Table 1.

Factors influencing the cellular apoptosis in breast cancer

Factors	Expression level	Impact on tumor development	Detailed impact on mechanism	References
Fas/FasL	Fas↓	Induce apoptosis	Activate apoptosis signaling and induce apoptosis in the cells in which this receptor interacts with its ligand – FasL	28
	FasL↑	Decrease immunity	Maintain a proapoptotic environment	29
			Induce effector T lymphocytes to death and stimulate activation-induced cell death and escape immune recognition and interference	8, 30
PD-1/PD-1L	↑	Inhibit apoptosis	Inhibit the activation of effector T cells, which induce FasL and interleukin-10	32
			Attenuate T cell apoptosis	34
			Stimulate tumor regression, improve the outcomes, and prove clinically effective when PD-1/PD-L1 pathway is targeted and PD-1 is blocked	46, 49–51
Bcl-2	↑	Inhibit apoptosis	Inhibit the release of cytochrome C from mitochondria to the cytoplasm and the TRAIL-induced cellular apoptosis	55, 56
		Promote growth	Promote neoplastic transformation and prolong the life span of tumor cells by allowing them to accumulate oncogene mutations and stimulate the growth of BC cells	57, 58
Survivin	↑	Inhibit apoptosis	Associated with poorer outcome, advanced tumor grade, worse metastasis, and lower survival rate	59, 60
Caspase	↓	Promote apoptosis	Resist apoptosis by the downregulation of caspase activation	61

Notes: Various factors that can influence the programmed apoptosis are listed in the table along with their impacts on the cellular apoptosis in breast cancer. ↑ means upregulation and ↓ means downregulation.

Abbreviations: Fas, factor-associated suicide; FasL, Fas ligand; PD-1, programmed death receptor 1; PD-1L, PD-1 ligand; TRAIL, TNF-related apoptosis-inducing ligand; BC, breast cancer.