NT21MP negatively regulates paclitaxel-resistant cells by targeting miR‑155‑3p and miR‑155-5p via the CXCR4 pathway in breast cancer.
作者： Yueyue Wang , Lei Yan , Lingyu Zhang , Henan Xu , Tiantian Chen
关键词:
摘要: Evidence has shown that microRNAs (miRNAs) are vital in cell growth, migration, and invasion by inhibiting their target genes. A previous study demonstrated miRNA (miR)-155‑3p miR‑155-5p exerted opposite effects on proliferation, apoptosis, migration breast cancer lines. An microarray was used to show miR‑155‑3p downregulated whereas upregulated paclitaxel-resistant (PR) cells compared with parental cells. However, the role of miR‑155 metastasis remains be elucidated. 21-residue peptide derived from viral macrophage inflammatory protein II (NT21MP), competes ligand CXC chemokine receptor 4 (CXCR4) its stromal cell-derived factor-1α, inducing apoptosis cancer. The present aimed identify underlying mechanism action miR‑155‑3p/5p NT21MP PR Quantitative polymerase chain reaction, western blotting, wound-healing, cycle assays, Cell Counting kit-8 assay were achieve this goal. combined overexpression decreased ability increased number apoptotic arrested G0/G1 phase transition vitro. knockdown had a similar effect Furthermore, ectopic expression gene myeloid differentiation primary response 88 (MYD88) or tumor 53-induced nuclear 1 (TP53INP1) enhanced sensitivity paclitaxel. Taken together, these findings suggested genes MYD88 TP53INP1 may serve as novel biomarkers for therapy through CXCR4 pathway improving paclitaxel
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