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pmid:35094292

The promotional effect of microRNA-103a-3p in cervical cancer cells by regulating the ubiquitin ligase FBXW7 function.

Li Ren · Jinjin Yang · Xiyan Meng · Junjun Zhang · Yiran Zhang

Human cell · 2022 doi:10.1007/s13577-021-00649-2

Paper

complete

Experiment

complete

Data

partial

Analysis

complete

Execution

absent

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Record details sci_version · id · kind · revision · content_hash · schema · created_at · updated_at · generator
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pmid:35094292
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science-record
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title
The promotional effect of microRNA-103a-3p in cervical cancer cells by regulating the ubiquitin ligase FBXW7 function.
doi
10.1007/s13577-021-00649-2
pmid
35094292
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[0]
Li Ren
[1]
Jinjin Yang
[2]
Xiyan Meng
[3]
Junjun Zhang
[4]
Yiran Zhang
journal
Human cell
year
2022
abstract
MicroRNAs (miRNAs) have been reported to be involved in the initiation and progression of human tumors including cervical cancer (CC). However, the mechanisms underlying of their actions in CC remain to be fully elucidated. Herein, the differentially expressed miRNAs that were screened based on GSE55940 microarray data retrieved from Gene Expression Omnibus (GEO), and miR-103a-3p was significantly upregulated in CC tissues which was selected as the target miRNA for further research. We also found that high expression of miR-103a-3p was closely associated with histological grades, FIGO stage and distant metastasis as well as reflected poor overall survival. Moreover, miR-103a-3p inhibition decreased the growth capacity of SiHa and HeLa cells by inducing cell apoptosis. And F-box and WD repeat-domain containing protein 7 (FBXW7), a well-known tumor suppressor in many cancer types, was identified as a direct target of miR-103a-3p. It was further found that FBXW7 was significantly downregulated in CC tissues, and it was inversely correlated with miR-103a-3p expression levels. Further investigation demonstrated that FBXW7 upregulation could simulate the roles of miR-103a-3p knockdown in cell viability and apoptosis. Moreover, FBXW7 knockdown efficiently abrogated the influences of CC cells proliferation caused by miR-103a-3p inhibition. Notably, miR-103a-3p could block FBXW7 mediated the downstream transcription factor pathways. Taken together, these findings suggest that miR-103a-3p functions as an oncogene in CC by targeting FBXW7.
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Differences between two groups were analyzed by unpaired t test and continuous data from multiple groups were analyzed using a one-way ANOVA, followed by Tukey’s post hoc test. The correlation between FBXW7 and miR-103a-3p expression was analyzed using Pearson’s correlation coefficient. Survival curves were calculated by the Kaplan–Meier method by the log-rank test.
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Differences between two groups were analyzed by unpaired t test and continuous data from multiple groups were analyzed using a one-way ANOVA, followed by Tukey’s post hoc test. The correlation between FBXW7 and miR-103a-3p expression was analyzed using Pearson’s correlation coefficient. Survival curves were calculated by the Kaplan–Meier method by the log-rank test.
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miR-103a-3p functions as an oncogene in cervical cancer by targeting FBXW7.
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Taken together, these findings suggest that miR-103a-3p functions as an oncogene in CC by targeting FBXW7.
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miR-103a-3p functions as an oncogene in cervical cancer by targeting FBXW7.
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Human transcriptome expression analysis of cervical cancer
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Differences between two groups were analyzed by unpaired t test and continuous data from multiple groups were analyzed using a one-way ANOVA, followed by Tukey’s post hoc test. The correlation between FBXW7 and miR-103a-3p expression was analyzed using Pearson’s correlation coefficient. Survival curves were calculated by the Kaplan–Meier method by the log-rank test.
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Complete file
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