ArticleCancer management and research2020
ANLN Directly Interacts with RhoA to Promote Doxorubicin Resistance in Breast Cancer Cells.
Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- VIRMA/IGF2BP3-mediated ANLN upregulation promotes intrahepatic cholangiocarcinoma growth by forming a positive feedback loop with RhoA/YAP1/TEAD1 signaling pathway.Cell death & disease · 2026Article
- Integrative analysis of fatty acid metabolism and identification ofJournal of thoracic disease · 2025Article
- Functions of RhoA in the female reproductive system.Reproductive and developmental medicine · 2025Review
- Drug Resistance Analysis of Pancreatic Cancer Based on Universally Differentially Expressed Genes.International journal of molecular sciences · 2025Article
- Anillin interacts with RhoA to promote tumor progression in anaplastic thyroid cancer by activating the PI3K/AKT pathway.Endocrine · 2025Article
- The role of ANLN in malignant tumors: pathogenesis, treatment resistance and targeted strategies.Frontiers in cell and developmental biology · 2025Review
- Comprehensive characterization of stemness-related lncRNAs in triple-negative breast cancer identified a novel prognostic signature related to treatment outcomes, immune landscape analysis and therapeutic guidance: a silico analysis with in vivo experiments.Journal of translational medicine · 2024Article
- Anillin contributes to prostate cancer progression through the regulation of IGF2BP1 to promote c-Myc and MAPK signaling.American journal of cancer research · 2024Article
- BMSCs overexpressed ISL1 reduces the apoptosis of islet cells through ANLN carrying exosome, INHBA, and caffeine.Cellular and molecular life sciences : CMLS · 2022Article
- ANLN and UBE2T are prognostic biomarkers associated with immune regulation in breast cancer: a bioinformatics analysis.Cancer cell international · 2022Article
- A Four-Gene Prognostic Signature Based on the TEAD4 Differential Expression Predicts Overall Survival and Immune Microenvironment Estimation in Lung Adenocarcinoma.Frontiers in pharmacology · 2022Article
- Comprehensive bioinformatics analysis reveals the prognostic value, predictive value, and immunological roles of ANLN in human cancers.Frontiers in genetics · 2022Article
- Alternatively spliced ANLN isoforms synergistically contribute to the progression of head and neck squamous cell carcinoma.Cell death & disease · 2021Article
- Integrated Chromatin Accessibility and Transcriptome Landscapes of Doxorubicin-Resistant Breast Cancer Cells.Frontiers in cell and developmental biology · 2021Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChemotherapy resistance is the leading cause of cancer treatment failure. This research was conducted to explore a potential link between actin-binding protein anillin (ANLN) and doxorubicin resistance in breast cancer. MATERIALS AND
methodsWe compared ANLN expression and 50% inhibition concentration (IC50) of doxorubicin in human breast cancer cells (MDA-MB-231) and human breast cancer cells with doxorubicin resistance (MDA-MB-231/ADM). Co-immunoprecipitation was used to investigate the interaction between ANLN and RhoA. The cell viability, apoptosis, gene and protein expression were estimated by MTT, flow cytometry, quantitative real-time PCR and western blot.
resultsThe doxorubicin resistance in MDA-MB-231/ADM cells (IC50 = 19.40 ± 1.16 μg/mL) was significantly higher than that in MDA-MB-231 cells (IC50 = 1.65 ± 0.23 μg/mL). ANLN was up-regulated in MDA-MB-231/ADM cells compared to MDA-MB-231 cells. Furthermore, ANLN overexpression promoted cell viability and inhibited apoptosis of MDA-MB-231 cells. The gene and protein expression of multidrug resistance (MDR1) and cancer resistance protein (BCRP) were enhanced by ANLN overexpression in MDA-MB-231 cells. ANLN silencing suppressed cell viability and the expression of MDR1 and BCRP and facilitated apoptosis in MDA-MB-231/ADM cells. Moreover, ANLN promoted RhoA activation by interacting with RhoA. ANLN up-regulation enhanced cell viability and the expression of MDR1 and BCRP and decreased apoptosis of MDA-MB-231 cells. The influence conferred by ANLN overexpression was effectively abolished by C3 transferase.
conclusionThis work revealed that ANLN promoted doxorubicin resistance in breast cancer cells by activating RhoA. Thus, our study suggests a novel target for breast cancer treatment.
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