ABSTRACT
Esophageal squamous cell carcinoma (ESCC) is the leading pathologic type in China. miR-145 has been reported to be downregulated in multiple tumors. This study was aimed to investigate the role of miR-145 in ESCC. miR-145 expression was investigated in 65 ESCC samples as well as four ESCC cell lines by quantitative real-time polymerase chain reaction (qRT-PCR). Targetscan 6.2 website (http://www.targetscan.org/) was used to predict the targets of miR-145. Expression of phospholipase C epsilon 1 (PLCE1) messenger RNA and protein was detected by qRT-PCR or Western blot. MTT and wound healing assay were conducted to explore the effects of miR-145 on the proliferation and migration of ESCC cell lines, respectively. miR-145 was significantly decreased in ESCC tissues. An inverse correlation between miR-145 and invasion depth and TNM stage were observed. PLCE1 was a direct target of miR-145, and the expression of PLCE1 was inversely correlated with miR-145 expression in ESCC tissues. In addition, overexpression of miR-145 suppressed cell proliferation and migration in ESCC cells. The enforced expression of PLCE1 partially reversed the suppressive effect of miR-145. These results prove that miR-145 may perform as a tumor suppressor in ESCC by targeting PLCE1.
Subject(s)
Esophageal Neoplasms/genetics , Esophageal Squamous Cell Carcinoma/genetics , Gene Expression Regulation, Neoplastic , MicroRNAs/genetics , Phosphoinositide Phospholipase C/genetics , Aged , Base Sequence , Cell Line, Tumor , Cell Movement , Cell Proliferation , Epithelial Cells/metabolism , Epithelial Cells/pathology , Esophageal Neoplasms/metabolism , Esophageal Neoplasms/pathology , Esophageal Neoplasms/surgery , Esophageal Squamous Cell Carcinoma/metabolism , Esophageal Squamous Cell Carcinoma/pathology , Esophageal Squamous Cell Carcinoma/surgery , Female , Humans , Lymphatic Metastasis , Male , MicroRNAs/metabolism , Middle Aged , Neoplasm Staging , Phosphoinositide Phospholipase C/antagonists & inhibitors , Phosphoinositide Phospholipase C/metabolism , RNA, Messenger/genetics , RNA, Messenger/metabolism , RNA, Small Interfering/genetics , RNA, Small Interfering/metabolism , Signal TransductionABSTRACT
OBJECTIVE: To compare compensatory sweating after lowering or restricting the level of sympathectomy. METHOD: A systematic review and meta-analysis were conducted of all randomized controlled trials published in English that compared compensatory sweating after lowering or restricting the level of sympathectomy. The Cochrane collaboration tool was used to assess the risk of bias, and the Mantel-Haenszel odds ratio method was used for the meta-analysis. RESULTS: A total of 11 randomized controlled trials were included, including a total of 1079 patients. Five of the randomized controlled trials studied restricting the level of sympathectomy, and the remaining six studied lowering the level of sympathectomy. CONCLUSIONS: The compiled randomized controlled trial results published so far in the literature do not support the claims that lowering or restricting the level of sympathetic ablation results in less compensatory sweating.
Subject(s)
Hyperhidrosis/physiopathology , Hyperhidrosis/surgery , Sweating/physiology , Sympathectomy/methods , Humans , Publication Bias , Randomized Controlled Trials as Topic , Risk Factors , Severity of Illness Index , Treatment OutcomeABSTRACT
OBJECTIVE: To compare compensatory sweating after lowering or restricting the level of sympathectomy. METHOD: A systematic review and meta-analysis were conducted of all randomized controlled trials published in English that compared compensatory sweating after lowering or restricting the level of sympathectomy. The Cochrane collaboration tool was used to assess the risk of bias, and the Mantel-Haenszel odds ratio method was used for the meta-analysis. RESULTS: A total of 11 randomized controlled trials were included, including a total of 1079 patients. Five of the randomized controlled trials studied restricting the level of sympathectomy, and the remaining six studied lowering the level of sympathectomy. CONCLUSIONS: The compiled randomized controlled trial results published so far in the literature do not support the claims that lowering or restricting the level of sympathetic ablation results in less compensatory sweating. .
Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Young Adult , Health Services Accessibility/statistics & numerical data , Indians, North American/statistics & numerical data , Medicaid/statistics & numerical data , United States Indian Health Service/statistics & numerical data , Alaska , Health Services Needs and Demand , United StatesABSTRACT
OBJECTIVE: To investigate the expression of two major alternative transcripts of RASSF1 gene (RASSF1A and RASSF1C) in human primary ovarian cancers and their biological implication as a new tumor suppressor gene. METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) and laser capture microdissection (LCM) were used to determine mRNA expression of the two major alternative transcripts of RASSF1 gene (RASSF1A and RASSF1C) in 3 ovarian cancer cell lines and 80 cases of primary ovarian cancers. RESULTS: RASSF1A mRNA was undetectable in SK-OV-3 cell line. Expression of RASSF1A and RASSF1C in 80 primary ovarian cancers were 40.0% (32/80) and 91.3% (73/80) respectively. RASSF1A mRNA expression was detectable more frequently in stage I and II (71.4%, 10/14; 75.0%, 9/12) than in stage III and IV ovarian cancers (26.7%, 12/45; 14.1%, 1/9) (P < 0.05). The expression level was also higher in well and moderately differentiated tumor groups (58.6%, 17/29; 50.0%, 10/20) than in poorly differentiated tumor group (16.1%, 5/31) (P < 0.05). CONCLUSION: There is a preferential loss of RASSF1A expression in human ovarian cancers and its expression is correlated with the tumor stage and the degree of histological differentiation which, as a tumor suppressor gene, might play an important role in the tumorigenesis of human primary ovarian cancer.
Subject(s)
Cystadenocarcinoma, Serous/metabolism , Genes, Tumor Suppressor , Ovarian Neoplasms/metabolism , Tumor Suppressor Proteins/biosynthesis , Carcinoma, Endometrioid/metabolism , Carcinoma, Endometrioid/pathology , Cell Line, Tumor , Cystadenocarcinoma, Mucinous/metabolism , Cystadenocarcinoma, Mucinous/pathology , Cystadenocarcinoma, Serous/pathology , Female , Gene Expression Regulation, Neoplastic , Humans , Neoplasm Staging , Ovarian Neoplasms/pathology , Prognosis , RNA, Messenger/biosynthesis , RNA, Messenger/genetics , Reverse Transcriptase Polymerase Chain Reaction , Tumor Suppressor Proteins/geneticsABSTRACT
OBJECTIVE: To investigate hypermethylation of promoter region of RASSF1A and its relationship with ovarian malignant epithelial tumors. METHODS: Methylation-specific PCR (MSP) was used to determine the hypermethylation of promoter region of ras association domain family 1 (RASSF1A) gene in 80 cases of ovarian malignant epithelial tumors. RESULTS: No methylation of promoter region of RASSF1A gene was found in all 80 normal control tissues (0). Of 80 ovarian malignant epithelial tumors 42 were hypermethylated in promoter region of RASSF1A gene (52.5%). There was no statistically significant difference in the frequency of hypermethylation of RASSF1A gene among serious adenocarcinomas, mucinous adenocarcinomas and endometrioid adenocarcinomas (54.2%, 52.4% and 45.5%, respectively; P > 0.05). Hypermethylation of RASSF1A gene happened more often in tumors in stage III and IV (66.7% and 77.8%) than that in stage I and II (21.4% and 16.7%; P < 0.05). It was less frequently observed in well and moderately differentiated tumors (34.5% and 35.0%) than in poorly differentiated tumors (80.6%; P < 0.05). CONCLUSION: High frequency of methylation of RASSF1A promoter exists in ovarian malignant epithelial tumors as a tumor suppressor gene, its suppressor activity may be abrogated by an epigenetic mechanism. Hypermethylation of RASSF1A promoter in patients with epithelial malignant ovarian tumors is related to clinical stage and histopathological grade. It indicates poor prognosis.
