Profilin 2 (PFN2) promotes the proliferation, migration, invasion and epithelial-to-mesenchymal transition of triple neg
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ORIGINAL ARTICLE
Profilin 2 (PFN2) promotes the proliferation, migration, invasion and epithelial‑to‑mesenchymal transition of triple negative breast cancer cells Yuwei Ling1 · Qi Cao2 · Yihan Liu2 · Jing Zhao1 · Ye Zhao1 · Kaifu Li1 · Zhiqiang Chen1 · Xiaoyan Du2 · Xueyun Huo2 · Hua Kang1 · Zhenwen Chen2 Received: 24 March 2020 / Accepted: 1 October 2020 © The Japanese Breast Cancer Society 2020
Abstract Background Triple negative breast cancer (TNBC) is the most aggressive subtype with the worst prognosis. The role of profilin 2 (PFN2) in TNBC is very controversial. The current study is to explore the role of PFN2 in TNBC. Methods PFN2 expression in TNBC and normal breast tissues were evaluated by immunohistochemical analysis. The association between PFN2 expression and prognosis in TNBC patients was analyzed from the TCGA database. A cell counting kit-8 (CCK8) assay was employed to investigate the effects of PFN2 in TNBC cell proliferations. The migration and invasion capability of TNBC cells was evaluated by transwell assays. Western blot was performed to assess the related protein expression of TGF-β/Smad signaling and epithelial to mesenchymal transition. Finally, TNBC xenografts were established to determine the tumorigenicity in vivo using female Nod/Scid mice. Results PFN2 is upregulated in TNBC and the higher expression was associated with worse survival. CCK8 assays and Transwell assays demonstrated that PFN2 promoted the proliferation, migration and invasion of TNBC cells. Smad2 and Smad3 were upregulated in PFN2 overexpressing TNBC cells, which further induced the process of epithelial‑to‑mesenchymal transition. Similarly, the overexpressing PFN2 TNBC cells exhibited stronger tumorigenicity in vivo. Conclusions Higher PFN2 expression is associated with a worse 10-year overall survival and relapse-free survival in breast cancer patients, as well as worse 10-year relapse-free survival in TNBC patients. PFN2 promotes the proliferation, migration and invasion of TNBC cells by regulating epithelial-to-mesenchymal transition. Keywords Triple negative breast cancer · PFN2 · Epithelial-to-mesenchymal transition
Senior author: Zhenwen Chen. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s12282-020-01169-x) contains supplementary material, which is available to authorized users. * Xueyun Huo [email protected] * Hua Kang [email protected] Zhenwen Chen [email protected] 1
Department of General Surgery, Center for Thyroid and Breast Surgery, Xuanwu Hospital, Capital Medical University, Beijing 100053, China
School of Basic Medical Sciences, Beijing Key Laboratory of Cancer Invasion and Metastasis Research, Capital Medical University, Beijing 100069, China
2
Introduction Triple negative breast cancer (TNBC) accounts for approximately 15–20% of the more than 2 million breast cancer cases diagnosed worldwide each year. TNBC is defined by the absence of estrogen and progesterone receptor expression and the amplification of human epiderma
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