ArticleCell death & disease2021
LncRNA MALAT1 promotes gastric cancer progression via inhibiting autophagic flux and inducing fibroblast activation.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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.
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.
Who cites it
46 citing papers in PubMed, 54 citations in OpenAlex.
- Exploring the Clinical Landscape of Long Non-coding RNAs in Cancer Diagnosis and Therapy.Biochemical genetics · 2026Review
- Interpretable Cancer Survival Prediction by Fusing Semantic Labelling of Cell Types and Whole Slide Images.Interdisciplinary sciences, computational life sciences · 2026Article
- Linc-ROR orchestrates autophagy suppression and marks gastric cancer via the miR-145-5p/CARMIL1 axis.Cell biology and toxicology · 2026Article
- Pericytes as key mediators of microenvironmental signaling crosstalk: implications in vascular diseases and cancer.Frontiers in cell and developmental biology · 2026Review
- From Tumor Biology to Clinical Perspectives: Novel Biomarkers and Therapeutic Insights in Gastric Cancer.Oncology research · 2026Review
- Remodeling the Stroma: The Role of ncRNAs in Cancer-Associated Fibroblasts and Therapeutic Implications for Digestive Tumors.Drug design, development and therapy · 2026Review
- Advances in protein microarray-based proteomics for gastric cancer applications in biomarker discovery, molecular subtyping, and precision oncology.Frontiers in oncology · 2026Review
- The RNA-binding protein ELAVL1 promotes Beclin1-mediated cellular autophagy and thus endometrial cancer development by affecting LncRNA-neat stability.Cancer biology & therapy · 2025Article
- Radiotherapy affects the ELAVL1-mediated autophagy pathway by promoting the release of LINC01943 exosomes in breast cancer cells to accelerate the M2 polarization of macrophages.Medical oncology (Northwood, London, England) · 2025Article
- MALAT1 as a molecular driver of tumor progression, immune evasion, and resistance to therapy.Molecular cancer · 2025Review
- Construction and Analysis of Immune Infiltration and Competing Endogenous RNA Network in Moyamoya Disease.International journal of molecular sciences · 2025Article
- The mechanism by which MALAT1/CREG1 regulates premature rupture of fetal membrane through autophagy mediated differentiation of amniotic fibroblasts.Non-coding RNA research · 2025Article
- Fluorescence imaging of MALAT1 expression using a Cy5.5-labeled antisense oligonucleotide in lung cancer and epidermal carcinoma cells.Cancer imaging : the official publication of the International Cancer Imaging Society · 2025Article
- LncRNA-Protein Interactions: A Key to Deciphering LncRNA Mechanisms.Biomolecules · 2025Review
- Autophagy mediated immune response regulation and drug resistance in cancer.Molecular biology reports · 2025Review
- Macrophage-Derived Exosomal MALAT1 Regulates Autophagy through miR-204-5p/ATG7 Axis in H9C2 Cardiomyocytes and Diabetic Rat Heart.Acta Cardiologica Sinica · 2025Article
- Exploring the Putative Involvement of MALAT1 in Mediating the Beneficial Effect of Exendin-4 on Oleic Acid-Induced Lipid Accumulation in HepG2 Cells.Biomedicines · 2025Article
- Integrative single-cell atlas unveils heterogeneity and prognostic value of cancer-associated fibroblasts in gastric cancer.Frontiers in oncology · 2025Article
- LncRNA in gastric cancer drug resistance: deciphering the therapeutic strategies.Frontiers in oncology · 2025Review
- Deciphering the Landscape of GATA-Mediated Transcriptional Regulation in Gastric Cancer.Antioxidants (Basel, Switzerland) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy defection contributes to inflammation dysregulation, which plays an important role in gastric cancer (GC) progression. Various studies have demonstrated that long noncoding RNA could function as novel regulators of autophagy. Previously, long noncoding RNA MALAT1 was reported upregulated in GC cells and could positively regulate autophagy in various cancers. Here, we for the first time found that MALAT1 could promote interleukin-6 (IL-6) secretion in GC cells by blocking autophagic flux. Moreover, IL-6 induced by MALAT1 could activate normal to cancer-associated fibroblast conversion. The interaction between GC cells and cancer-associated fibroblasts in the tumour microenvironment could facilitate cancer progression. Mechanistically, MALAT1 overexpression destabilized the PTEN mRNA in GC cells by competitively interacting with the RNA-binding protein ELAVL1 to activate the AKT/mTOR pathway for impairing autophagic flux. As a consequence of autophagy inhibition, SQSTM1 accumulation promotes NF-κB translocation to elevate IL-6 expression. Overall, these results demonstrated that intercellular interaction between GC cells and fibroblasts was mediated by autophagy inhibition caused by increased MALAT1 that promotes GC progression, providing novel prevention and therapeutic strategies for GC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.