ArticleJournal of experimental & clinical cancer research : CR2018
SP1-induced lncRNA AGAP2-AS1 expression promotes chemoresistance of breast cancer by epigenetic regulation of MyD88.
Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 88 papers.
What it found
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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.
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Who cites it
88 citing papers in PubMed, 184 citations in OpenAlex.
- Multi-payload antibody-drug conjugates for photothermal dynamic and chemotherapy of HER2-positive breast cancer.Materials today. Bio · 2026Article
- A coagulation-related long non-coding RNA signature to predict prognosis and immune features of breast cancer.Discover oncology · 2025Article
- Epigenetic and epitranscriptomic role of lncRNA in carcinogenesis (Review).International journal of oncology · 2025Review
- Crosstalk between RNA-binding proteins and non-coding RNAs in tumors: molecular mechanisms, and clinical significance.International journal of biological sciences · 2025Review
- A mathematical model for predicting the spatiotemporal response of breast cancer cells treated with doxorubicin.Cancer biology & therapy · 2024Article
- STAT3-induced upregulation of lncRNA TTN-AS1 aggravates podocyte injury in diabetic nephropathy by promoting oxidative stress.Toxicology research · 2024Article
- Review
- H3K27ac-activated LncRNA NUTM2A-AS1 Facilitated the Progression of Colorectal Cancer CellsCurrent cancer drug targets · 2024Article
- Landscape of NcRNAs involved in drug resistance of breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Retraction Note: Exosome-mediated transfer of lncRNA PART1 induces gefitinib resistance in esophageal squamous cell carcinoma via functioning as a competing endogenous RNA.Journal of experimental & clinical cancer research : CR · 2023Article
- LncRNA SNHG4 Modulates EMT Signal and Antitumor Effects in Endometrial Cancer through Transcription Factor SP-1.Biomedicines · 2023Article
- Metformin and long non-coding RNAs in breast cancer.Journal of translational medicine · 2023Review
- EIF4A3 stabilizes the expression of lncRNA AGAP2-AS1 to activate cancer-associated fibroblasts via MyD88/NF-κb signaling.Thoracic cancer · 2023Article
- STAT3-mediated upregulation of LINC00520 contributed to temozolomide chemoresistance in glioblastoma by interacting with RNA-binding protein LIN28B.Cancer cell international · 2022Article
- LncRNA CRNDE hinders the progression of osteoarthritis by epigenetic regulation of DACT1.Cellular and molecular life sciences : CMLS · 2022Article
- H3K27ac-activated lncRNA KTN1-AS1 aggravates tumor progression by miR-505-3p/ZNF326 axis in ovarian cancer.Annals of translational medicine · 2022Article
- Long non-coding RNA AGAP2-AS1 promotes cell proliferation and invasion through regulating miR-193a-3p/LOXL4 axis in laryngeal squamous cell carcinoma.Cell cycle (Georgetown, Tex.) · 2022Article
- Article
- FOXO3-induced lncRNA LOC554202 contributes to hepatocellular carcinoma progression via the miR-485-5p/BSG axis.Cancer gene therapy · 2022Article
- New insights into the interplay between long non-coding RNAs and RNA-binding proteins in cancer.Cancer communications (London, England) · 2022Review
28 more citing papers are in PubMed but not listed here.
Corrections and comments
- Retraction · 2023-01-11Duplication of/in Image · Investigation by Third Party · Paper Mill · Unreliable Results and/or Conclusions · · see also: https://pubpeer.com/publications/C317EF3416E524BACA3D529F7C13C9
- Retracted
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundResistance to trastuzumab has become a leading cause of mortality in breast cancer patients and is one of the major obstacles for improving the clinical outcome. Cell behavior can be modulated by long non-coding RNAs (lncRNAs), but the contribution of lncRNAs in trastuzumab resistance to breast cancer is largely unknown. To this end, the involvement and regulatory function of lncRNA AGAP2-AS1 in human breast cancer are yet to be investigated.
methodsTrastuzumab-resistant SKBR-3 and BT474 cells were obtained by continuous culture with 5 mg/mL trastuzumab for 6 months. RT-qPCR assay was used to determine the expression of AGAP2-AS1 in tissues and cells. RNA fluorescence in situ hybridization was used to investigate the subcellular location of AGAP2-AS1 in breast cancer cells. Bioinformatic analysis, chromatin immunoprecipitation (ChIP), RNA immunoprecipitation (RIP), western blotting, and immunofluorescence were carried out to verify the regulatory interaction of AGAP2-AS1, CREB-binding protein (CBP), and MyD88. In addition, a series of in vitro assays and a xenograft tumor model were used to analyze the functions of AGAP2-AS1 in breast cancer cells.
resultsAGAP2-AS1 was upregulated and transcriptionally induced by SP1 in breast cancer. Overexpression of AGAP2-AS1 promoted cell growth, suppressed apoptosis, and caused trastuzumab resistance, whereas knockdown of AGAP2-AS1 showed an opposite effect. MyD88 was identified as a downstream target of AGAP2-AS1 and mediated the AGAP2-AS1-induced oncogenic effects. Mechanistically, the RIP assay revealed that AGAP2-AS1 could bind to CBP, a transcriptional co-activator. ChIP assays showed that AGAP2-AS1-bound CBP increased the enrichment of H3K27ac at the promoter region of MyD88, thus resulting in the upregulation of MyD88. Gain- and loss-of-function assays confirmed that the NF-κB pathway was activated by MyD88 and AGAP2-AS1. Furthermore, high AGAP2-AS1 expression was associated with poor clinical response to trastuzumab therapy in breast cancer patients.
conclusionAGAP2-AS1 could promote breast cancer growth and trastuzumab resistance by activating the NF-κB signaling pathway and upregulating MyD88 expression. Therefore, AGAP2-AS1 may serve as a novel biomarker for prognosis and act as a therapeutic target for the trastuzumab treatment.
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