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Background: Emerging evidence have illustrated the vital role of long noncoding RNAs (lncRNAs) long intergenic non-protein coding RNA 00511 (LINC00511) on the human cancer progression and tumorigenesis. However, the role of LINC00511 in breast cancer tumourigenesis is still unknown. This research puts emphasis on the function of LINC00511 on the breast cancer tumourigenesis and stemness, and investigates the in-depth mechanism.
Methods: The lncRNA and RNA expression were measured using RT-PCR. Protein levels were measured using western blotting analysis. CCK-8, colony formation assays and transwell assay were performed to evaluate the cell proliferation ability and invasion. Sphere-formation assay was also performed for the stemness. Bioinformatic analysis, chromatin immunoprecipitation (ChIP) and luciferase reporter assays were carried to confirm the molecular binding.
Results: LINC00511 was measured to be highly expressed in the breast cancer specimens and the high-expression was correlated with the poor prognosis. Functionally, the gain and loss-of-functional experiments revealed that LINC00511 promoted the proliferation, sphere-formation ability, stem factors (Oct4, Nanog, SOX2) expression and tumor growth in breast cancer cells. Mechanically, LINC00511 functioned as competing endogenous RNA (ceRNA) for miR-185-3p to positively recover E2F1 protein. Furthermore, transcription factor E2F1 bind with the promoter region of Nanog gene to promote it transcription.
Conclusion: In conclusion, our data concludes that LINC00511/miR-185-3p/E2F1/Nanog axis facilitates the breast cancer stemness and tumorigenesis, providing a vital insight for them.
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http://dx.doi.org/10.1186/s13046-018-0945-6 | DOI Listing |
Mol Cancer Ther
September 2025
Case Western Reserve University School of Medicine, Cleveland, OH, United States.
The estrogen receptor (ER or ERα) remains the primary therapeutic target for luminal breast cancer, with current treatments centered on competitive antagonists, receptor down-regulators, and aromatase inhibitors. Despite these options, resistance frequently emerges, highlighting the need for alternative targeting strategies. We discovered a novel mechanism of ER inhibition that targets the previously unexplored interface between the DNA-binding domain (DBD) and ligand-binding domain (LBD) of the receptor.
View Article and Find Full Text PDFJ Med Chem
September 2025
Department of Natural Products and Medicinal Chemistry, CSIR-Indian Institute of Chemical Technology, Hyderabad 500007, India.
Nitric oxide (NO) is a multifunctional signaling molecule in oncology, influencing tumor progression, apoptosis, and immune responses. In contrast, chlorambucil (Cbl), a DNA-alkylating chemotherapeutic, induces cytotoxicity through DNA damage. Here, we report a photoresponsive nanoparticle platform for sequential codelivery of NO and Cbl, where NO is released within 10 min of irradiation, followed by Cbl release within 30 min.
View Article and Find Full Text PDFJ Am Acad Audiol
September 2025
Paraneoplastic cerebellar degeneration (PCD) is a rare neurological disorder caused by tumor-mediated antibodies targeting the cerebellum, often leading to irreversible cerebellar damage. The most common antibody implicated in PCD is anti-Purkinje cell cytoplasmic antibody type-1, associated with malignancies such as breast, gynecological, and lung cancers. Symptoms often include dizziness, imbalance, progressive ataxia, and other cerebellar signs/symptoms, but early presentations may mimic acute vestibular syndrome, thus complicating diagnosis.
View Article and Find Full Text PDFStem Cell Rev Rep
September 2025
Paris Cité University, INSERM UMR-S 970, Paris Cardiovascular Research Centre, Paris, France.
Endothelial Colony-Forming Cells (ECFCs) are recognized as key vasculogenic progenitors in humans and serve as valuable liquid biopsies for diagnosing and studying vascular disorders. In a groundbreaking study, Anceschi et al. present a novel, integrative strategy that combines ECFCs loaded with gold nanorods (AuNRs) to enhance tumor radiosensitization through localized hyperthermia.
View Article and Find Full Text PDFAnn Surg Oncol
September 2025
Department of Surgery, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.