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A Cu/Zn co-incorporated BCP scaffold-derived GDF-5 sustained release system was successfully prepared and exhibited improved angiogenic and osteogenic capacities.

Microstructure and chemical constitution are important factors affecting the biological activity of biomaterials. This study aimed to fabricate hydroxyapatite (HAp) particles with both micro/nanohybrid structure and Cu doping to promote osteogenic differentiation and antibacterial property. In the presence of inositol hexakisphosphate (IP6), micro/nano-structured and Cu-doped HAp (HAp-IP6-Cu) microspheres were successfully fabricated via hydrothermal method. Morphological observation showed that HAp-IP6-Cu microspheres with a diameter of 3.1-4.1 μm were chrysanthemum-like and composed of nano-flakes approximately 50 nm in thickness. Compared with the HAp micro-rods or IP6 modified HAp (HAp-IP6) microspheres, HAp-IP6-Cu microspheres had a larger specific surface area, better hydrophilicity and stronger ability to adsorb bovine serum albumin. To evaluate the synergistic effects of micro/nanohybrid structure and Cu on cell behavior, rat calvarial osteoblasts (RCOs) were cultured on HAp-IP6-Cu, HAp-IP6 and HAp layers as well as their extracts, respectively. Results demonstrated that HAp-IP6-Cu layer promoted the adhesion, proliferation and osteogenic differentiation of RCOs. The cells grew on HAp-IP6-Cu and HAp-IP6 layers exhibited greater spreading than those on HAp layer. In addition, quantitative test by the agar disk diffusion technique found that HAp-IP6-Cu microspheres were effectively against S taphylococcus aureus and E scherichia coli. These results demonstrated that HAp-IP6-Cu microspheres may be a potential candidate as a bioactive and anti-infective biomaterial for bone regeneration.

Testis expressed 10 (Tex10), a new core component of the pluripotency circuitry, has been reported to positively regulate embryonic stem cell (ESC) super-enhancers to promote ESC self-renewal; however, the expression and function of Tex10 in hepatocellular carcinoma (HCC) and liver cancer stem cells remains unclear. The present study was designed to investigate the expression patterns of Tex10 with immunohistochemistry, western blotting and RT-qPCR in samples from HCC patients and HCC cell lines. The results obtained show that Tex10 was highly expressed in HCC tissues, and elevated Tex10 protein levels positively correlate with the poorly differentiated carcinoma. Likewise, we found that Tex10 expression in the high-metastasis HCCLM3 potential cell line was higher than that in the low-metastasis HepG2 potential cell line, and Tex10 expression in liver cancer stem cells was also higher than that in adhered HCC cells. In addition, Tex10 knockdown decreased stem cell marker expression and drug resistance. Tex10 promoted cancer stemness through activation of the STAT3 signaling pathway. Taken together, our study demonstrates that Tex10 plays a potent carcinogenic role in HCC tumorigenesis by maintaining cancer stem cell properties through activation of the STAT3 signaling pathway and promoting chemo-resistance. Thus, targeting Tex10 may provide a novel and effective therapeutic strategy to suppress the tumorigenicity of advanced HCC.

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A previous study by our group suggested that testis expressed 10 (Tex10) contributes to tumor progression by promoting stem cell-like features in hepatocellular carcinoma. However, the relevance of pluripotency factor Tex10 in esophageal squamous cell carcinoma (ESCC) has remained elusive. The objective of the present study was to investigate the role of Tex10 in ESCC. For this purpose, the mRNA and protein expression of Tex10 was detected by reverse transcription-quantitative PCR, western blot analysis and immunohistochemistry. In a loss-of-function experiment, EC109 cells were transfected with lentiviral vectors containing Tex10 short hairpin RNA or negative control. Cell proliferation was assessed using a Cell Counting kit-8, and flow cytometry was used to analyze apoptosis and the cell cycle. Transwell assays were employed to examine the migratory and invasive capacity, and a sphere formation assay was performed to assess the clonogenicity of the EC109 cells. The results revealed that the elevated expression of Tex10 was positively associated with malignancy and with epithelial-mesenchymal transition (EMT)-associated mesenchymal markers in human ESCC specimens. The knockdown of Tex10 led to the inhibition of cell proliferation, the induction of apoptosis and cell cycle arrest, and decreased the stemness, migratory and invasive capacity of the EC109 cells. Furthermore, the silencing of Tex10 enhanced the sensitivity of the ESCC cells to 5-fluorouracil. In addition, the present study revealed that Tex10 plays an essential role in regulating EMT via the activation of Wnt/β-catenin signaling. On the whole, the findings of the present study suggest that the downregulation of Tex10 in ESCC specimens is significantly associated with tumor malignancy, and that Tex10 promotes stem cell-like features and induces the EMT of ESCC cells through the enhancement of Wnt/β-catenin signaling.