ArticleOncoTargets and therapy2020
Tumor-Derived Exosome-Educated Hepatic Stellate Cells Regulate Lactate Metabolism of Hypoxic Colorectal Tumor Cells via the IL-6/STAT3 Pathway to Confer Drug Resistance.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- The avatar principle: exosomal dynamics guiding tumor adaptation and next-generation therapeutic strategies.Journal of nanobiotechnology · 2026Review
- Colorectal cancer cells-derived exosomal miR-188-3p promotes liver metastasis by creating a pre-metastatic niche via activation of hepatic stellate cells.Journal of translational medicine · 2025Article
- Extracellular Vesicles as Mediators and Potential Targets in Combating Cancer Drug Resistance.Molecules (Basel, Switzerland) · 2025Review
- Probing the Depths of Molecular Complexity: STAT3 as a Key Architect in Colorectal Cancer Pathogenesis.Current gene therapy · 2025Review
- Unveiling the tumor microenvironment in colorectal cancer therapeutic resistance.Frontiers in cell and developmental biology · 2025Review
- New roles of tumor-derived exosomes in tumor microenvironment.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024Article
- Emerging roles of small extracellular vesicles in metabolic reprogramming and drug resistance in cancers.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- The biological function of tumor-derived extracellular vesicles on metabolism.Cell communication and signaling : CCS · 2023Review
- Unraveling the Emerging Niche Role of Hepatic Stellate Cell-derived Exosomes in Liver Diseases.Journal of clinical and translational hepatology · 2023Review
- Extracellular Vesicles in Colorectal Cancer: From Tumor Growth and Metastasis to Biomarkers and Nanomedications.Cancers · 2023Review
- Exosomes derived from MDR cells induce cetuximab resistance in CRC via PI3K/AKT signaling‑mediated Sox2 and PD‑L1 expression.Experimental and therapeutic medicine · 2023Article
- Role of exosomes in hepatocellular carcinoma and the regulation of traditional Chinese medicine.Frontiers in pharmacology · 2023Review
- Extracellular Vesicles in Cancer Drug Resistance: Roles, Mechanisms, and Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Review
- Exosomes in the hypoxic TME: from release, uptake and biofunctions to clinical applications.Molecular cancer · 2022Review
- The prognostic value of preoperative serum lactate dehydrogenase levels in patients underwent curative-intent hepatectomy for colorectal liver metastases: A two-center cohort study.Cancer medicine · 2021Article
- Targeting STAT3 Signaling Pathway in Colorectal Cancer.Biomedicines · 2021Review
- Regulation of signal transduction pathways in colorectal cancer: implications for therapeutic resistance.PeerJ · 2021Article
- The Mechanism of Warburg Effect-Induced Chemoresistance in Cancer.Frontiers in oncology · 2021Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeColorectal cancer cells spread to the liver and crosstalk with the microenvironment, and hepatic stellate cells (HSCs) are the major stromal components in the liver. However, the role of the interaction between colorectal tumor cells and HSCs in chemotherapeutic resistance remains unclear. The present study aimed to determine the mechanism of colorectal tumor cells educating the HSCs to reprogram the metabolism of adjacent tumor cells and fuel themselves in the metastatic microenvironment of the liver. PATIENTS AND
methodsImmunohistochemistry (IHC) examined the expression of the monocarboxylate transporters 1 (MCT1) and lactate dehydrogenase B (LDHB) in colorectal liver metastases (CRLM). The Mann-Whitney
resultsThe expression of MCT1 and LDHB was high in the liver metastases of irinotecan-resistant patients, and the high level of IL-6 in the plasma of patients with CRLM was associated with poor response to irinotecan-based chemotherapy. The colorectal tumor-derived exosomes activated HSCs to secrete excessive IL-6. Furthermore, the conditioned medium of activated HSCs enhanced the lactate metabolism of hypoxic tumor cells by activating the IL-6/STAT3 pathway and upregulating the downstream MCT1 and LDHB, in order to confer the resistance of SN38, which is the active metabolite of irinotecan.
conclusionTaken together, the cultured supernatant of normoxic exosome-educated HSCs enhances the lactate metabolism of hypoxic tumor cells via the IL-6/STAT3 pathway, in order to confer the SN38 resistance in a mimic liver metastatic microenvironment.
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