Jianghong Wu,Ziwen Long,Hong Cai,Shengjia Yu,Xiaowen Liu
Aim: To study the carcinogenetic mechanism of HOXB7 in gastric cancer (GC) remains. Methods: Two human GC cell lines — SGC7901 and SNU1 — were used for this study. SGC7901 cells were transfected with siRNA-HOXB7 (siHOXB7) to knock down HOXB7 expression, whereas, SNU1 cells were transduced with pCDNA3.1-HOXB7 to overexpress HOXB7. After transfection, cancer progression was assessed by determining cell proliferation, wound-healing process, cell cycle, apoptosis, invasion, and migration. The effect of HOXB7 on epithelial–mesenchymal transition (EMT) was measured by observing changes in F-actin cytoskeleton and evaluating the expression of EMT markers. p-Scr and p-FAK were evaluated to assess the mechanism. Results: Knockdown of HOXB7 suppressed cell proliferation, alleviated the wound-healing process, inhibited cell migration and invasion, and arrested the cell cycle while promoting cell apoptosis, suggesting the tumor-suppressive effect of siHOXB7 in human GC cells. On the contrary, HOXB7 overexpression showed a tumor-promoting effect on human GC cells. Moreover, we confirmed an inhibitory effect of siHOXB7 on the EMT process by preventing epithelial cells from acquiring a mesenchymal phenotype and downregulating mesenchymal markers (vimentin, β-catenin, N-cadherin, Twist) while upregulating epithelial markers (E-cadherin). Our data revealed that HOXB7 was associated with Src/FAK and favored the activation of the Src–FAK pathway in human GC cells. Conclusion: HOXB7 accelerated the malignancy of GC, by facilitating EMT and regulating the Scr–FAK pathway.
Polyetheretherketone (PEEK) has been widely used in the preparation of orthopedic implants due to its biological inertness and similar mechanical modulus to natural bone. However, the affinity between biological tissue (bone and soft tissue) and PEEK surface is weak, leading to low osseointegration and an increased risk of inflammation. The situation could be improved by modifying PEEK surface. Surfaces with good hydrophilicity and proper microtopography would promote cellular adhesion and proliferation. This work presented a two-step surface modification method to achieve the effect. Polyacrylic acid (PAA) chains were grafted on PEEK surface by UV irradiation. Then, ethylenediamine (EDA) was added to introduce amino groups and promote the cross-linking of PAA chains. Furthermore, a mathematical model was built to describe and regulate the surface topography growth process semi-quantitatively. The model fits experimental data quite well (adjusted R 2 = 0.779). Results showed that the modified PEEK surface obtained superhydrophilicity. It significantly improved the adhesion and proliferation of BMSCs and MFBs by activating the FAK pathway and Rho family GTPase. The cellular affinity performed better when the surface topography was in network structure with holes in about 25 μm depth and 20–50 μm diameter. Good hydrophilicity seems necessary for the FAK pathway activation, but simply improving surface hydrophilicity might not be enough for cellular affinity improvement. Surface topography at micron scale should be a more important cue. This simple surface modification method could be contributed to further study of cell-microtopography interaction and have potential applications in clinical PEEK orthopedic implants.
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