Abstract Objectives Human salivary adenoid cystic carcinoma ( SACC ) is one of the most common malignant tumours of the salivary gland and has strong migratory and invasive ability, which often lead to poor prognosis and lower survival rate. Tumour tissue tends to stiffen during solid tumour progression. This study aimed to investigate the influence of various substrate stiffness on the migration and invasion of SACC . Methods Salivary adenoid cystic carcinoma cell line ACC 2 cells were cultured on polydimethylsiloxane substrates ( PDMS ) with varying stiffness for investigating the effects of substrate stiffness on the activities of MMP s and TIMP s. The underlying mechanism was also explored. Results When ACC 2 cells were cultured on various stiffness of PDMS , the expressions of matrix metalloproteinases 2 ( MMP 2), MMP 9, MMP 14, R hoA, R ac1, Rho‐associated protein kinase 1 ( ROCK 1) and ROCK 2 were up‐regulated with increasing substrate stiffness, whereas that of tissue inhibitor of matrix metalloproteinase 1 ( TIMP 1), TIMP 2 and TIMP 4 were down‐regulated with increasing substrate stiffness. Conclusions Our results showed that substrate stiffness regulated the activities of MMP s and TIMP s and then modulate migratory and invasive ability of ACC 2 cells via RhoA/ ROCK pathway. This work indicate that matrix stiffness played an important role in progression of SACC , which not only can help understand the strong invasive ability of SACC , but also suggested that therapeutically targeting matrix stiffness may help reduce migration and invasion of SACC and improve effective therapies.
Although BMP9 is highly capable of promoting osteogenic differentiation of mesenchymal stem cell (MSCs), the molecular mechanism involved remains to be fully elucidated. Here, we explore the possible involvement and detail role of JNKs (c-Jun N-terminal kinases) in BMP9-induced osteogenic differentiation of MSCs. It was found that BMP9 stimulated the activation of JNKs in MSCs. BMP9-induced osteogenic differentiation of MSCs was dramatically inhibited by JNKs inhibitor SP600125. Moreover, BMP9-activated Smads signaling was decreased by SP600125 treatment in MSCs. The effects of inhibitor are reproduced with adenoviruses expressing siRNA targeted JNKs. Taken together, our results revealed that JNKs was activated in BMP9-induced osteogenic differentiation of MSCs. What is most noteworthy, however, is that inhibition of JNKs activity resulted in reduction of BMP9-induced osteogenic differentiation of MSCs, implying that activation of JNKs is essential for BMP9 osteoinductive activity.
Phytochemical studies on the rhizomes of Actaea asiatica led to the isolation of seven new cycloartane triterpenes, actaticas A−G ( 1−7 ). Their structures were determined by NMR, HRESIMS, and chemical analysis. All the isolates were evaluated for their antiproliferative activity against HT-29 and McF-7 cell lines. The results showed that all the compounds displayed cytotoxicity. All compounds showed significant inhibitory effects with IC 50 values of 9.2–26.4 μM.
Bone tissue engineering based on adipose-derived stem cells (ASCs) is expected to become a new treatment for diabetic osteoporosis (DOP) patients with bone defects. However, compared with control ASCs (CON-ASCs), osteogenic potential of DOP-ASCs is decreased, which increased the difficulty of bone reconstruction in DOP patients. Moreover, the cause of the poor osteogenesis of ASCs in a hyperglycemic microenvironment has not been elucidated. Therefore, this study explored the molecular mechanism of the decline in the osteogenic potential of DOP-ASCs from the perspective of epigenetics to provide a possible therapeutic target for bone repair in DOP patients with bone defects.
To study the expression and significance of basic fibroblast growth factor(bFGF)and transforming growth factor-beta 1 (TGF-beta1) in mucoepidermoid carcinomas with different malignant degree.Using immunohistochemistry (IHC) staining technique, bFGF and TGF-beta1 proteins in the mucoepidermoid carcinoma tissues with different malignant degree, including well-differentiated, moderately differentiated and poorly differentiated mucoepidermoid carcinoma, and normal salivary gland tissue were detected.The positive rate of bFGF and TGF-beta1 in normal salivary glands were apparently lower than those in malignant mucoepidermoid carcinomas (P<0.05). The positive rate of bFGF in moderately and poorly differentiated mucoepidermoid carcinoma was higher than that in the well-differentiated carcinoma (P <0.05). However, the positive expression of bFGF showed no relationship between the moderately and poorly differentiated mucoepidermoid carcinomas. The positive rate of TGF-beta1 in moderately and poorly differentiated mucoepidermoid carcinomas was lower than that in the well-differentiated carcinoma (P<0.05). The positive expression of TGF-beta1 showed no relationship between the moderately and poorly differentiated mucoepidermoid carcinomas. The expression of bFGF and TGF-beta1 showed negative correlation (r=- 0.471, P=0.0003).The expression of TGF-beta1 may inhibit the development of the mucoepidermoid carcinoma, contrariwise, the expression of bFGF may prompt the development of the mucoepidermoid carcinoma. The expression of bFGF and TGF-beta1 has a negative correlation.
Pharmaceutical analysis is a main course of pharmacy major.This papers discussed our teaching experience and reflection of the course based on our several years of teaching experiences.The teaching of pharmaceutical analysis should seize the main line of the knowledge, think highly of the summary, enrich the teaching methods and be good at using the multimedia technology.Beside, some advice was given.These experience and advice can provide the reference for other teachers or students.
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