ArticlePeerJ2020
Ginsenoside panaxatriol reverses TNBC paclitaxel resistance by inhibiting the IRAK1/NF-κB and ERK pathways.
Article in PeerJ, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 27 citations in OpenAlex.
- Targeting the tumor microenvironment: a new strategy for natural products in breast cancer therapy.Natural products and bioprospecting · 2026Review
- CXCL1 in triple‑negative breast cancer: Mechanisms, challenges, and therapeutic opportunities (Review).Oncology reports · 2026Review
- Tumor-Associated Macrophage-Derived CXCL1 Promotes Endometrial Cancer Progression Through the CXCR2/NF-κB Pathway.Cancer science · 2026Article
- The Significance of CXCL1 in Cancer: An Overview of Molecular Mechanisms.International journal of molecular sciences · 2026Review
- Research progress of ginseng active ingredients combined with chemotherapy in cancer therapy.Journal of ginseng research · 2026Review
- Panaxatriol exerts anti-senescence effects and alleviates osteoarthritis and cartilage repair fibrosis by targeting UFL1.Journal of advanced research · 2025Article
- Review
- Review
- IRE1α inhibitor enhances paclitaxel sensitivity of triple-negative breast cancer cells.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- The therapeutic potential of natural metabolites in targeting endocrine-independent HER-2-negative breast cancer.Frontiers in pharmacology · 2024Review
- Astragaloside IV enhances the sensitivity of breast cancer stem cells to paclitaxel by inhibiting stemness.Translational cancer research · 2023Article
- Ginsenosides: changing the basic hallmarks of cancer cells to achieve the purpose of treating breast cancer.Chinese medicine · 2023Review
- Natural-Product-Derived Adjunctive Treatments to Conventional Therapy and Their Immunoregulatory Activities in Triple-Negative Breast Cancer.Molecules (Basel, Switzerland) · 2023Review
- Involvement in Tumorigenesis and Clinical Significance of CXCL1 in Reproductive Cancers: Breast Cancer, Cervical Cancer, Endometrial Cancer, Ovarian Cancer and Prostate Cancer.International journal of molecular sciences · 2023Review
- Targeting regulated cell death (RCD) with small-molecule compounds in triple-negative breast cancer: a revisited perspective from molecular mechanisms to targeted therapies.Journal of hematology & oncology · 2022Review
- Zinc complex of 3,5-di-tert-butyl salicylate inhibits viability, migration, and invasion in triple-negative breast cancer cells.Scientific reports · 2022Article
- Ginsenosides: Allies of gastrointestinal tumor immunotherapy.Frontiers in pharmacology · 2022Review
- Anti-cancer effect and potential microRNAs targets of ginsenosides against breast cancer.Frontiers in pharmacology · 2022Review
- Growth Inhibitory Efficacy of Chinese Herbs in a Cellular Model for Triple-Negative Breast Cancer.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPaclitaxel (PTX) resistance is a major obstacle in the treatment of triple-negative breast cancer (TNBC). Previously, we have reported that interleukin-1 receptor-associated kinase 1 (IRAK1) and its downstream pathways are associated with PTX resistance in TNBC cells. In this study, we sought to investigate the combination treatment of ginsenoside panaxatriol (GPT), one of the main active components in
methodsCellTiter-Glo and colony formation assays were used to assess cell viability. Flow cytometry was used to analyze subG1 and apoptosis. Western blot was used to detect expressions of proteins involved in apoptosis and the IRAK1/NF-κB and ERK pathways. The mRNA expression of inflammatory cytokines, S100A7/8/9 and cancer stem cell (CSC)-related genes were examined by qPCR. Stem cells were identified by tumor sphere assay. Cell invasion ability was examined by transwell assay.
resultsWe show that GPT inhibits MDA-MB-231 PTX resistant (MB231-PR) cell viability in a dose-dependent manner. When combined with PTX, GPT synergistically causes more cell death, induces subG1 accumulation and cell apoptosis. Besides, up-regulation of BAX/BCL-2 ratio, and down-regulation of MCL-1 are also observed. Moreover, this combination inhibits IRAK1, NF-κB and ERK1/2 activation, and leads to down-regulation of inflammatory cytokines (IL6, IL8, CXCL1, CCL2), S100A7/9 and CSC-related genes (OCT4, SOX2, NANOG, ALDH1, CD44) expression. In addition, the combination treatment suppresses MB231-PR cell invasion ability, and impairs tumor sphere growth both in MB231-PR and SUM159 PTX resistant (SUM159-PR) cells.
conclusionOur study demonstrates that GPT can resensitize TNBC PTX resistant cells to PTX by inhibiting the IRAK1/NF-κB and ERK pathways and reducing stem cell characteristics.
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