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Role of the tumor microenvironment in mediating de novo resistance to drugs and physiological mediators of cell death
Abstract
The emergence of clinical drug resistance continues to be an obstacle for the successful treatment of cancer. Our current understanding of mechanisms associated with drug resistance has been ascertained by investigating drug-resistant models created by exposing a parental population to increasing concentrations of a cytotoxic. These unicellular drug-resistant models have been critical in elucidating drug-resistant mechanism and in some cases have aided in the identification of drug targets. However, these models do not address resistance mechanisms that contribute to de novo drug resistance. We propose that specific niches within the tumor microenvironment may provide a sanctuary for subpopulations of tumors cells that affords a survival advantage following initial drug exposure and may facilitate the acquisition of acquired drug resistance. More specifically, we propose that the bone marrow microenvironment is a sanctuary for hema-topoietic cancers. This review will focus on the bone marrow microenvironment and its role in conferring resistance to cytotoxics and physiological mediators of cell death.
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“CAFs comprise the majority of cell types within the TME, and their reciprocal interactions with cancer cells have been well documented (Whiteside, 2008; Hazlehurst et al., 2003; Karnoub et al., 2007).”
From Tumor microenvironment derived exosomes pleiotropically modulate cancer cell metabolism (2016) · cites this paper as Hazlehurst et al., 2003
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“The role of integrin signaling in cancer cell survival and chemoresistance has also been demonstrated (Hazlehurst et al., 2003), including using 3D glioblastoma in vitro models (Janouskova et al., 2012).”
BackgroundMethodHumanized chondroitinase ABC sensitizes glioblastoma cells to temozolomide
Jaime‐Ramirez, A. C., Dmitrieva, N., Yoo, J. Y., Banasavadi‐Siddegowda, Y., Zhang, J., Relation, T., Bolyard, C. M., Wojton, J., & Kaur, B. (2017) · The Journal of Gene Medicine · doi:10.1002/jgm.2942 · Cited by 49
“Briefly three different glioma cell lines (Gli36ΔEGFR, U251 and U87ΔEGFR) grown in a three‐dimensional cell culture were incubated with β‐D‐xylopyranoside to reduce CSPG glycosylation.(17,18) Forty‐ eight hours post treatment, a moderate decrease in glioma sphere aggregation was observed in cells treated with β‐D‐xylo…”
A New α5β1 Integrin-Dependent Survival Pathway Through GSK3β Activation in Leukemic Cells
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“many tumors [23].”
Osteopontin-mediated enhanced hyaluronan binding induces multidrug resistance in mesothelioma cells
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“For instance, it has been reported that small cell lung cancer cells, myeloma cells, glioma cells and colon cancer cells were protected from apoptosis induced by various anticancer agents when the cells were plated on ECM (Damiano et al., 1999; Sethi et al., 1999; Uhm et al., 1999; Kouniavsky et al., 2002).”
InfluentialUltrasound-activated nanomaterials for sonodynamic cancer theranostics
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“Recently, accumulating evidence suggests that the extracellular microenvironment may also influence the drug response and acquisition of drug resistance in cancer cells [5,6].”
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“Accordingly, multidrug resistance and survival of tumor cells remain challenges in the treatment of various tumors (Groot et al., 2007, Hazlehurst et al., 2003).”
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“The interaction between tumours and stromal cells in the TME is mediated through cell adhesion molecules and/or soluble factors 49 .”
The mesenchymal tumor microenvironment
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Miniaturized pre-clinical cancer models as research and diagnostic tools
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“Given the ability of CAFs to change the extracellular matrix topology as a main component of tumor progression and anticancer drug resistance (42, 43), it was highly likely that the SCCs recruited fibroblasts in the TME to evade tumor dormancy and promote chemoresistance.”
BackgroundMony, U., Jawad, M., Seedhouse, C., Russell, N. H., & Pallis, M. (2008) · Leukemia · doi:10.1038/leu.2008.125 · Cited by 43
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“…(Allinen et al., 2004; Liao et al., 2018; Wang et al., 2017), tumor growth (Lyssiotis and Kimmelman, 2017; Whiteside, 2008), drug resistance (Hazlehurst et al., 2003; Sun, 2016; Trédan et al., 2007), immunosuppression (Arina et al., 2016; Cohen et al., 2017; Wang and DuBois, 2015), and…”
Intracellular trafficking of integrins in cancer cells
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Ovarian ascites-derived Hospicells promote angiogenesis via activation of macrophages
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“The complex interactions between cell types in this microenvironment regulate tumor growth, progression, metastasis, angiogenesis and resistance to chemotherapies [10–14].”
BackgroundKnock-down of P-glycoprotein reverses taxol resistance in ovarian cancer multicellular spheroids
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“We propose that et al (19) indicated the importance the microenvironment in mediating the expression of a functional drug resistance phenotype.”
Targeting Integrin α6 Stimulates Curative-Type Bone Metastasis Lesions in a Xenograft Model
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“Targeting laminin-binding integrins is particularly relevant to bone metastatic lesions as bone is a laminin-rich environment that provides a protective adhesion site for early metastatic tumors to survive standard chemotherapeutic agents (38-40).”
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“It has been well investigated in many malignancies that the lements of the tumor microenvironment could protect the tumor rom chemotherapy and death receptor-mediated apoptosis [7,8].”
BackgroundTargeting the bone marrow microenvironment in hematologic malignancies
Dalton, W. S., Hazlehurst, L., Shain, K. H., Landowski, T. H., & Alsina, M. (2004) · Seminars in Hematology · doi:10.1053/j.seminhematol.2004.02.001 · Cited by 40
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“It has been shown that cell-cell or cell-matrix adhesion processes are involved in chemoresistance (1).”
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A microarray based expression profiling of paclitaxel and vincristine resistant MCF-7 cells
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“Stromal cells may modulate the reaction of tumor cells to chemotherapy in various ways [2-5].”
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Extracellular Matrix Proteins Modulate Antimigratory and Apoptotic Effects of Doxorubicin
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“Dalton was the first to show that ECM is able to confer resistance to chemotherapy [3, 22, 23].”
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MSC-NPRA loop drives fatty acid oxidation to promote stemness and chemoresistance of gastric cancer
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Gender-specific differences in expression in human lymphoblastoid cell lines
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“drug classes [13,14] and may limit the translational potential of”
Background
Metadata
- Authors
- Hazlehurst, L. A., Landowski, T. H., & Dalton, W. S.
- Affiliations
- University of South Florida (US)
- Corresponding author
- Dalton, William S
- Venue
- Oncogene
- Published
- 2003-10-20
- Volume
- 22
- Issue
- 47
- Pages
- 7396-7402
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2041997066
- Cited by
- 203
- References
- 61
- Citations by year
- 2026: 2 · 2024: 2 · 2023: 8 · 2022: 5 · 2021: 6 · 2020: 19 · 2019: 2 · 2018: 3 · 2017: 9 · 2016: 14 · 2015: 9 · 2014: 10 · 2013: 12 · 2012: 18
- FWCI
- 1.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Keywords
- tumor microenvironment, acquired drug resistance, bone marrow microenvironment, hematopoietic tumors, cytotoxic drugs, cell death, cancer stem cells, hematopoietic stem cells
- MeSH terms
- Animals, Antineoplastic Agents, Cell Adhesion, DNA Damage, Humans, Neoplasms, Signal Transduction, Integrins, Apoptosis, Drug Resistance, Neoplasm
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