Abnormal expression of long non-coding RNAs (lncRNAs) is involved in many pathological processes of cancers. However, the role of lncRNA LINC00052 in breast cancer progression is still unclear. Here, LINC00052 expression was detected by in situ hybridization and quantitative real-time PCR assays. Cell Counting Kit-8, wound healing, and transwell assays were used to investigate changes in the proliferation, migration, and invasion of breast cancer cells. MiR-548p was found associated with LINC00052 or Notch2 by RNA pull-down, dual-luciferase reporter, and qRT-PCR assays. The effect of LINC00052 on lung metastasis was explored through in vivo experiments. High LINC00052 expression was observed in breast cancer tissues and cells. LINC00052 silencing inhibited the proliferation, migration, and invasion of MCF7 cells, and LINC00052 overexpression produced the opposite results. MiR-548p, a target gene of LINC00052, partially rescued the effects of LINC00052 on proliferation, migration, and invasion of MCF7. Notch2 was the target of miR-548p and LINC00052 could promote Notch2 expression. Moreover, the phosphorylation of proline-rich tyrosine kinase 2 (Pyk2), a downstream factor of Notch2, was increased by LINC00052, and a Pyk2 mutant could inhibit the cell migration and invasion induced by LINC00052 overexpression in MDA-MB-468 cells, which was similar to the function of the miR-548p mimic. We further demonstrated that LINC00052 exacerbated the metastases of breast cancer cells in vivo. Our research demonstrated that LINC00052 is highly expressed in breast cancer and promotes breast cancer proliferation, migration, and invasion via the miR-548p/Notch2/Pyk2 axis. LINC00052 could serve as a potential therapeutic target for breast cancer.

长链非编码 RNA (lncRNA) 的异常表达参与癌症的许多病理过程。然而，lncRNA LINC00052 在乳腺癌进展中的作用仍不清楚。此处，LINC00052 表达通过原位杂交和定量实时 PCR 检测进行检测。Cell Counting Kit-8、伤口愈合和 transwell 检测用于研究乳腺癌细胞增殖、迁移和侵袭的变化。通过 RNA pull-down、双荧光素酶报告基因和 qRT-PCR 检测发现 MiR-548p 与 LINC00052 或 Notch2 相关。通过体内实验探索LINC00052对肺转移的影响。在乳腺癌组织和细胞中观察到高 LINC00052 表达。LINC00052 沉默抑制了 MCF7 细胞的增殖、迁移和侵袭，和 LINC00052 过表达产生相反的结果。LINC00052 的靶基因 MiR-548p 部分挽救了 LINC00052 对 MCF7 增殖、迁移和侵袭的影响。Notch2 是 miR-548p 的靶标，LINC00052 可以促进 Notch2 的表达。此外，LINC00052 增加了 Notch2 的下游因子富含脯氨酸的酪氨酸激酶 2 (Pyk2) 的磷酸化，并且 Pyk2 突变体可以抑制 MDA-MB-468 细胞中 LINC00052 过表达诱导的细胞迁移和侵袭，这类似于 miR-548p 模拟物的功能。我们进一步证明 LINC00052 加剧了体内乳腺癌细胞的转移。我们的研究表明，LINC00052 在乳腺癌中高表达，并通过 miR-548p/Notch2/Pyk2 轴促进乳腺癌的增殖、迁移和侵袭。