Tumor microenvironment-mediated chemoresistance in breast cancer.
Therapy resistance or tumor relapse in cancer is common. Tumors develop resistance to chemotherapeutic through a variety of mechanisms, with tumor microenvironment (TM) serving pivotal roles. Using breast cancer as a paradigm, we propose that responses of cancer cells to drugs are not exclusively determined by their intrinsic characteristics but are also controlled by deriving signals from TM. Affected microenvironment by chemotherapy is an avenue to promote phenotype which tends to resist on to be ruined. Therefore, exclusively targeting cancer cells does not demolish tumor recurrence after chemotherapy. Regardless of tumor-microenvironment pathways and their profound influence on the responsiveness of treatment, diversity of molecular properties of breast cancer also behave differently in terms of response to chemotherapy. And also it is assumed that there is cross-talk between phenotypic diversity and TM. Collectively, raising complex signal from TM in chemotherapy condition often encourages cancer cells are not killed but strengthen. Here, we summarized how TM modifies responses to chemotherapy in breast cancer. We also discussed successful treatment strategies have been considered TM in breast cancer treatment.
Department of Anatomical Science, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran; Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Kobra
K
Velaei
Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Nasser
N
Samadi
Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Balal
B
Barazvan
Department of Anatomical Science, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran; Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: soleimanirj@yahoo.com.
Jafar
J
Soleimani Rad
D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001943:Breast Neoplasms / Q000188:drug therapy*; D018925:Chemokines / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D019008:Drug Resistance, Neoplasm / Q000276:immunology / Q000502:physiology*; D042783:Endothelial Cells / Q000166:cytology; D005109:Extracellular Matrix / Q000502:physiology; D005347:Fibroblasts / Q000166:cytology; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000502:physiology; D016246:Lymphocytes, Tumor-Infiltrating / Q000166:cytology / Q000276:immunology; D008264:Macrophages / Q000166:cytology / Q000276:immunology; D059630:Mesenchymal Stem Cells / Q000166:cytology; D017154:Stromal Cells / Q000166:cytology; D000072258:Tumor Hypoxia / Q000502:physiology; D059016:Tumor Microenvironment / Q000276:immunology / Q000502:physiology*
D000970:Antineoplastic Agents; D018925:Chemokines; D016207:Cytokines; D036341:Intercellular Signaling Peptides and Proteins
Breast cancer; Chemoresistance; Stromal cells; Tumor microenvironment