Evidence map›Paper›PMID 41622408›Full record

ArticleJournal of the Egyptian National Cancer Institute2026

Significance of MALAT1 long non-coding RNA and miR-20a-5p in regulating epithelial mesenchymal transition in luminal breast cancer patients.

Gehad Tarek, Manar Fouda, Mohamed Omran, Gehan Safwat, Mahmoud Kamel, Abdel Hady Abdel Wahab

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Article in Journal of the Egyptian National Cancer Institute, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Gehad TarekDepartment of Chemistry, Faculty of Science, Helwan University, Cairo, Egypt.
Manar FoudaDepartment of Chemistry, Faculty of Science, Helwan University, Cairo, Egypt.
Mohamed OmranDepartment of Chemistry, Faculty of Science, Helwan University, Cairo, Egypt.
Gehan SafwatFaculty of Biotechnology, October University of Modern Sciences and Arts, Cairo, Egypt.
Mahmoud KamelDepartment of Clinical Pathology,, National Cancer Institute, Cairo University, Cairo, Egypt.
Abdel Hady Abdel WahabDepartment of Cancer Biology, National Cancer Institute, Cairo University, Cairo, Egypt. abdelhady.abdelwahab@nci.cu.edu.eg.

Funding

National Strategy for Biotechnology and Genetic Engineering, Academy of Science and Research (ASRT), Ministry of Higher Education and Scientific Research, Egypt 75D21
6 · The paper itself

Abstract

backgroundLuminal breast cancer (LBC) is the most common subtype of breast cancer affecting women worldwide. Although luminal breast cancer typically has a better prognosis, it mostly responds poorly to neoadjuvant chemotherapy. Non-coding RNAs, especially long non-coding RNAs and microRNAs are crucial in regulating biological processes that contribute to breast cancer development. MALAT1, a long non-coding RNA, is pivotal in the progression of breast cancer. Epithelial-mesenchymal transition (EMT) is critical for cell movement during embryonic development. Clarifying this role could pave various avenues for developing innovative strategies for combating this subtype of malignancy. The present study aimed to investigate the expression profiles and clinical relevance of MALAT1 level and EMT-related miRNAs (miR-17-5p, miR-20a-5p, miR-93-5p, miR-135b-5p, and miR-146a-5p) alongside EMT markers (E-cadherin, N-cadherin, vimentin, fibronectin, twist, SNAI1, Slug, ZEB1, and ZEB2) in LBC patients.

methodsFresh tissues were collected from fifty patients and twenty noncancerous controls. Differential expression of the markers was evaluated using qRT-PCR assay. Spearman Rho test assessed the relationship between the expression levels. Linear regression test evaluated the correlation between the parameters and various clinico-pathological features.

resultsOur results revealed an overall upregulation of MALAT1 in breast cancer tissues although this increase did not reach statistical significance. Overexpression of miR-20a-5p, miR-135b, and ZEB2 was reported, whereas miR146a-5p, ZEB1 and Vimentin levels were suppressed. Correlation analysis demonstrated that miR-20a-5p was positively correlated with SNAI1, E-cadherin, N-cadherin and Slug also it was significantly associated with family history and tumor laterality.

conclusionsOur findings suggest that miR-20a-5p plays an oncogenic role in luminal breast cancer by promoting EMT, while MALAT1 may contribute to disease progression through indirect regulatory mechanisms. Finally, MALAT1 and miR-20a-5p might serve as potential therapeutic and prognostic targets in LBC.

Indexed as

Breast NeoplasmsEpithelial-Mesenchymal TransitionMicroRNAsRNA, Long NoncodingAdultBiomarkers, TumorFemaleGene Expression Regulation, NeoplasticHumansMiddle AgedPrognosisBiomarkers, TumorMALAT1 long non-coding RNA, humanMicroRNAsMIRN20a microRNA, humanRNA, Long NoncodingBreast cancerLuminal subtypeMALAT1MicroRNAmiR-20a-5pNon-coding RNA

Identifiers

PMID41622408
PMCPMC13262381

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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.