ArticleScientific reports2023
A1BG-AS1 promotes adriamycin resistance of breast cancer by recruiting IGF2BP2 to upregulate ABCB1 in an m6A-dependent manner.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- The role, regulatory mechanisms, and therapeutic implications of FTO in gastrointestinal cancer.Genes & diseases · 2026Review
- Potential regulatory role of the mActa biochimica et biophysica Sinica · 2025Review
- Reciprocal regulation between m6 A modifications and non-coding RNAs: emerging roles in cancer therapeutic resistance.Discover oncology · 2025Review
- Interactions between long non-coding RNAs and m6 A modification in cancer.Discover oncology · 2025Review
- IGF2BP2: an mCellular & molecular biology letters · 2025Review
- Article
- Multifaceted roles of insulin‑like growth factor 2 mRNA binding protein 2 in human cancer (Review).Molecular medicine reports · 2025Review
- Decoding breast cancer treatment resistance through genetic, epigenetic, and immune-regulatory mechanisms: from molecular insights to translational perspectives.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Epitranscriptomic RNA mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- The Emerging Role of IGF2BP2 in Cancer Therapy Resistance: From Molecular Mechanism to Future Potential.International journal of molecular sciences · 2024Review
- Decoding the epitranscriptome: a new frontier for cancer therapy and drug resistance.Cell communication and signaling : CCS · 2024Review
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Adriamycin (ADR) resistance is an obstacle for chemotherapy of breast cancer (BC). ATP binding cassette subfamily B member 1 (ABCB1) expression is indicated to be closely related to the drug resistance of cancer cells. The current work intended to explore the molecular mechanisms to regulate ABCB1 in BC cells with ADR resistance. We found that long noncoding RNA (lncRNA) A1BG antisense RNA 1 (A1BG-AS1) is upregulated in ADR resistant BC cell lines (MCF-7/ADR, MDA-MB-231/ADR). A1BG-AS1 knockdown enhanced the ADR sensitivity by suppressing the viability, proliferation potential and migration ability, and facilitating cell apoptosis in BC. Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) is known to be an m6A reader to modulate the stability of mRNA transcripts in an m6A-dependent manner, which was a shared RNA binding protein (RBP) for A1BG-AS1 and ABCB1. The interaction of IGF2BP2 with A1BG-AS1 or ABCB1 was explored and verified using RNA pulldown and RNA immunoprecipitation (RIP) assays. ABCB1 mRNA and protein expression was positively regulated by A1BG-AS1 and IGF2BP2 in BC cells. ABCB1 mRNA expression was stabilized by A1BG-AS1 via recruiting IGF2BP2 in an m6A-dependent manner. Moreover, rescue assays demonstrated that A1BG-AS1 enhanced BC ADR resistance by positively modulating ABCB1. Xenograft mouse models were used to explore whether A1BG-AS1 affected the ADR resistance in BC in vivo. The findings indicated that A1BG-AS1 silencing inhibited tumor growth and alleviated ADR resistance in vivo. In conclusion, A1BG-AS1 enhances the ADR resistance of BC by recruiting IGF2BP2 to upregulate ABCB1 in an m6A-dependent manner.
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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.