Dataset Information

[Expression profile of miR-501-5p in lung adenocarcinoma patients from Xuanwei area].

ABSTRACT: OBJECTIVE:To investigate the relationship between miR-501-5p expression and the clinicopathological factors in patients with lung adenocarcinoma in Xuanwei area. METHODS:Surgical specimens of lung adenocarcinoma and paired adjacent tissues from 24 patients with lung adenocarcinoma from Xuanwei area were examined for miR-501-5p expression using microRNA microarray technique and qPCR. Chi-square test was used to analyze the association of miR-501-5P expression with the clinicopathological characteristics of the patients. Multiple regression analysis was performed to analyze the association of miR-501-5p expression with the patients' gender, age, tumor stage, and preoperative CEA level. RESULTS:MicroRNA microarray analysis and qPCR validation results revealed significantly upregulated expressions of miR-501-5p in patients with lung adenocarcinoma from Xuanwei area (Plt;0.01). The microarray data showed an up-regulation of miR-501-5p by 3.17 folds in lung adenocarcinoma tissue compared with the adjacent tissue (P=0.22376, FDR=0.071395). Chi-square test indicated that miR-501-5p expression level was associated with the patients' age (f=7.168, P=0.014), TNM stage (f=36.627, P<0.01), and preoperative serum CEA level (f=30.045, Plt;0.01), but not with the patients' gender (f=3.612, P=0.071). Multiple regression analysis revealed that miR-501-5p expression was positively correlated with the patients' age, TNM stage of the tumor, and serum CEA (Plt;0.05). CONCLUSION:miR-501-5p expression is up-regulated in lung adenocarcinoma with significant associations with the patients' age, TNM stages and serum CEA level in patients from Xuanwei area, suggesting its potential role in the tumorigenesis and progression of lung adenocarcinoma in Xuanwei area.

SUBMITTER: Chen S

PROVIDER: S-EPMC6780435 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature

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[Expression profile of miR-501-5p in lung adenocarcinoma patients from Xuanwei area].

Chen Shuai S Zhou Yong-Chun YC Chen Ying Y Chen Xiao-Bo XB Li Guang-Jian GJ Lei Yu-Jie YJ Tian Lin-Wei LW Zhao Guang-Qiang GQ Huang Qiubo Q Huang Yunc-Hao YH

Nan fang yi ke da xue xue bao = Journal of Southern Medical University 20170301 3

<h4>Objective</h4>To investigate the relationship between miR-501-5p expression and the clinicopathological factors in patients with lung adenocarcinoma in Xuanwei area.<h4>Methods</h4>Surgical specimens of lung adenocarcinoma and paired adjacent tissues from 24 patients with lung adenocarcinoma from Xuanwei area were examined for miR-501-5p expression using microRNA microarray technique and qPCR. Chi-square test was used to analyze the association of miR-501-5P expression with the clinicopathol ...[more]

PMID: 28377352

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Project description:BackgroundLung adenocarcinoma (LUAD) is currently the leading cause of cancer-related death worldwide. Long noncoding RNAs (lncRNAs) play key roles in tumor occurrence and development as crucial cancer regulators. The present study aimed to explore the molecular mechanism and regulatory network of Linc00511 in LUAD and to identify new potential therapeutic targets for LUAD.MethodsReal-time quantitative polymerase chain reaction (RT-qPCR) was performed to determine the relative Linc00511 levels in LUAD tissues and cells. The proliferation, apoptosis, migration, and invasion abilities of LUAD cells were assessed by a Cell Counting Kit-8 (CCK-8) assay, a colony formation assay, flow cytometry, and a Transwell assay. Changes in hsa_miR-126-5p, hsa_miR-218-5p, and COL1A1 expression were analyzed using western blotting and RT-qPCR. Targeted binding between miR-126-5p/miR-218-5p and Linc00511 or COL1A1 was verified with a luciferase reporter system and confirmed by an RNA pulldown assay. The participation of the PI3K/AKT signaling pathway was confirmed via western blotting. Xenograft animal experiments were performed to detect the impact of Linc00511 on LUAD tumor growth in vivo.ResultsIn the present work, we observed that Linc00511 was upregulated in LUAD tissues and cells. Loss/gain-of-function experiments indicated that knockdown of Linc00511 significantly inhibited LUAD cell proliferation, migration and invasion and promoted LUAD cell apoptosis, whereas overexpression of Linc00511 showed the opposite effects. In addition, we determined that Linc00511 promoted COL1A1-mediated cell proliferation and cell motility by sponging miR-126-5p and miR-218-5p. Moreover, Linc00511 activated the PI3K/AKT signaling pathway through upregulation of COL1A1. Finally, silencing of Linc00511 inhibited LUAD tumor growth in vivo.ConclusionsLinc00511 acts as a competing endogenous RNA to regulate COL1A1 by targeting miR-126-5p and miR-218-5p, thereby promoting the proliferation and invasion of LUAD cells.

Project description:ObjectivesLung adenocarcinoma (LUAD) exhibits a higher fatality rate among all cancer types worldwide, yet the precise mechanisms underlying its initiation and progression remain unknown. Mounting evidence suggests that long non-coding RNAs (lncRNAs) exert significant regulatory roles in cancer development and progression. Nevertheless, the precise involvement of lncRNA CYP4A22-AS1 in LUAD remains incompletely comprehended.MethodsBioinformatics analyses evaluated the expression level of CYP4A22-AS1 in lung adenocarcinoma and paracancer. The LUAD cell line with a high expression of CYP4A22-AS1 was constructed to evaluate the role of CYP4A22-AS1 in the proliferation and metastasis of LUAD by CCK8, scratch healing, transwell assays, and animal experiments. We applied transcriptome and microRNA sequencing to examine the mechanism of CYP4A22-AS1 enhancing the proliferation and metastasis of LUAD. Luciferase reporter gene analyses, west-blotting, and qRT-PCR were carried out to reveal the interaction between CYP4A22-AS1, miR-205-5p/EREG, and miR-34c-5p/BCL-2 axes.ResultsCYP4A22-AS1 expression was significantly higher in LUAD tissues than in the adjacent tissues. Furthermore, we constructed a LUAD cell line with a high expression of CYP4A22-AS1 and noted that the high expression of CYP4A22-AS1 significantly enhanced the proliferation and metastasis of LUAD. We applied transcriptome and microRNA sequencing to examine the mechanism of CYP4A22-AS1 enhancing the proliferation and metastasis of LUAD. CYP4A22-AS1 increased the expression of EREG and BCL-2 by reducing the expression of miR-205-5p and miR-34-5p and activating the downstream signaling pathway of EGFR and the anti-apoptotic signaling pathway of BCL-2, thereby triggering the proliferation and metastasis of LUAD. The transfection of miR-205-5p and miR-34-5p mimics inhibited the role of CYP4A22-AS1 in enhancing tumor progression.ConclusionThis study elucidates the molecular mechanism whereby CYP4A22-AS1 overexpression promotes LUAD progression through the miR-205-5p/EREG and miR-34c-5p/BCL-2 axes.

Dataset Information

[Expression profile of miR-501-5p in lung adenocarcinoma patients from Xuanwei area].

Publications

[Expression profile of miR-501-5p in lung adenocarcinoma patients from Xuanwei area].

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