环状 RNA circPTK2 通过 miR-136/NFIB 信号通路调控三阴性乳腺癌细胞的迁移和侵袭。
Circular RNA circPTK2 modulates migration and invasion via miR-136/NFIB signaling on triple-negative breast cancer cells in vitro.
机构信息
Department of General Surgery, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Chaoyang District, Beijing, 100029, China.
出版信息
Inflamm Res. 2022 Apr;71(4):409-421. doi: 10.1007/s00011-022-01548-4. Epub 2022 Mar 2.
OBJECTIVE AND BACKGROUND
Triple-negative breast cancer (TNBC) is an aggressive breast type of cancer with poor prognosis and high mortality rates. CircRNAs have been widely investigated, due to their crucial role in cancer progression. We aimed to elucidate the function of circPTK2 (has_circ_0003221) in TNBC and explore the mechanism in progression of TNBC.
METHODS
qPCR was performed to validate the expression of circPTK2 and related mRNA in TNBC tissue and cell lines. CCK-8, EdU, Transwell assay were conducted to detect the proliferation, migration and invasion of circPTK2 and miR-136 on TNBC cells. RIP and dual-luciferase reporter assay were used to confirm the interaction among circPTK2, miR-136 and NFIB. Si-circPTK2, mimic and inhibitor of miR-136 were transfected in TNBC cells to confirm the mechanism of circPTK2 and miR-136 in TNBC cells.
RESULTS
CircPTK2 were downregulated in TNBC tissues and cell lines. CircPTK2 significantly promoted the proliferation, migration, and invasion of TNBC cells. CircPTK2 was confirmed to be a sponge of miR-136, and directly regulated NFBI and AKT/PI3K pathway. A rescue assay validated circPTK2/miR-136/NFIB axis in TNBC cells.
CONCLUSION
CircPTK2 promoted TNBC progression and development. circPTK2/miR-136/NFIB might be an effective biomarker for TNBC.
目的和背景
三阴性乳腺癌（TNBC）是一种侵袭性乳腺癌，预后差，死亡率高。环状 RNA（circRNAs）由于在癌症进展中的重要作用而受到广泛研究。我们旨在阐明 circPTK2（has_circ_0003221）在 TNBC 中的功能，并探讨其在 TNBC 进展中的机制。
方法
qPCR 用于验证 circPTK2 和相关 mRNA 在 TNBC 组织和细胞系中的表达。CCK-8、EdU、Transwell 测定用于检测 circPTK2 和 miR-136 对 TNBC 细胞的增殖、迁移和侵袭的影响。RIP 和双荧光素酶报告基因测定用于证实 circPTK2、miR-136 和 NFIB 之间的相互作用。在 TNBC 细胞中转染 Si-circPTK2、miR-136 的模拟物和抑制剂，以验证 circPTK2 和 miR-136 在 TNBC 细胞中的作用机制。
结果
circPTK2 在 TNBC 组织和细胞系中表达下调。circPTK2 显著促进 TNBC 细胞的增殖、迁移和侵袭。circPTK2 被证实是 miR-136 的海绵体，直接调节 NFBI 和 AKT/PI3K 通路。挽救试验验证了 circPTK2/miR-136/NFIB 轴在 TNBC 细胞中的作用。
结论
circPTK2 促进了 TNBC 的进展和发展。circPTK2/miR-136/NFIB 可能是 TNBC 的有效生物标志物。
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