Meng Wang1, Di Chen1, Hanchao Zhang1, Chengyu Luo2. 1. Department of General Surgery, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Chaoyang District, Beijing, 100029, China. 2. Department of General Surgery, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Chaoyang District, Beijing, 100029, China. luochengyu@163.com.
Abstract
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.
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.
Authors: Mark Lee; Brian R Untch; Bin Xu; Ronald Ghossein; Catherine Han; Fengshen Kuo; Cristina Valero; Zaineb Nadeem; Neal Patel; Vladimir Makarov; Snjezana Dogan; Richard J Wong; Eric J Sherman; Alan L Ho; Timothy A Chan; James A Fagin; Luc G T Morris Journal: Mol Cancer Res Date: 2021-10-11 Impact factor: 6.333