| Abstract: Over the past decade, there have been remarkable advances in understanding the signaling pathways involved in cancer development. It is well-established that cancer is caused by the
dysregulation of cellular pathways involved in proliferation, cell cycle, apoptosis, cell metabolism,
migration, cell polarity, and differentiation. Besides, growing evidence indicates that extracellular
matrix signaling, cell surface proteoglycans, and angiogenesis can contribute to cancer development.
Given the genetic instability and vast intra-tumoral heterogeneity revealed by the single-cell sequencing of tumoral cells, the current approaches cannot eliminate the mutating cancer cells. Besides,
the polyclonal expansion of tumor-infiltrated lymphocytes in response to tumoral neoantigens cannot
elicit anti-tumoral immune responses due to the immunosuppressive tumor microenvironment.
Nevertheless, the data from the single-cell sequencing of immune cells can provide valuable insights
regarding the expression of inhibitory immune checkpoints/related signaling factors in immune
cells, which can be used to select immune checkpoint inhibitors and adjust their dosage. Indeed,
the integration of the data obtained from the single-cell sequencing of immune cells with immune
checkpoint inhibitors can increase the response rate of immune checkpoint inhibitors, decrease the
immune-related adverse events, and facilitate tumoral cell elimination. This study aims to review key
pathways involved in tumor development and shed light on single-cell sequencing. It also intends to
address the shortcomings of immune checkpoint inhibitors, i.e., their varied response rates among
cancer patients and increased risk of autoimmunity development, via applying the data from the
single-cell sequencing of immune cells. |