scholarly journals Arenobufagin activates p53 to trigger esophageal squamous cell carcinoma cell apoptosis in vitro and in vivo

2017 ◽  
Vol Volume 10 ◽  
pp. 1261-1267 ◽  
Author(s):  
Junhong Lv ◽  
Shaohuan Lin ◽  
Panli Peng ◽  
Changqing Cai ◽  
Jianming Deng ◽  
...  
2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e15571-e15571
Author(s):  
L. Ke ◽  
H. Wei ◽  
L. Na ◽  
L. Na ◽  
W. Xin ◽  
...  

e15571 Background: Cell adhesion molecules are of crucial importance in cancer invasion and metastasis. Epithelial to mesenchymal transition, characterized by reduced E-cadherin and increased N-cadherin expression, has been recognized as a feature of aggressive tumors, but the importance of this phenotype has not been settled in esophageal squamous cell carcinoma. Aim: To examine the expressions of N-cadherin and E-cadherin in 62 normal esophageal epithelium specimens, 31 adjacent atypical hyperplasia epithelium specimens and 62 esophageal squamous cell carcinoma specimens, and to investigate the roles of N-cadherin in the invasiveness of esophageal squamous cell carcinoma cell line EC9706 transfected by N-cadherin shRNA.. Methods: PV immunohistochemistry was used to detect the expression pattern of N-cadherin and E-cadherin in 62 normal esophageal epithelium specimens, 31 adjacent atypical hyperplasia epithelium specimens and 62 esophageal squamous cell carcinoma specimens. The invasiveness of esophageal squamous cell carcinoma cell line EC9706 in vitro and in vivo was determined by transwell assay and nude mice experiments after EC9706 was transfected by N-cadherin shRNA. Results: The positive rates of N-cadherin decreased in the sequence of carcinoma, adjacent atypical hyperplasia and normal esophageal tissue, which were 75.8%, 61.3%, 29.0% (P < 0.05), respectively, while those of E-cadherin increased in sequence, which were 40.3%, 71.0% and 95.2% (P < 0.05). The increased expression of N-cadherin and decreased expression of E-cadherin were related to the invasion, differentiation, and lymph node metastasis (P < 0.05). The expression level of N-cadherin decreased in the N- cadherin knocked down cells, and the invasiveness of those cells decreased significantly as well in vitro and in vivo. Conclusions: These results suggest that N-cadherin is an important factor in the invasiveness of esophageal squamous cell carcinoma and N-cadherin may serves as a potential molecular target for biotherapy of esophageal squamous cell carcinoma. No significant financial relationships to disclose.


2021 ◽  
Vol 11 ◽  
Author(s):  
Yun-Zhu Zeng ◽  
Yong-Qu Zhang ◽  
Jiong-Yu Chen ◽  
Li-Ying Zhang ◽  
Wen-Liang Gao ◽  
...  

Background and ObjectivesIn China, over 90% of esophageal cancer (EC) cases are esophageal squamous cell carcinoma (ESCC). ESCC is a frequently malignant tumor with poor prognosis despite the development of comprehensive therapeutic strategies, for which there is still a lack of effective prognostic factors. Previous studies found that the abnormal expression of TRPC1 is closely related to the proliferation, invasion, metastasis, and differentiation of various tumors. However, the relationship between TRPC1 and ESCC is currently unclear. The present study aimed to clarify the clinical significance of TRPC1 and to preliminarily assess the molecular mechanism by which TRPC1 regulates cell proliferation, migration, and invasion in ESCC.Materials and MethodsImmunohistochemistry (IHC) was used to determine the expression of TRPC1 and Ki-67 in 165 cases of ESCC. The correlations between TRPC1 expression and clinicopathological characteristics were determined, and both univariate and multivariate analyses were utilized to quantify the impact of TRPC1 expression on patient survival. Cell Counting Kit-8, scratch wound healing, and transwell assays were used to determine the effects of TRPC1 on proliferation, migration, and invasion in ESCC in vitro, respectively.ResultsThe positive expression rate of TRPC1 showed significantly decreased in ESCC (45.50%) compared with the levels in normal esophageal mucosa (NEM; 80.80%) and high-grade intraepithelial neoplasia (HGIEN; 63.20%) (P&lt;0.001). Higher expression rate of TRPC1 was associated with low lymph node metastasis (P&lt;0.001), high differentiation (rs= 0.232, P=0.003), and low Ki-67 (rs = −0.492, P&lt;0.001). We further revealed that low expression of TRPC1 was associated with poor prognosis (Disease-free survival, DFS: 95% CI=0.545–0.845, P=0.001; Overall survival, OS: 95% CI=0.553–0.891, P=0.004). Furthermore, we showed that downregulation of TRPC1 promoted the proliferation, migration, and invasion of human esophageal squamous cell carcinoma cell line EC9706 in vitro. In contrast, overexpression of TRPC1 inhibited the proliferation, migration, and invasion of human esophageal squamous cell carcinoma cell line KYSE150 (P&lt;0.01), in a manner at least in part mediated through the AKT/p27 pathway.ConclusionTRPC1 inhibited the proliferation, migration, and invasion of EC9706 and KYSE150 cells, at least, in part mediated through the AKT/p27 pathway in vitro. The downregulation of TRPC1 may be one of the most important molecular events in the malignant progression of ESCC. TRPC1 could be a new candidate tumor suppressor gene and a new prognostic factor of ESCC.


2016 ◽  
Vol 5 (10) ◽  
pp. 2879-2885 ◽  
Author(s):  
Hong‐lei Luo ◽  
Ming‐de Huang ◽  
Jia‐ni Guo ◽  
Rui‐hua Fan ◽  
Xiao‐tian Xia ◽  
...  

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