ArticleCell & bioscience2015
Hypoxia and TGF-β1 lead to endostatin resistance by cooperatively increasing cancer stem cells in A549 transplantation tumors.
Article in Cell & bioscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Targeting myeloid-derived suppressor cells by inhibiting hypoxia-inducible factor 1α could improve tumor progression.Annals of medicine and surgery (2012) · 2024Article
- Hypoxic microenvironment in cancer: molecular mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2023Review
- Review
- Roles of the Exosomes Derived From Myeloid-Derived Suppressor Cells in Tumor Immunity and Cancer Progression.Frontiers in immunology · 2022Review
- Targeting Myeloid-Derived Suppressor Cells to Enhance the Antitumor Efficacy of Immune Checkpoint Blockade Therapy.Frontiers in immunology · 2021Review
- Green Synthesized Honokiol Transfersomes Relieve the Immunosuppressive and Stem-Like Cell Characteristics of the Aggressive B16F10 Melanoma.International journal of nanomedicine · 2021Article
- TGF-β1 mediates the effects of aspirin on colonic tumor cell proliferation and apoptosis.Oncology letters · 2018Article
- The Antiproliferative and Colony-suppressive Activities of STAT3 Inhibitors in Human Cancer Cells Is Compromised Under Hypoxic Conditions.Anticancer research · 2017Article
- MMP-14 and TGFβ-1 methylation in pituitary adenomas.Oncology letters · 2016Article
- The accumulation of macrophages attenuates the effect of recombinant human endostatin on lung cancer.OncoTargets and therapy · 2016Article
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13 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundLung cancer is the leading cause of cancer-related deaths worldwide, and treatments for lung cancer have a high failure rate. Anti-angiogenic therapy is also often ineffective because of refractory disease. Endostatin (ES) is one of the most widely-used anti-angiogenic drugs for lung cancer in China, and resistance to it is a barrier that needs to be resolved. It has been shown that myeloid-derived suppressor cells (MDSCs) are involved in resistance to ES. Whether other cells and/or cell factors in the tumor microenvironment that have been shown to be related to resistance to other anti-cancer drugs are also involved in ES resistance is unknown.
resultsIn this study, we showed that after continuously treatment with ES for 12 days, volumes of A549 transplantation tumors of mice reached the sizes of tumors which were borne by mice that were treated with normal saline and this meant that resistance to ES appeared. Cancer stem cells (CSCs), which have been widely accepted as one of reasons responsible for resistance to many anti-tumor drugs were also being discovered increased proportionally in A549 transplantation tumors after ES treatment for 12 days. During further exploration of reasons for this increase, we discovered that after ES treatment, microvessel density and vascular endothelial growth factor level was decreased in tumors, whereas transforming growth factor (TGF)-β1 level was elevated, and MDSCs, one of the sources of TGF-β1, were also increased. We speculate that hypoxia and TGF-β1 are responsible for the increased CSC number in A549 transplantation tumors. By using cobalt chloride to mimic hypoxia and human recombinant TGF-β1 in vitro, we found that hypoxia and TGF-β1can indeed enhance the stemness of A549 cells. In addition, the inductive effect of hypoxia is stronger than TGF-β1, and the combination of both is stronger than either alone, which is first report of such a finding, to our knowledge.
conclusionsIncreased TGF-β1 and strengthened hypoxia in A549 transplantation tumors, as a result of ES therapy, cooperatively increase proportion of CSCs that are involved in ES resistance which was revealed by failure of tumor volume repression after continuously treatment with ES for 12 days.
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