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Abstract: Palladin was a novel binding partner of ILKAP in eukaryotic cells. Palladin’s C-terminal fragment including only its last three Ig domains (residues 710–1106) and the PP2C domain of ILKAP (residues 108–392) were necessary and sufficient for their interaction. The biological significance of the interaction between palladin and ILKAP was that palladin recruited the cytoplasmic ILKAP to initiate ILKAP-induced apoptosis. Our results suggested that palladin played a specific role in modulating the subcellular localization of the cytoplasmic ILKAP and promoting the ILKAP-induced apoptosis. [Copyright &y& Elsevier]

Hairy and enhancer of split homolog-1 (Hes1) is a member of an extensive family of basic helix-loop-helix (bHLH) proteins and plays a crucial role in neurogenesis, myogenesis, hematopoiesis, and sex determination. It has been reported that Hes1 is essential for precursors maintenance, optic cup-stalk boundary maintenance, and morphogenesis of the retina. However, it still reminds questions about the role and mechanism of Hes1 in the development of retinal pigment epithelial cells. In our study, We generated Hes1 −/− human embrsyonic stem cells, and attempted to induce them into retinal pigment epithelial cells by our previous protocol, found that the cells induced by Hes1 −/− hESCs hardly expressed RPE-related genes, and rarely appeared RPE cell morphology. Additionally, Hes1 may affect the development of RPE cells via Wnt4 pathway by analyzing the RNA-seq data of differently expressed genes between normal RPE cells development and Hes1 −/− RPE cells development. Overall, depletion of Hes1 may result in the failure of Wnt4 signal activation, and contributed to the developmental disorder in retinal pigment epithelium morphogenesis and specification. • The absence of Hes 1 caused developmental disorders in RPE in morphogenesis and specification. • Lake of Hes1 in the differentiation of RPE showed premature neural precursors. • The depletion of Hes1 expression blocked the up-regulation expression of RPE-specific genes. • The up-regulation failure of the Wnt4 pathway emerged during RPE development by Hes1 deletion. [ABSTRACT FROM AUTHOR]

Bone metastasis occurs in approximately 30–40% patients with advanced non-small cell lung cancer (NSCLC), but the mechanism underlying this bone metastasis remains poorly understood. The chemokine super family is believed to play an important role in tumor metastasis in lung cancer. The chemokine receptor XCR1 has been identified to promote cell proliferation and migration in oral cancer and ovarian carcinoma, but the role of XCR1 in lung cancer has not been reported. In this study, we demonstrated for the first time that XCR1 was overexpressed in lung cancer bone metastasis as compared with that in patients with primary lung cancer. In addition, the XCR1 ligand XCL1 promoted the proliferation and migration of lung cancer cells markedly, and knockdown of XCR1 by siRNA abolished the effect of XCL1 in cell proliferation and migration. Furthermore, we identified JAK2/STAT3 as a novel downstream pathway of XCR1, while XCL1/XCR1 increased the mRNA level of the downstream of JAK2/STAT3 including PIM1, JunB, TTP, MMP2 and MMP9. These results indicate that XCR1 is a new potential therapeutic target for the treatment of lung cancer bone metastasis. [ABSTRACT FROM AUTHOR]

RunX2 has been identified to crucially regulate the osteolysis in giant cell tumor of bone. MiR-30a is an intronic miRNA identified as tumor suppressor, but little is known about its role in giant tumor cell of bone. In our research, we reported miR-30a was down-regulated in GCT whereas RunX2 was highly expressed. Further research proved that miR-30a can regulate the expression of RunX2 by binding to its 3′-UTR, which influence the osteoclast differentiation and osteolysis formation. Thus, these results suggest that miR-30a could directly target RunX2 and participate in osteolysis in GCT. [ABSTRACT FROM AUTHOR]

Highlights: [•] MiR-126-5p was expressed at low level in GCT. [•] MMP-13 is consistently and highly expressed by the GCTSCs in GCT. [•] MiR-126-5p could negatively regulate MMP-13 expression. [•] MiR-126-5p can regulate OC differentiation and osteolysis formation in GCT. [ABSTRACT FROM AUTHOR]