MiR-495-3p and miR-143-3p co-target CDK1 to inhibit the development of cervical cancer

Tang, Jun; Pan, Huagang; Wang, W; Qi, Chunrun; Gu, Chenzheng; Shang, Anquan; Zhu, Jinlian

doi:10.1007/s12094-021-02687-6

Cited by 31 publications

(16 citation statements)

References 24 publications

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“…Hsa-miR-27b-3p upregulation could suppress the CC cell stemness by suppressing VEGF-C [29]. Has-miR-495-3p was reported to suppress the occurrence and development of CC through downregulating the CDK1 expression [30]. Low survival rate, high stage, and lymph node metastasis of CC were signi cantly related to downregulation of has-miR-30e-5p.…”

Section: Discussionmentioning

confidence: 97%

Prognostic value and mechanism of EPHB2 overexpression in cervical cancer

Zhao

Cong

et al. 2022

Preprint

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Background Cervical cancer (CC) still represents an important challenge for female malignant tumors. In recent years, increasing evidence has indicated that EPHB2 plays a significant part in the origin and progression of many types of cancer in humans. Nevertheless, the mechanism of EPHB2 in CC remains inexplicable. The purpose of this study is to determine the prognostic value and related regulatory mechanism of EPHB2 in CC. Methods The basic clinical information and transcriptome data related to CC patients were downloaded from TCGA database and conducted standardization processing. TIMER2.0 was used for analyzing the EPHB2 expression differences of between 38 cancer types and corresponding normal tissues. The expression and prognostic value (including OS and RFS) of EPHB2 in different cancer types were determined by GEPIA2. And the starbase database was used for exploring the upstream miRNAs and lncRNAs of EPHB2. Then, The correlation analysis of EPHB2, miRNA and lncRNA and the exploration of prognostic value and expression of miRNAs in CESC was conducted using the R language packages. We also analyzed the prognostic value and expression difference of 187 lncRNAs based on the UALCAN database. Finally, we performed the correlation analysis between EPHB2 and multiple immune cells using the R language package. Results In our study, the AC073957.3/hsa-miR-150-5p axis was found to be the most potential upstream ncRNA-related regulator of EPHB2 in CC. And the results of immune correlation infiltration analysis suggest that as EPHB2 copy numbers fluctuate in CESC there is an obvious difference in immune cell infiltration levels, and EPHB2 was markedly positively correlated with Th2 cell, NK cell, Eosinophils, Tgd, Mast cell, NK CD56bright cells and Tem while negatively correlated with Tcm and B cell in CC. Conclusion Our study shows that EPHB2 is a potential prognostic marker, and its overexpression is related to poor prognosis of CC, which is expected to be a new therapeutic target for CC.

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Section: Discussionmentioning

confidence: 97%

Prognostic value and mechanism of EPHB2 overexpression in cervical cancer

Zhao

Cong

et al. 2022

Preprint

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“… 20 Moreover, overexpressing miR-143-3p inhibited the progression of cervical cancer, while CDK1 offset this effect. 21 However, until now, the relationship between miR-143-3p and CDK1 had not been reported in TNBC. Our results also revealed that miR-139-5p and miR-155-5p were associated with SMARCA4 across all four databases.…”

Section: Discussionmentioning

confidence: 97%

Microarray data reveal potential genes that regulate triple-negative breast cancer

Chi

Cong

2022

J Int Med Res

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Objective Triple-negative breast cancer (TNBC) is characterized by a lack of targeted therapies and poor patient prognosis, and its underlying pathological mechanisms remain unclear. This study aimed to identify potential key genes and related pathways that are required for TNBC development. Methods We screened the Gene Expression Omnibus database for transcriptome data and identified differently expressed genes in TNBC. Then, we performed Gene Ontology analysis to determine the genes and pathways involved in TNBC development. We correlated significantly expressed genes and miRNAs using miRDB, TargetScan, miRWalk, and DIANA, and then validated the expression of CDK1 and miR-143-3p in TNBC patients. Results Eighteen genes were significantly upregulated in TNBC patients, and these were found to be enriched in cell metabolic process, cell division, mitochondrion, and respiratory chain. MiR-143-3p was found to be an upstream regulator of CDK1. Validation experiments revealed that CDK1 was upregulated while miR-143-3p was downregulated in clinical TNBC specimens. Conclusions Collectively, our results revealed 18 upregulated genes in TNBC. Notably, CDK1 and its related microRNA miR-143-3p could be potential therapeutic targets for TNBC.

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“…Potential binding sites for CREB1 in the promoter of miR-495-3p, miR-495-3p and KPNA2 were predicted by using StarBase bioinformatics software. Plasmid construction and luciferase activity assays were performed as previously reported [5].…”

Section: Dual-luciferase Reporter Assaymentioning

confidence: 99%

“…MiRNAs inhibit gene expression at the post-transcriptional level by binding to the 3' untranslated region. An imbalance of miRNAs is related to tumorigenesis, proliferation, metastasis and drug resistance [5]. It has been reported that miR-495-3p dysregulation is closely related to tumour occurrence.…”

Section: Introductionmentioning

confidence: 99%

CREB1 regulates KPNA2 by inhibiting mir-495-3p transcription to control melanoma progression

Geng

Qiu

Gao

et al. 2022

BMC Mol and Cell Biol

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Background Melanoma is a common type of skin cancer, and its incidence is increasing gradually. Exploring melanoma pathogenesis helps to find new treatments. Objective We aimed to explore the potential molecular mechanisms by which CREB1 regulates melanoma. Methods TransmiR and ALGGEN were used to predict targets of CREB1 in the promoter of miR-495-3p or miR-495-3p and KPNA2, and a dual-luciferase reporter assay was performed to detect binding of CREB1 to these promoters. In addition, binding of CREB1 to the miR-495-3p promoter was confirmed by a ChIP assay. qRT‒PCR was carried out to detect mRNA levels of miR-495-3p, CREB1 and KPNA2. An EdU assay was conducted to detect cell viability. Transwell assays and flow cytometry were performed to assess cell migration and invasion and apoptosis, respectively. Moreover, factors associated with overall survival were analysed by using the Cox proportional hazards model. Results Our results show miR-495-3p to be significantly decreased in melanoma. Additionally, miR-495-3p overexpression inhibited melanoma cell viability. CREB1 targeted miR-495-3p, and CREB1 overexpression enhanced melanoma cell viability by inhibiting miR-495-3p transcription. Moreover, miR-495-3p targeted KPNA2, and CREB1 regulated KPNA2 by inhibiting miR-495-3p transcription to enhance melanoma cell viability. Conclusion CREB1 regulates KPNA2 by inhibiting miR-495-3p transcription to control melanoma progression. Our results indicate the molecular mechanism by which the CREB1/miR-495-3p/KPNA2 axis regulates melanoma progression.

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MiR-495-3p and miR-143-3p co-target CDK1 to inhibit the development of cervical cancer

Cited by 31 publications

References 24 publications

Prognostic value and mechanism of EPHB2 overexpression in cervical cancer

Prognostic value and mechanism of EPHB2 overexpression in cervical cancer

Microarray data reveal potential genes that regulate triple-negative breast cancer

CREB1 regulates KPNA2 by inhibiting mir-495-3p transcription to control melanoma progression

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