ArticleCell cycle (Georgetown, Tex.)2017
MALAT1 promotes osteosarcoma development by regulation of HMGB1 via miR-142-3p and miR-129-5p.
Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 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
77 citing papers in PubMed.
- Deciphering lncRNA and circRNA control of autophagy in osteosarcoma mechanisms and clinical translation.Discover oncology · 2026Review
- HMGB1 and Its Signaling Pathway in Osteosarcoma: Current Advances in Targeted Therapy.Current issues in molecular biology · 2025Review
- Potential Regulation ofInternational journal of molecular sciences · 2025Article
- Targeting and engineering long non-coding RNAs for cancer therapy.Nature reviews. Genetics · 2024Review
- Osteosarcoma in a ceRNET perspective.Journal of biomedical science · 2024Review
- Deconstructing the role of MALAT1 in MAPK-signaling in melanoma: insights from antisense oligonucleotide treatment.Oncotarget · 2023Article
- Signal Pathways and microRNAs in Osteosarcoma Growth and the Dual Role of Mesenchymal Stem Cells in Oncogenesis.International journal of molecular sciences · 2023Review
- miR-29a-3p mitigates the development of osteosarcoma through modulating IGF1 mediated PI3k/Akt/FOXO3 pathway by activating autophagy.Cell cycle (Georgetown, Tex.) · 2022Article
- Circ-FOXM1 promotes the proliferation, migration and EMT process of osteosarcoma cells through FOXM1-mediated Wnt pathway activation.Journal of orthopaedic surgery and research · 2022Article
- Navigating the genomic instability mine field of osteosarcoma to better understand implications of non-coding RNAs.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2022Article
- Long noncoding RNA SNHG4: a novel target in human diseases.Cancer cell international · 2021Review
- Circulating Long Non-Coding RNAs as Novel Potential Biomarkers for Osteogenic Sarcoma.Cancers · 2021Review
- Downregulation of high mobility group box 1 enhances the radiosensitivity of non-small cell lung cancer by acting as a crucial target of microRNA-107.Experimental and therapeutic medicine · 2021Article
- The role of biomechanical forces and MALAT1/miR-329-5p/PRIP signalling on glucocorticoid-induced osteonecrosis of the femoral head.Journal of cellular and molecular medicine · 2021Article
- Damage-Associated Molecular Patterns Modulation by microRNA: Relevance on Immunogenic Cell Death and Cancer Treatment Outcome.Cancers · 2021Review
- HMGB1 as a therapeutic target in disease.Journal of cellular physiology · 2021Review
- Mechanism of Cyclic Tensile Stress in Osteogenic Differentiation of Human Periodontal Ligament Stem Cells.Calcified tissue international · 2021Article
- How metformin affects various malignancies by means of microRNAs: a brief review.Cancer cell international · 2021Review
- The Involvement of Long Non-Coding RNAs in Bone.International journal of molecular sciences · 2021Review
- miR-142-3p reduces the viability of human cervical cancer cells by negatively regulating the cytoplasmic localization of HMGB1.Experimental and therapeutic medicine · 2021Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, emerging evidence has demonstrated that metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNAs (lncRNAs), contributes to the initiation and development of tumors, including osteosarcoma (OS). Multiple studies have suggested an oncogenic role of MALAT1 and high-mobility group protein B1 (HMGB1) in OS tumorigenesis and metastasis, but the effects and mechanisms are not unanimous. Here, we showed that MALAT1 and HMGB1 were significantly increased in human OS cell lines and knockdown of MALAT1 reduced HMGB1 expression. By using online tools, we screen out 2 candidate miRNAs, miR-142-3p and miR-129-5p which may be associated with both MALAT1 and HMGB1. Luciferase reporter assay revealed a direct interaction between the 2 miRNAs and MALAT1, respectively, via a putative binding site within MALAT1. Meanwhile, both the 2 miRNAs could bind to HMGB1 3'-untranslated region (3'-UTR) and regulate HMGB1 expression. Moreover, knockdown of MALAT1 decreased HMGB1 expression, inhibited OS cell growth and promoted apoptosis, while miR-142-3p and miR-129-5p inhibitor partly restored the inhibitory effect of MALAT1 knockdown on HMGB1 expression, OS cell growth and the promotion of apoptosis. In OS tissues, the expression of MALAT1 and HMGB1 was upregulated while the expression of miR-142-3p and miR-129-5p was downregulated. Together, our results support a MALAT1/miR-142-3p/miR-129-5p/HMGB1 axis in OS cell proliferation and tumor progression. MALAT1 promoted OS cell growth through inhibition of miR-142-3p or miR-129-5p and by targeting HMGB1.
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.