ABSTRACT
[This retracts the article DOI: 10.3892/ol.2018.8109.].
ABSTRACT
Developments in cancer therapy have greatly improved the survival time for patients with pancreatic ductal adenocarcinoma (PDAC); however, the prognosis of patients with PDAC remains poor. Understanding the expression patterns and functions of microRNAs may provide strategies for the diagnosis and treatment of patients with PDAC. The present study aimed to explore the expression and functions of microRNA-216b (miR-216b) in PDAC. The expression of miR-216b in PDAC tissues and cell lines was quantified with reverse transcription-quantitative polymerase chain reaction. An miR-216b mimic was introduced into PDAC cells to induce the effects of miR-21b overexpression. The effects of miR-216b overexpression on growth, migration and invasion of PDAC cells were evaluated by cell proliferation assay, migration and invasion assays, respectively. The molecular mechanism underlying the suppressive effects of miR-216b on PDAC was also examined; a direct target gene of miR-216b, ρ-associated coiled-coil containing protein kinase 1 (ROCK1), was downregulated by ROCK1 short interfering RNA to investigate the effects on growth, migration and invasion of PDAC cells. The present study revealed that miR-216b was significantly downregulated in PDAC tissues and cell lines. Overexpression of miR-216b inhibited growth, migration and invasion of PDAC cells in vitro. ROCK1 was identified as a direct target gene of miR-216b in pancreatic cancer and the downregulation of ROCK1 resembled the effects of miR-216b overexpression in PDAC cells. Taken together, miR-216b acted as a tumor suppressor in PDAC and may represent a novel therapeutic target in PDAC.
ABSTRACT
BACKGROUND: Our previous study suggested that N-cadherin was downregulated in hepatocellular carcinoma (HCC). Our aim in this study was to investigate the correlation between N- and E-cadherin expression in HCC and its clinical significance. METHODS: Eighty-six patients with HCC undergoing liver resection were retrospectively studied. N- and E-cadherin expression in HCC and adjacent liver tissue were investigated using immunohistochemistry and immunofluorescence. The correlation between the expression status of both cadherins and surgical outcomes was analyzed. RESULTS: In 23 patients negative for E-cadherin expression, 19 of them (82.6%) were also negative for N-cadherin expression. In 30 patients with heterogeneous expression of E-cadherin, 20 of them (66.7%) also had heterogeneous expression of N-cadherin. In 33 patients with uniformly positive expression of E-cadherin, 19 of them (57.6%) also had uniformly positive expression of N-cadherin. Therefore, there was a positive correlation between expression patterns of N- and E-cadherins. Concurrent loss of both N- and E-cadherin expressions was significantly associated with absence of the tumor capsule, vascular invasion, and poor differentiation. The 1- and 3-y disease-free survival rates were 27% and 9%, respectively, and the 1- and 3-y overall survival rates were 64.3% and 14.3%, respectively, in patients with concurrent loss of both cadherins, which were significantly worse than those with concurrent uniformly positive expression or heterogeneous expression of both cadherins. CONCLUSIONS: Loss of N-cadherin was positively correlated with loss of E-cadherin in HCC. Concurrent loss of both N- and E-cadherin expressions was associated with poor surgical outcomes of HCC patients undergoing liver resection.
Subject(s)
Antigens, CD/analysis , Cadherins/analysis , Carcinoma, Hepatocellular/surgery , Hepatectomy , Liver Neoplasms/surgery , Adult , Aged , Carcinoma, Hepatocellular/chemistry , Carcinoma, Hepatocellular/mortality , Female , Humans , Liver Neoplasms/chemistry , Liver Neoplasms/mortality , Male , Middle Aged , Neoplasm InvasivenessABSTRACT
OBJECTIVES: To compare the outcomes after liver resection for a single small hepatocellular carcinoma (HCC) (≤ 5 cm) between non-cirrhotic patients and cirrhotic patients, and to explore the influence of liver cirrhosis on recurrence and overall survival after liver resection in patients with a single small HCC. METHODS: A consecutive series of 256 patients with a single small HCC undergoing liver resection from April 2001 to October 2009 was retrospectively reviewed. Among the 256 patients, 227 patients were male, and 29 were female. The medium age was 49 years (ranged, 14 - 79 years); 224 (87.5%) patients were positive for hepatitis B surface antigen, 241 (94.1%) patients were with preoperative liver function of Child-Pugh grade A. The entire cohort were divided into non-cirrhosis group (n = 44) and cirrhosis group (n = 212). Univariate analysis and then multivariate analysis were performed to determine the prognostic factors of recurrence and overall survival after liver resection for all patients. RESULTS: The 1-, 3-, 5-year recurrence-free survival rates after liver resection were 93.0%, 85.3%, and 68.5%, respectively, in non-cirrhosis group, while 81.1%, 58.6%, and 45.0%, respectively, in cirrhosis group. The 1-, 3-, 5-year overall survival rates after liver resection were 100%, 92.5%, and 92.5%, respectively, in non-cirrhosis group, while 93.8%, 78.7%, and 67.8%, respectively, in cirrhosis group. Both the recurrence-free survival and overall survival of non-cirrhosis group were significantly better than those of cirrhosis group (χ(2) = 8.756, P = 0.003; χ(2) = 8.603, P = 0.003). Cirrhosis, absence of tumor capsule, presence of microvascular invasion and moderate/poor tumor differentiation were the independent adverse prognostic factors for recurrence-free survival and overall survival in patients with a single small HCC after liver resection. CONCLUSIONS: Cirrhosis is an important adverse prognostic factor for long-term survival in patients with a single small HCC after liver resection. Liver resection resulted in much worse survival for cirrhotic patients compared to non-cirrhotic patients.