Tripartite motif-containing 22 (TRIM22) is reported to participate in numerous cellular activities. Recent studies confirm that TRIM22 is a target gene for P53, and inhibits clonogenic growth of leukemic U-937 cells. The current study aims to discover the effect of TRIM22 in progression of human chronic myeloid leukemia (CML) and explore the related mechanism. TRIM22 was knocked down by siRNA transfection in CML cell K562. We observed that TRIM22 knockdown decreased proliferation and invasion in K562 cells. TRIM22 knockdown significantly induced cell cycle arrest by regulating the level of CDK4, Cyclin D1, P70S6K, and P53 in K562 cell. Moreover, loss of TRIM22 also promoted apoptosis through modulation of Bcl-2, Bax and active Caspase 3 in K562 cell. Furthermore, we demonstrated that TRIM22 knockdown inhibited the activation of PI3K/Akt/mTOR pathway by decreasing the level of the phosphorylated form p-Akt and p-mTOR in K562 cell. In conclusion, loss of TRIM22 suppresses the progression and invasion of CML through regulation of PI3K/Akt/mTOR pathway, suggesting that TRIM22 might be as a potential target for the treatment strategy of CML.

Aim The purpose of this study is to consider the function of cytoskeleton-associated protein 2-like (CKAP2L) in lung adenocarcinoma (LAD) development and its prognostic value. Methods The mRNA expression of CKAP2L and its correlation with clinical factors in LAD patients were analyzed from the data taken from The Cancer Genome Atlas and The First Affiliated Hospital of Kunming Medical University. We constructed H460 and A549 cell lines with silenced CKAP2L using RNA interference. Cell counting kit-8 assay and colony formation assays were carried out to determine the function of CKAP2L in H460 and A549 cell proliferation. Transwell and wound healing assays were applied to determine the effect of CKAP2L on H460 and A549 cell invasion and migration. The influences of CKAP2L on mitogen-activated protein kinase signaling pathway-related proteins were tested by Western blotting. Results CKAP2L expression is enhanced in LAD tissues and is predictive of poor prognosis in LAD patients. High expression of CKAP2L is associated with stage ( P <0.001), lymph node status ( P =0.002), and metastasis ( P =0.025). Depletion of CKAP2L dramatically suppressed the proliferation, migration, and invasion of H460 and A549 cells. Moreover, the ratio of p-MEK/ MEK and p-ERK/ERK reduced obviously in A549 cells after depleting CKAP2L. Conclusion Our findings implied that CKAP2L might be a promoter of LAD and could serve as a predictor for LAD patients.

Abstract:In this paper a novel laser impact spot welding (LISW) method is described, in which a hump was formed on the flyer plate on the intended welding spot location by local pre-forming. When the flyer and base plates were placed together to perform welding, the two plates kept in contact over their entire surfaces except at the hump, where a local air gap was enough to guarantee the impact velocity and collision angle to achieve spot welding using laser pulse energy. The presented approach was implemented to join thin titanium foils to copper foils under low laser energy system. Joints with regular shapes were obtained. The microstructure in the weld interface was studied with scanning electron microscopy (SEM) and energy dispersive spectroscopy (EDS). It was found that the jetting occurred at the central region of the weld spots due to oblique impact. Wave features were observed in the weld interfaces. The impact energy was found to have significant influence on the wave's characteristics. Moreover, SEM images and EDS analysis did not show apparent element diffusion across the weld interface. Besides, the lap shearing test was used to characterize the mechanical properties of the spot welded joints.

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Abstract:Laser flexible shock micro-bulging (LFSB) is a novel micro fabrication technology, which combines laser dynamic forming and flexible die forming, which is a type of high strain rate micro-forming. The LFSB of 304 stainless steel foils was investigated in this paper. Experimental and simulated results indicated that the bulging depth and thickness thinning rate of bulging parts increased with an increase of laser energy and a decrease of workpiece thickness. Experimental results also showed the surface morphology of bulging parts. The hardness distribution in the cross section of bulging parts was revealed by nanoindentation experiments. The internal microstructure of micro bulging parts was observed by TEM. In addition, the equivalent stress and plastic strain distribution of bulging parts were shown in the numerical simulation under different workpiece thicknesses and laser energies.