Objective:To investigate the roles and regulation mechanism of miR-31 in human cutaneous squamous cell carcino-ma (cSCC) growth. Methods:cSCC cells were transfected with the antisense oligonucleotide (ASO) of miR-31, and the cSCC growth was tested by colony formation and in vivo tumor formation assays. The target gene of miR-31 was validated by Western blot and green fluorescent protein (GFP) reporter assay. The cells were then transfected with the siRNA of the target gene, and the effect of the target gene on cell growth was preformed by colony formation assay. Finally, real-time PCR and immunohistochemistry were used for analy-sis of the expression of miR-31 and its target gene. Results:miR-31 ASO resulted in a low number of cell colonies and small tumor vol-ume (P<0.05). Western blot showed that the cells with miR-31 ASO had a higher protein level of large tumor suppressor homolog 2 (LATS2) than the control. The 3' UTR of LATS2 had a binding site with miR-31, and miR-31 ASO increased the GFP intensity con-trolled by LATS2 3' UTR, whereas no effect was observed on the mutant LATS2 3' UTR. Western blot showed that LATS2 siRNA inhib-ited the expression of LATS2 protein by about 80%. Knocking down of LATS2 increased the colony number by about 70%or 1.3-fold in cSCC cells. Real-time PCR showed that miR-31 was overexpressed in most cSCC tissues, compared with normal tissues. An inverse relationship existed between miR-31 and LATS2 expression levels. Immunohistochemistry validated that LATS2 was downregulated in cSCC tissues. Conclusion:miR-31, which functions as an oncogene, promotes cSCC growth by suppressing LATS2 expression. Our da-ta suggest that miR-31 is a potential miRNA-based therapeutic target for cSCC growth.

Objective To investigate the role of the p38 MAPK pathway in the formation of cytoplasmic vacuoles .Methods Af-ter treated with Anisomycin ,SB203580 or SP600125 ,images of HepG2 ,LM3 ,QBC939 ,Hela and A549 cells were recorded by light microscopy and taken at a magnification of 400 × .The effects of anisomycin ,SB203580 and SP600125 on the activity of p38 and JNK were measured by Western blot .LM3 and A549 cells were stained with the ER-tracker red and the lyso-tracker red and subjec-ted to confocal microscopy analysis .Results (1)Anisomycin could abolish cytoplasmic vacuolization of HepG2 cells .(2)p38 MAPK activation was responsible for anisomycin-induced cytoplasmic vacuolization abolishment .(3)p38 MAPK blocking initiated cytoplas-mic vacuoles formation in various cancer cell lines .(4)p38 MAPK blocking-induced cytoplasmic vacuoles disrupted the integrity of endoplasmic reticulum .(5)p38 MAPK blocking reversibly induced cytoplasmic vacuoles formation .Conclusion These observations provide direct evidence for a role of p38 MAPK signaling in regulating the formation of cytoplasmic vacuoles .

The clinical characteristics of the pneumonia includes hyperthermia, cough and pectoralgia, etc with simultaneous mixed signs of inflammatory infiltration, consolidation, cavity/air sac and abscess in pulmonary CT scan, and these signs change rapidly. Respiratory failure and septic shock frequently occur in severe such patients, resulting in refractory management and relatively long therapeutic course. The timely diagnosis, use of sensitive antibiotics, respiratory and nutritional support, etc comprehensive effective measures can elevate the rescue success rate with severe hematogenous staphylococcus aureus pneumonia.