ABSTRACT
Objective To study the expression and clinical significance of miR-183-5p, TβRⅠ and TβRⅡ in esophageal squamous cell carcinoma (ESCC). Methods The mRNA and protein expression of miR-183-5p, TβRⅠ and TβRⅡ were examined in ESCC cell lines ECA-109, TE-1, normal esophageal epithelial cells, tumor tissues and tumor-free tissues from 72 ESCC patients. Their clinical significance and the relationship between miR-183-5p and the latter two were analyzed. The effects of miR-183-5p on the expression of TβRⅠand TβRⅡ in ECA-109 cells and the cell functions of ECA-109 were also investigated. Results Compared with the normal esophageal epithelia cells, ESCC cell lines TE-1 and ECA-109 were statistically characterized by a high expression of miR-183-5p (all P<0.05) and low expression of TβRⅠand TβRⅡ(all P<0.05). The expression of miR-183-5p in ESCC tissues was higher than that in adjacent normal tissues, while the expressions of TβRⅠ and TβRⅡ were lower (all P< 0.05). The expression of miR-183-5p was closely related to sex, tumor differentiation, tumor staging, distant metastasis, lymphatic metastasis, and tumor location (all P<0.05). TβRⅠlevel was associated with sex, lymph node metastasis and tumor size (all P<0.05). Experimental data showed the negative correlation between the expression of miR-183-5p and TβRⅠin ESCC tissues (r= -0.521, P< 0.05). Over expression of miR-183-5p significantly inhibited the expression of TβRⅠ in ECA-109 cells (P< 0.05) and promoted the growth, invasion and metastasis of ECA-109 cells (P< 0.05). Low expression of miR-183-5p significantly promoted the expression of TβRⅠ in ECA-109 cells (P< 0.05), and suppressed the growth, invasion and metastasis of ECA-109 cells (P< 0.05). There was no significant change in the expression of TβRⅡ in the transfection experiments. Conclusion MiR-183-5p is closely related to the abnormal expression of TβRⅠ, which may exert an important role in the progression of lymphatic metastasis.
ABSTRACT
Objective To investigate the role of Jiawei-sini Dection on expression of rat transforming growth factor-β1 receptor Ⅰ,Ⅱ(TβRⅠ,TβR Ⅱ), and study its treatment of anti-HF and the possible mechanisms. Methods The model of rat hepatic fibrosis was setup by subcutaneous injection of carbon tetrachloride and drinking alcohol freely;According to random block method, the successful model rats were divided into three groups:pathological model group (group B),Fufangbiejiarangan tablet group (group C), and Jiawei Sini Decoction group (group D), each group containing ten rats. Group A and group B were given two milliliters saline, group C was given Fufangbiejiarangan tablets 0.625 grams per kilogram of body weight, group D was given Jiawei Sini liquid 15.625 grams per kilogram of body weight.Each rat was fed once a day for 8 weeks.In order to avoid the natural repair of the hepatic affecting the experimental results, the rats,except group A, were still injected 40% CCl4 three milliliters per kilogram of body weight after feeding drug once a week. Fufang-Biejia-Ruangan Ttablet group was set as a positive control;The effects on expression of TβRⅠ,TβR Ⅱ were determined by immunohistochemical method. Changes of alanine aminotransferase (ALT), aspartate aminotransferase(AST),alkaline phosphatase(ALP) and TβRⅠ,TβR Ⅱ were observed in rats. Results The expression of TβRⅠ、Ⅱ, compared with the pathological model(16.63±2.69)%, (14.57±1.09)%, were significantly reduced in Jiawei-Sini Dection group[they are(8.09±0.71)%,(6.51±0.48)%, the difference was statistically significant(P＜0.05).The effects of Jiawei-Sini Dection was equal to the effect of Fufang-Biejia-Ruangan Tablets on expression of TβRⅠ,TβR Ⅱ(P＞0.05). Conclusion Jiawei-Sini Dection was able to inhibit the expression of TβRⅠ and TβR Ⅱ, thus affected the combination of TGFβ1, and their receptors.