Objective To investigate the relationship between Wnt5a gene and E-cadherin or vimentin gene in breast cancer cell line MCF-7. Methods RT-PCR was used to detect the mRNA expression of Wnt5a, E-cadherin and vimentin in breast cancer MCF-7 cells and the normal human mammary epithelial cell line MCF-10A, respectively, and their correlation was analyzed. Results The mRNA expression levels of Wnt5a and E-cadherin in cell line MCF-7 were significantly lower than those in cell line MCF-10A [(16.93± 2.97)%vs. (27.47±2.76) %, (12.97±1.35) % vs. (20.43±2.60) %, both P<0.05]. The mRNA expression level of vimentin in cell line MCF-7 was significantly higher than that in cell line MCF-10A [(16.53±0.85)%(6.33± 2.08) %, P<0.05 ]. In cell line MCF-7, the expression of Wnt5a was positively related to E-cadherin (г=0.997, P<0.05), but it was negatively related to vimentin (г=-0.998, P<0.05). Conclusions The expression of Wnt5a in human breast cancer cell line MCF-7 is significantly lower than that in cell line MCF-10A, which indicates that Wnt5a is a cancer suppressor gene in breast cancer. The expression of Wnt5a in cell line MCF-7 is positively related with E-cadherin, and it is negatively related with vimentin. Wnt5a may cause invasion and metastasis of breast cancer cell through the breast epithelial mesenchymal transitions.

The pathophysiological process of immune inflammatory response after severe trauma is extremely complex, especially manifested in the dynamic changes. In the physiological response state, the inflammatory and anti-inflammatory conditions are in a dynamic balance. The immune inflammatory response is relatively stable, avoiding excessive inflammatory reactions or immunosuppression and reducing further damage to the body. In the pathological response state, the dynamic balance between inflammatory and anti-inflammatory is broken, and it can also lead to persistent inflammatory-immunosuppression-catabolism syndrome (PICS). As a result, it increases serious complications such as uncontrolled inflammatory reactions, sepsis, multiple organ dysfunction syndrome (MODS), and multiple organ failure (MOF). Current researches on post-traumatic immune inflammatory response have also expanded to the genetic level, indicating that the over-expression of genes and the generation and increase of immune response media are likely to be the key reasons for the disorder of immune inflammatory response. The author reviews the research progress of immune inflammatory response mechanism and related clinical intervention after severe trauma, in order to summarize the previous research results and explore the future research direction.

The amygdala is an important hub for regulating emotions and is involved in the pathophysiology of many mental diseases, such as depression and anxiety. Meanwhile, the endocannabinoid system plays a crucial role in regulating emotions and mainly functions through the cannabinoid type-1 receptor (CB₁R), which is strongly expressed in the amygdala of non-human primates (NHPs). However, it remains largely unknown how the CB₁Rs in the amygdala of NHPs regulate mental diseases. Here, we investigated the role of CB₁R by knocking down the cannabinoid receptor 1 (CNR1) gene encoding CB₁R in the amygdala of adult marmosets through regional delivery of AAV-SaCas9-gRNA. We found that CB₁R knockdown in the amygdala induced anxiety-like behaviors, including disrupted night sleep, agitated psychomotor activity in new environments, and reduced social desire. Moreover, marmosets with CB₁R-knockdown had up-regulated plasma cortisol levels. These results indicate that the knockdown of CB₁Rs in the amygdala induces anxiety-like behaviors in marmosets, and this may be the mechanism underlying the regulation of anxiety by CB₁Rs in the amygdala of NHPs.
Animals ; Callithrix ; Receptors, Cannabinoid ; Anxiety ; Amygdala ; Cannabinoids ; Phenotype