Degradation behavior of 2D auxetic structure with biodegradable polymer under mechanical stress.

Coronary heart disease is serious harm to human health. Vascular scaffold implantation is the main treatment. Biodegradable polymers are widely used in vascular scaffolds for good biodegradability and biocompatibility. However, whether the mechanical properties and radial expansion ability can successfully implant the scaffold without acute elastic retraction remains to be further studied. Because of the unique deformation mechanism, shear resistance, and resilience, auxetic structures can effectively avoid the restenosis of degraded vascular scaffolds. Firstly, the plane isotropic and plane anisotropic auxetic structural scaffolds were designed. The control structures (traditional structures) scaffolds were taken as the contrast. PCL was used to prepare the vascular auxetic by 3D printing. The printing parameters of fused deposition 3D printing, such as printing temperature, printing speed, and printing pressure, were studied to determine the optimal printing parameters of PCL. A self-assembled cyclic tensile stress loading device was used to investigate the degradation behavior of different scaffolds under different sizes of cyclic tensile stress, such as surface morphology, pH changes, mass loss rate, and mechanical properties. The increase of stress, surface roughness, and mass loss rate of the scaffolds all showed an increasing trend. pH gradually decreased from the fifth week, and the decrease was proportional to the stress. A large level of stress loading intensifies the decline of elastic modulus and the ultimate strength of the scaffold. In conclusion, the increase of periodic tensile stress will accelerate the degradation of scaffolds, and the degradation behavior of scaffolds with different configurations is different. The degradation rate of dilatant scaffolds was higher than that of control scaffolds, and the degradation rate of anisotropic auxetic scaffolds was higher than that of isotropic auxetic scaffolds, which provides a theoretical reference for the application of auxetic structure in the degradation of vascular scaffolds.

[Eukaryotic expression of human Y-box binding protein 1 (YB-1) promotes the proliferation and migration of human HepG2 cells].

Objective To establish the eukaryotic expression vector of Y-box-binding protein 1 (YB-1) with FLAG-tagged and transfect it into hepatocellular carcinoma HepG2 cells to identify the effects of YB-1 on the proliferation and migration. Methods Human YB-1 gene was amplified from the human ovary library by PCR. YB-1 fraction was double enzyme digested and connected with pcDNA3.0-FLAG vector to construct eukaryotic expression vector pcDNA3.0-FlAG-YB-1, which was transfected into HepG2 cells. The expression of YB-1 was detected by Western blotting, and the effect of YB-1 on the proliferation of HepG2 cells was determined by CCK-8 assay and clone formation. The effect of YB-1 on the migration of HepG2 cells was analyzed by wound healing assays. Results The eukaryotic expression vector pcDNA3.0-FLAG-YB-1 was successfully established. YB-1 protein can be expressed in HepG2 cells, and YB-1 promoted the proliferation and migration of HepG2 cells. Conclusion YB-1 promotes the proliferation and migration of HepG2 cells.

Interaction between BEND5 and RBPJ suppresses breast cancer growth and metastasis via inhibiting Notch signaling.

High frequent metastasis is the major cause of breast cancer (BC) mortality among women. However, the molecular mechanisms underlying BC metastasis remain largely unknown. Here, we identified six hub BC metastasis driver genes (BEND5, HSD11B1, NEDD9, SAA2, SH2D2A and TNFSF4) through bioinformatics analysis, among which BEND5 is the most significant gene. Low BEND5 expression predicted advanced stage and shorter overall survival in BC patients. Functional experiments showed that BEND5 could suppress BC growth and metastasis in vitro and in vivo. Mechanistically, BEND5 inhibits Notch signaling via directly interacting with transcription factor RBPJ/CSL. BEN domain of BEND5 interacts with the N-terminal domain (NTD) domain of RBPJ, thus preventing mastermind like transcriptional coactivator (MAML) from forming a transcription activation complex with RBPJ. Our study provides a novel insight into regulatory mechanisms underlying Notch signaling and suggests that BEND5 may become a promising target for BC therapy.

RHOV promotes lung adenocarcinoma cell growth and metastasis through JNK/c-Jun pathway.

Lung adenocarcinoma (LUAD) is a common type of lung cancer with high frequent metastasis and a high death rate. However, genes responsible for LUAD metastasis are still largely unknown. Here, we identify an important role of ras homolog family member V (RHOV) in LUAD metastasis using a combination of bioinformatic analysis and functional experiments. Bioinformatic analysis shows five hub LUAD metastasis driver genes (RHOV, ZIC5, CYP4B1, GPR18 and TCP10L2), among which RHOV is the most significant gene associated with LUAD metastasis. High RHOV expression predicted shorter overall survival in LUAD patients. RHOV overexpression promotes proliferation, migration, and invasion of LUAD cells, whereas RHOV knockdown inhibits these biological behaviors. Moreover, knockdown of RHOV suppresses LUAD tumor growth and metastasis in nude mice. Mechanistically, RHOV activates Jun N-terminal Kinase (JNK)/c-Jun signalling pathway, an important pathway in lung cancer development and progression, and regulates the expression of markers of epithelial-to-mesenchymal transition, a process involved in cancer cell migration, invasion and metastasis. RHOV-induced malignant biological behaviors are inhibited by pyrazolanthrone, a JNK inhibitor. Our findings indicate a critical role of RHOV in LUAD metastasis and may provide a biomarker for prognostic prediction and a target for LUAD therapy.