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Contribution of Tumor Microenvironment (Tme) to Tumor Apoptosis, Angiogenesis, Metastasis, and Drug Resistance Publisher Pubmed



Xiao Y1 ; Hassani M2 ; Moghaddam MB3 ; Fazilat A4 ; Ojarudi M5 ; Valilo M5
Authors
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Authors Affiliations
  1. 1. Harbin Medical University Cancer Hospital, Heilongjiang Province, Harbin, 150006, China
  2. 2. Faculty of Pharmacy, Near East University, Nicosia, Cyprus
  3. 3. School of Pharmacy, Yeditepe University, Istanbul, Turkey
  4. 4. Department of Genetics, Motamed Cancer Institute, Breast Cancer Research Center, ACECR, Tehran, Iran
  5. 5. Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran

Source: Medical Oncology Published:2025


Abstract

The tumor microenvironment (TME) contains tumor cells, surrounding cells, and secreted factors. It provides a favorable environment for the maintenance of cancer stem cells (CSCs), the spread of cancer cells to metastatic sites, angiogenesis, and apoptosis, as well as the growth, proliferation, invasion, and drug resistance of cancer cells. Cancer cells rely on the activation of oncogenes, inactivation of tumor suppressors, and the support of a normal stroma for their growth, proliferation, and survival, all of which are provided by the TME. The TME is characterized by the presence of various cells, including cancer-associated fibroblasts (CAFs), tumor-associated macrophages (TAMs), CD8 + cytotoxic T cells (CTLs), regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), mesenchymal stem cells (MSCs), endothelial cells, adipocytes, and neuroendocrine (NE) cells. The high expression of inflammatory cytokines, angiogenic factors, and anti-apoptotic factors, as well as drug resistance mechanisms in the TME, contributes to the poor therapeutic efficacy of anticancer drugs and tumor progression. Hence, this review describes the mechanisms through which the TME is involved in apoptosis, angiogenesis, metastasis, and drug resistance in tumor cells. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2025.
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