ABSTRACT
Objective To study the effects of Twist gene silencing on migration and invasion of human triple-nega-tive breast cancer cell Hs578T and its potential mechanisms. Methods The lentiviral vectors with Twist gene-targe-ted specific shRNA and the negative control were constructed,then transfected into the human triple-negative breast cancer cell line Hs578T to establish the stable cell lines of Twist gene silencing. The blank group(blank),negative control group(shNC) and Twist gene silencing group(shTwist) were set up.After screening by puromycin,the fluo-rescence expression and the infection efficiency of each group cells were observed by inverted fluorescence micro-scope. The expression of Twist mRNA and protein level was detected by quantitative real-time PCR and Western blot.Transwell migration and invasion experiments were performed to measure cell migration and invasion abilities, re-spectively. Western blot was used to detect the levels of p-AKT, AKT, p-ERK1/2 and ERK1/2 proteins. Results Twist gene was successfully knockdown in human triple-negative breast cancer cell line Hs578T. Compared with the blank group and shNC group cells,the cell migration and invasion ability of the shTwist group cells were decreased significantly(P<0.05,P<0.05),and the expression of Twist downstream p-AKT and p-ERK1/2 proteins were al-so reduced notably in the shTwist group cells(P<0.05,P<0.05). Conclusions Twist promotes cell migration and invasion via AKT/ERK signaling axis in human triple-negative breast cancer cell line Hs578T.
ABSTRACT
PURPOSE: G-protein coupled estrogen receptor 1 (GPER) probably play important roles in the progression of breast cancer including endocrine therapeutic resistance. We evaluated GPER in primary breast cancers. METHODS: Immunohistochemistry was used to detect GPER in paraffin-embedded tissues of primary breast cancers from 423 patients and GPER expression was correlated with clinicopathological factors. RESULTS: GPER was expressed in 63.8% of specimens, coexpressed with estrogen receptor alpha (ERalpha) in 36.6% of tumors and was positive in 62.5% of the ERalpha-negative tumors. The expression of GPER had no relationship with the status of ERalpha, progesterone receptor and HER2. Although the expression of GPER was significantly inversely related with nodal status (p=0.045), no correlation between GPER expression and other clinicopathological variables (age, menstruation status, tumor size, stage, histologic grade, Nottingham Prognostic Index or pathological type) was found. CONCLUSION: GPER and ERalpha exhibited independent expression pattern of distribution in primary breast cancers. A long-term follow-up and a more definite molecular phenotype for ER are necessary in confirming studies.