作者: Junyun Wang , Nan Ding , Yongjun Li , Hua Cheng , Dong Wang
关键词: Insulin-like growth factor 1 receptor 、 Cell growth 、 Carcinogenesis 、 KLF4 、 Melanoma 、 Metastasis 、 Biology 、 Cancer research 、 Insulin-like growth factor-binding protein 、 Growth factor
摘要: The insulin-like growth factor binding protein 5 (IGFBP5), which is often dysregulated in human cancers, plays a crucial role carcinogenesis and cancer development. However, the function underlying mechanism of IGFBP5 tumor metastasis has been elusive, particularly malignant melanoma. Here, we reported that acts as an important suppressor melanoma tumorigenicity by series experiments including transwell assay, xenograft model, vivo experiment, RNA-Seq. Overexpression A375, typical cell line, inhibited behaviors significantly, vitro proliferation, anchorage-independent growth, migration invasion, well pulmonary metastasis. In addition, overexpression suppressed epithelial-mesenchymal transition (EMT), decreased expression E-cadherin key stem markers NANOG, SOX2, OCT4, KLF4, CD133. Furthermore, exerts its inhibitory activities reducing phosphorylation IGF1R, ERK1/2, p38-MAPK kinases abating HIF1α target genes, VEGF MMP9. All these findings were confirmed knockdown line A2058. Taken together, results shed light on potential tumor-suppressor progression, indicating might be novel therapeutic for