Evidence map›Paper›PMID 41053822›Full record

ReviewMolecular cancer2025

MALAT1 as a molecular driver of tumor progression, immune evasion, and resistance to therapy.

Amirreza Bitaraf, Alireza Zafarani, Pardis Jahandideh, Benyamin Hakak-Zargar, Atousa Haghi, Golareh Asgaritarghi, Sadegh Babashah

Abstract readReview
In one paragraph

Review in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed.

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  8. Methylation marks breast cancer metastasis: The roles of mThe Journal of biological chemistry · 2026
    Review
  9. Integrating multi-omics data for next-generation cancer research and precision medicine.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
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  15. LncRNA AC098613.1 promotes acute myeloid leukemia cell differentiation through CDC5L/ADAP1/NRD1 axis.Apoptosis : an international journal on programmed cell death · 2026
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Amirreza Bitaraf *Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, 14115-154, Tehran, Iran.
Alireza Zafarani *Department of Hematology, Allied Medical School, Iran , University of Medical Sciences, Tehran, Iran.
Pardis JahandidehNeuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
Benyamin Hakak-ZargarSchool of Medicine, Faculty of Health, Deakin University, Geelong, VIC, Australia.
Atousa HaghiHematology-Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Golareh AsgaritarghiDepartment of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, 14115-154, Tehran, Iran.
Sadegh BabashahDepartment of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, 14115-154, Tehran, Iran. babashah@modares.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) are emerging as important regulators of gene expression in both normal biological systems and disease. Among them, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has attracted considerable attention due to its high nuclear expression and evolutionary conservation. It was first identified as a biomarker for lung cancer metastasis, but since then, its involvement has been reported in a wide range of cancers. MALAT1 influences several key cancer-related processes, including cell proliferation, migration, angiogenesis, apoptosis, epithelial-mesenchymal transition, and the behavior of cancer stem cells. In this review, we take a closer look at how MALAT1 functions through different mechanisms, such as regulating RNA splicing, altering chromatin states, acting as a sponge for microRNAs, or modifying protein interactions, to drive these changes. We also discuss its growing role in shaping the immune landscape of tumors, particularly its involvement in immune evasion, inflammatory signaling, and regulation of immunogenic cell death. In addition, MALAT1 contributes to resistance against therapy, rewiring of cellular metabolism, and communication between tumor and stromal cells via exosomes. While many studies describe MALAT1 as an oncogene, others suggest it may also play a suppressive role depending on the cancer type and biological context. Here, we aim to offer a comprehensive overview of MALAT1's diverse actions and evaluate its potential as a diagnostic marker and therapeutic target in cancer.

Indexed as

Biomarkers, TumorDrug Resistance, NeoplasmImmune EvasionNeoplasmsRNA, Long NoncodingTumor EscapeAnimalsDisease ProgressionGene Expression Regulation, NeoplasticHumansBiomarkers, TumorMALAT1 long non-coding RNA, humanRNA, Long NoncodingBiomarkerCancer immunologyDrug resistanceEpithelial-mesenchymal transitionLong noncoding RNAMALAT1MicroRNA

Identifiers

PMID41053822
PMCPMC12502584

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.