ArticleInternational journal of molecular and cellular medicine2021
Knockdown of SOX12 Expression Induced Apoptotic Factors is Associated with TWIST1 and CTNNB1 Expression in Human Acute Myeloid Leukemia Cells.
Article in International journal of molecular and cellular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- The oncogenic potential of SOX12: a comprehensive and perspective view.Journal of translational medicine · 2026Review
- Systematic profiling reveals distinct senescence signatures and regulators across human brain cell types.Nature communications · 2025Article
- Regulatory Network Inference of Induced Senescent Midbrain Cell Types Reveals Cell Type-Specific Senescence-Associated Transcriptional Regulators.bioRxiv : the preprint server for biology · 2025Article
- Non-Coding RNAs: Foes or Friends for Targeting Tumor Microenvironment.Non-coding RNA · 2023Review
- Effects of hsa-piR-32877 Suppression with Antisense LNA GapmeRs on the Proliferation and Apoptosis of Human Acute Myeloid Leukemia Cells.International journal of molecular and cellular medicine · 2023Article
- Bioinformatic Analyses of Broad H3K79me2 Domains in Different Leukemia Cell Line Data Sets.Cells · 2022Article
- CircRNAs as New Therapeutic Entities and Tools for Target Identification in Acute Myeloid Leukemia.Cancer genomics & proteomicsReview
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent improvements in molecular treatment and gene therapy led to discovering novel cancer remedies. Antisense LNA GapmeRs is a state-of-the-art molecular research field for diagnosing and treating various cancer types. Acute myeloid leukemia (AML) is a heterogeneous hematopoietic malignancy defined by the rapid accumulation and malignant proliferation of immature myeloid progenitors. SOX12 is a new potential target for acute myeloid leukemia. In this study, SOX12 was blocked by antisense LNA GapmeRs (ALG) in human AML cell lines (KG1 and M07e). Cells were transfected with Gapmer anti-
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