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Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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A stem cell is an unspecialized cell that can divide without limit as needed and can, under specific conditions, differentiate into specialized cells.
Adult stem cells
Adult stem cells are tissue-specific; hence, they divide to develop the tissue from which they originate. One type of adult stem cell is the epithelial stem cell, which gives rise to the keratinocytes in the multiple layers of epithelial cells in the epidermis of the skin. Adult bone marrow has three distinct types of stem cells:...
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Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
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Stem cells are undifferentiated cells that divide and produce more stem cells or progenitor cells that differentiate into mature, specialized cell types. All the cells in the body are generated from stem cells in the early embryo, but small populations of stem cells are also present in many adult tissues including the bone marrow, brain, skin, and gut. These adult stem cells typically produce the various cell types found in that tissue—to replace cells that are damaged or to continuously...
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Embryonic stem (ES) cells are undifferentiated pluripotent cells, meaning they can produce any cell type in the body. This gives them tremendous potential in science and medicine since they can generate specific cell types for use in research or to replace body cells lost due to damage or disease.
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Stem cells are undifferentiated cells that divide and produce different types of cells. Ordinarily, cells that have differentiated into a specific cell type are post-mitotic—that is, they no longer divide. However, scientists have found a way to reprogram these mature cells so that they “de-differentiate” and return to an unspecialized, proliferative state. These cells are also pluripotent like embryonic stem cells—able to produce all cell types—and are therefore...
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Cancer stem cell (CSC) resistance drivers.

Masoud Najafi1, Keywan Mortezaee2, Jamal Majidpoor3

  • 1Radiology and Nuclear Medicine Department, School of Paramedical Sciences, Kermanshah University of Medical Sciences, Kermanshah, Iran.

Life Sciences
|August 21, 2019
PubMed
Summary

Cancer stem cells (CSCs) are resistant to cancer therapies due to intrinsic and extrinsic factors. This review explores CSC resistance mechanisms and strategies to overcome therapy failure.

Keywords:
Cancer stem cell (CSC)ChemotherapyDedifferentiationEpithelial-mesenchymal transition (EMT)PlasticityRadiotherapyReactive oxygen species (ROS)ResistanceStemnessTumor microenvironment (TME)

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Area of Science:

  • Oncology
  • Cancer Biology
  • Cellular Biology

Background:

  • Cancer stem cells (CSCs) possess self-renewal and high tumorigenic potential.
  • CSCs exhibit resistance to conventional therapies, exacerbated by radio- and chemotherapy.
  • This resistance is influenced by both intrinsic cellular mechanisms and the tumor microenvironment (TME).

Purpose of the Study:

  • To review the intrinsic and extrinsic mechanisms driving CSC therapy resistance.
  • To explore the role of the tumor microenvironment in CSC resistance.
  • To propose strategies for overcoming CSC-mediated therapy failure.

Main Methods:

  • Literature review of scientific articles on cancer stem cells and therapy resistance.
  • Analysis of intrinsic CSC mechanisms including autophagy, cell cycling, EMT, ROS scavenging, drug transport, and DNA repair.
  • Examination of extrinsic factors, focusing on the tumor microenvironment's influence on CSC adaptation and resistance.

Main Results:

  • CSCs employ protective autophagy, efficient cell cycling, and robust DNA repair systems.
  • Epithelial-mesenchymal transition (EMT) regulators, ROS scavengers, and drug transporters contribute to CSC resistance.
  • The TME, through nutritional/metabolic deprivation and hypoxia, actively promotes CSC adaptation and resistance.

Conclusions:

  • CSC resistance is a complex interplay of intrinsic capabilities and extrinsic TME factors.
  • Understanding these mechanisms is crucial for developing effective cancer treatments.
  • Targeting CSC resistance pathways offers a promising strategy to improve therapeutic outcomes and prevent therapy failure.