CD44参与CXCL-12诱导的急性髓性白血病HL-60细胞极性。

Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al Pub Date : 2010-08-01 DOI:10.32604/BIOCELL.2010.34.091

Li-ping Zhou, Xiaolin Guo, B. Jing, Lianshuang Zhao

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引用次数: 14

摘要

CXCL-12及其受体CXCR4参与乳腺癌和黑色素瘤细胞向骨和淋巴结的转移。CD44是透明质酸的受体，参与淋巴细胞的再循环、归巢、粘附和迁移。但CD44在CXCL-12诱导的白血病细胞迁移中的作用仍不清楚。本研究表明，CXCL-12刺激可诱导急性白血病HL-60细胞株快速内化CXCR4，促进板足和尾足的形成。CXCL-12也诱导CD44易位到尾足，而CD44仍均匀分布在未处理的细胞膜上。结果表明，CD44参与了CXCL-12诱导的细胞极化和随后的细胞迁移。

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CD44 is involved in CXCL-12 induced acute myeloid leukemia HL-60 cell polarity.

CXCL-12 and its receptor CXCR4 participate in breast cancer and melanoma cell metastasis to bone and lymphoid nodes. CD44, as a receptor for hyaluronic acid, is involved in lymphocyte recirculation, homing, adhesion and migration. But the role of CD44 in CXCL-12 induced leukemia cell migration still remains unclear. The present study showed that CXCL-12 stimulation induced the rapid internalization of CXCR4 and facilitated the formation of lamellipodia and uropod in acute leukemia cell line HL-60. CXCL-12 also induced CD44 translocation into the uropod, while CD44 remained evenly distributed on the untreated cell membranes. Results suggest that CD44 participates in CXCL-12 induced cell polarization and subsequent cell migration.

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Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al

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