miR-2110通过调节CDT1影响肺腺癌的生物学行为

OBJECTIVE: To investigate the effect of miR-2110 on the biological behaviors, such as cell proliferation, apoptosis, and metastasis, of lung adenocarcinoma (LUAD) cells by means of cell and animal experiments. METHODS: Bioinformatics websites, including ENCORI, TargetScan, miRTarBase, and Tarbase, were used to analyze the changes in the expression of miR-2110 in LUAD samples and to predict miR-2110 target. LUAD tissue samples and cells were collected and the changes in the expression of miR-2110 were verified through PCR technology. CCK-8 assay, clonogenic assay, Transwell assay, and flow cytometry were conducted to analyze alterations in the functions of LUAD cells. In addition, 10 BALB/c female nude mice aged 6 to 8 weeks were randomly divided into 2 groups, and the effect of miR-2110 on LUAD was investigated by in vivo experiments. RESULTS: miR-2110 was significantly decreased in LUAD tissues and cells compared with the normal lung tissues. miR-2110 overexpression inhibited the proliferation and metastasis of LUAD cells and promoted the apoptosis of tumor cells (P<0.05). Bioinformatics prediction and dual luciferase reporter gene assay results confirmed that miR-2110 could target and bind to CDT1. In addition, overexpression of CDT1 gene reversed the proliferation, metastasis, and apoptosis of miR-2110 compared with the miR-2110 overexpression group (P<0.05). Nude mice in vivo experiments showed that miR-2110 overexpression significantly decreased the expression of Ki67, a tumor proliferation index, and vimentin and MMP9, two metastasis indices, compared with the control group. CONCLUSION: miR-2110 can inhibit proliferation and metastasis of LUAD by targeting CDT1, providing a new rationale for the treatment of LUAD.

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Journal
PubMed Central
Published
2024-09-20
DOI
https://doi.org/10.12182/20240960505
Primary Topic
Cancer-related molecular mechanisms research
Type
article
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article

miR-2110通过调节CDT1影响肺腺癌的生物学行为

Zhichao Zhao, Xiaofei Yan, Chenxi Lin, Xuzhe Li et al.
PubMed Central
Cancer-related molecular mechanisms research
article

miR-2110通过调节CDT1影响肺腺癌的生物学行为

Zhichao Zhao, Xiaofei Yan, Chenxi Lin, Xuzhe Li, Lei Wang, Yuan Mi, Ping Shi, Cong Wang
article en

Abstract

OBJECTIVE: To investigate the effect of miR-2110 on the biological behaviors, such as cell proliferation, apoptosis, and metastasis, of lung adenocarcinoma (LUAD) cells by means of cell and animal experiments. METHODS: Bioinformatics websites, including ENCORI, TargetScan, miRTarBase, and Tarbase, were used to analyze the changes in the expression of miR-2110 in LUAD samples and to predict miR-2110 target. LUAD tissue samples and cells were collected and the changes in the expression of miR-2110 were verified through PCR technology. CCK-8 assay, clonogenic assay, Transwell assay, and flow cytometry were conducted to analyze alterations in the functions of LUAD cells. In addition, 10 BALB/c female nude mice aged 6 to 8 weeks were randomly divided into 2 groups, and the effect of miR-2110 on LUAD was investigated by in vivo experiments. RESULTS: miR-2110 was significantly decreased in LUAD tissues and cells compared with the normal lung tissues. miR-2110 overexpression inhibited the proliferation and metastasis of LUAD cells and promoted the apoptosis of tumor cells (P<0.05). Bioinformatics prediction and dual luciferase reporter gene assay results confirmed that miR-2110 could target and bind to CDT1. In addition, overexpression of CDT1 gene reversed the proliferation, metastasis, and apoptosis of miR-2110 compared with the miR-2110 overexpression group (P<0.05). Nude mice in vivo experiments showed that miR-2110 overexpression significantly decreased the expression of Ki67, a tumor proliferation index, and vimentin and MMP9, two metastasis indices, compared with the control group. CONCLUSION: miR-2110 can inhibit proliferation and metastasis of LUAD by targeting CDT1, providing a new rationale for the treatment of LUAD.

PubMed Central
Hebei Medical University (CN), Fourth Hospital of Hebei Medical University (CN)
Openalex Percentile: Top 71%
Cancer-related molecular mechanisms research
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