According to the CSC hypothesis, cancer stem cells are pivotal in initiating, developing, and causing cancer recurrence. Since the identification of CSCs in leukemia, breast cancer, glioblastoma, and colorectal cancer in the 1990s, researchers have actively investigated the origin and biology of CSCs. However, the CSC hypothesis and the role of these cells in tumor development model is still in debate. These cells exhibit distinct surface markers, are capable of self-renewal, demonstrate unrestricted proliferation, and display metabolic adaptation. CSC phenotypic plasticity and the capacity to EMT is strictly connected to the stemness state. CSCs show high resistance to chemotherapy, radiotherapy, and immunotherapy. The plasticity of CSCs is significantly influenced by tumor microenvironment factors, such as hypoxia. Targeting the genetic and epigenetic changes of cancer cells, together with interactions with the tumor microenvironment, presents promising avenues for therapeutic strategies. See also the Graphical abstract(Fig. 1).
Keyphrases
- cancer stem cells
- induced apoptosis
- cell cycle arrest
- signaling pathway
- locally advanced
- epithelial mesenchymal transition
- endoplasmic reticulum stress
- radiation therapy
- stem cells
- cell death
- gene expression
- papillary thyroid
- genome wide
- cancer therapy
- squamous cell carcinoma
- oxidative stress
- atomic force microscopy
- drug delivery
- mass spectrometry
- squamous cell
- pi k akt
- copy number
- high speed