Evidence map›Paper›PMID 39373948›Full record

ArticleJournal of applied genetics2025

Profiling mRNA and miRNA expression variations associated with cyclin-dependent kinase pathway in the low-grade luminal early breast cancer.

Amir Mahdi Khamaneh, Nasrin Mohajeri, Behrooz Naghili, Nosratollah Zarghami

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Article in Journal of applied genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Amir Mahdi KhamanehDepartment of Molecular Medicine, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
Nasrin MohajeriRecombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran. Mohajeri.Nasrin@gmail.com.
Behrooz NaghiliDepartment of Molecular Medicine, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
Nosratollah ZarghamiDepartment of Medical Biochemistry, Faculty of Medicine, Istanbul Aydin University, Istanbul, Turkey. Zarghamin@gmail.com.ORCID http://orcid.org/0000-0002-4236-4537

Funding

Tabriz University of Medical Sciences IR.TBZMED.REC.1396.60
6 · The paper itself

Abstract

Luminal A and B subtypes of breast tumors have fluctuated in proliferation rates, which arise from cell cycle dysregulation in cancer. Besides, microRNAs can regulate various cell processes through integration with mRNA. miRNAs that target the cell cycle are significant because of their prediction capability of prognosis. The objective of this study is to discover the integration between miRNA-mRNA and miRNA-miRNA related to cyclin-dependent kinase. Thirty-four pairs of human primary breast cancer and tumor margin samples from luminal breast cancer patients were investigated to assess the expression levels of CCND1, E2F1, miR-124, miR-503, miR-449a, and miR-449b. Afterward, the expression levels of mRNAs and miRNAs were investigated by real-time PCR. Statistical analysis was conducted to compare the expression levels between breast cancer and corresponding normal tissues. The protein expressions of E2F1 and CCND1 were verified by western blotting. Further, the correlation between mRNAs and miRNAs was calculated. E2F1 was significantly increased in both luminal A and B patients, while CCND1 was upregulated only in luminal B. Significant differences in all miRNAs were detected in both luminal A and B biopsy specimens (p < 0.0001). The correlation analysis revealed a positive strong correlation between miR-124 and E2F1 in luminal A patient. Moreover, the correlation test confirmed the ability of miR-449a to increase the CCND1 gene in luminal B subtypes. Also, miRNA correlation exhibited the miRNA-miRNA interaction in luminal breast cancer. This study demonstrated the novel miRNA-mRNA and miRNA-miRNA interactions, providing new insights into the molecular integration in luminal A and B patients. The authors propose that this research could contribute to introducing valuable biomarkers for luminal cancerous cells.

Indexed as

Breast NeoplasmsCyclin-Dependent KinasesMicroRNAsRNA, MessengerAdultBiomarkers, TumorCyclin D1E2F1 Transcription FactorFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMiddle AgedBiomarkers, TumorCCND1 protein, humanCyclin D1Cyclin-Dependent KinasesE2F1 protein, humanE2F1 Transcription FactorMicroRNAsRNA, MessengerBreast cancerCyclin-dependent kinaseLuminalMicroRNA

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.