来促进STAT3介导的增殖和迁移，这可能是TNBC患者的潜在生物标志物。