[LncRNA SNHG11 promotes malignant progression of colorectal cancer cells through the PI3K/Akt/mTOR signaling pathway].

Objective: To investigate the effects of lncRNA SNHG11 on proliferation, migration, invasion and apoptosis of colorectal cancer cancer cells and possible mechanisms. Methods: qRT-PCR was performed to detect the expression level of lncRNA SNHG11 in colorectal cancer tissues and its related cell lines. The correlation between SNHG11 expression and clinical prognosis of patients was assessed by bioinformatics techniques. Cultured CRC cell lines were transfected with shCtrl (shCtrl group), shSNHG11#1 (shSNHG11#1 group), shSNHG11#2 (shSNHG11#2 group), Control cDNA (Control cDNA group), and SNHG11 cDNA (SNHG11 cDNA), respectively. Thiazolyl blue (MTT), clone formation assay, Transwell assay, cell scratch assay, and flow cytometry were used to detect the proliferation, migration, invasion, and apoptosis of CRC cells in each group. Western protein blotting was used to detect the expression of relevant proteins in each group, and the effect of lncRNA SNHG11 knockdown on the growth of tumour cells in vivo was analysed by nude mice tumouring assay. Phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signalling pathway inhibitor LY294002 was used for rescue experiments. Results: The expression of lncRNA SNHG11 was significantly higher in colorectal cancer cells and tissues than in normal tissues (P<0.05). Survival analysis showed that the expression level of SNHG11 was not statistically associated with CRC survival (P>0.05). shSNHG11#2 group compared with shCtrl group. MTT OD490/570 values decreased, the number of CRC cell clones decreased, the number of Transwell cells decreased, the area of cell scratch decreased, and the apoptosis rate increased (P<0.05). The mesenchymal markers matrix metalloproteinase (MMP9), N-cadherin and vimentin were significantly reduced, and the expression of the epithelial marker E-cadherin was upregulated. The expression of anti-apoptotic proteins Bcl-2 and Bcl-xl was decreased, and the expression of pro-apoptotic protein Bax was increased (P<0.05).In vivo experiments showed that lncRNA SNHG11 knockdown inhibited the growth of colorectal cancer cells, and the expression of Ki67 was reduced in tumours (P<0.05). LncRNA SNHG11 knockdown inhibited the expression of p-PI3K, p-Akt and p-mTOR.The PI3K/Akt/mTOR signaling pathway inhibitor LY294002 was able to restore the malignant cytological progression of colorectal cancer cells induced by the overexpression of lncRNA SNHG11. Conclusions: LncRNA SNHG11 is highly expressed in colorectal cancer. lncRNA SNHG11 can promote the malignant progression of colorectal cancer cells by regulating the PI3K/Akt/mTOR signaling pathway, and this finding provides a new theoretical basis for targeted therapy of colorectal cancer.

[Hemodynamics changes in proximal femur of patients with femoral head necrosis].

Intraosseous pressure of the proximal femur was measured with type II physical pressure detector in 46 patients with femoral head necrosis (Legg-perthes' disease 25, idiopathic necrosis 21) and in 49 normal persons (25 children and 24 adults). Fourteen of those with head necrosis and 9 of the normals were further surveyed by stress test, a test to see the pressure change following intraosseous injection of 5 ml heparinized normal saline solution. Again, intramedullary venography was done in 16 of those with diseased head and 12 of the normals to investigate their status of venous flow. The intraosseous pressure of normal hips was 20.56 +/- 8.13 mmHg in children and 17 +/- 8.72 mmHg in adults while that of diseased hips was 37.28 +/- 15.51 mmHg in children and 35 +/- 12.07 mmHg in adults. The results indicated the coexistence of intraosseous hypertension and femoral head necrosis. Intramedullary venogram showed diaphyseal reflux in those with femoral head necrosis. This finding was also proved by stress necrosis. This finding was also proved by stress test. The hindrance of venous return, whatever the cause may be, induced venous stasis, intraosseous hypertension and decreased arterial inflow. The necrosis of the femoral head was found to be due to insufficient and depletion of the nutrition supply in the femoral head.