Copyright
©The Author(s) 2024.
World J Clin Oncol. Feb 24, 2024; 15(2): 208-242
Published online Feb 24, 2024. doi: 10.5306/wjco.v15.i2.208
Published online Feb 24, 2024. doi: 10.5306/wjco.v15.i2.208
Gene | Full name | Role in ATP induced cell death | Ref. |
P2RX7 | Purinergic receptor P2X7 | Activate inflammatory mediators and increase calcium ions | Tamajusuku et al[22] |
CASP3 | Caspase-3 | Caspase-3 cleavage by caspase-1/4/5/11 forms pores, releasing pro-inflammatory cytokines | Souza et al[1] |
PANX1 | Pannexin-1 | P2X7 activation opens PANX1 channels, releasing ATP and triggering cell death pathways | Shoji et al[36] |
NLRP3 | NOD-like receptor family pyrin domain-containing protein 3 | NLRP3 activated by stimuli forms inflammasome, triggers caspase-1 activation, releases cytokines, and induces apoptosis | Sadatomi et al[37] |
CASP1 | Caspase-1 | Caspase-1 induces cytokine processing, pyrosis, and inflammation | Sadatomi et al[37] |
P2RY1 | P2Y purinoceptor 1 | P2RY1 can increase calcium ions in the Golgi apparatus | Ohishi et al[38] |
P2RY11 | P2Y purinoceptor 11 | Involved in immune inflammatory mechanisms | Yoon et al[39] |
ORAI1 | Calcium release-activated calcium channel protein 1 | Increased intracellular calcium ions | Peng et al[26] |
STIM1 | Stromal interaction molecule 1 | STIM1 responds to ATP-induced calcium influx, activating ORAI1 and promoting cell death | Peng et al[26] |
CASP8 | Caspase-8 | CASP8 causes apoptosis | Zhao et al[40] |
CASP9 | Caspase-9 | CASP9 causes apoptosis | Zhao et al[40] |
CASP7 | Caspase-7 | CASP7 causes apoptosis | Zhao et al[40] |
P2RX3 | Purinergic receptor P2X3 | NA | Ohishi et al[38] |
NLRP1 | NLR family pyrin domain-containing protein 1 | NLRP1 activates caspase-1, induces pyrodeath, and releases IL-1β and IL-18 | Zhao et al[41] |
P2RX4 | P2X purinoceptor 4 | P2RX4 contributes to AICD (pyroptosis) by activating the NLRP3 inflammasome, leading to IL-1β and IL-18 production | Ohishi et al[38] |
P2RX5 | P2X purinoceptor 5 | NA | Ohishi et al[38] |
SAPK | Stress-activated protein Kinase | ATP induces cell death via SAPK pathways, regulating apoptosis, necrosis, and stress signaling | Humphreys et al[42] |
p38 MAPK | p38 mitogen-activated protein kinases (p38 MAPK) | ATP activates p38 MAPK, which leads to cell death through apoptosis and necrosis | Noguchi et al[2] |
ASK1 | Apoptosis signal-regulating kinase 1. | Excessive ATP induces cellular stress, activating ASK1 and downstream pathways for cell death | Noguchi et al[2] |
NOX2 | NADPH oxidase 2 | ATP activates NOX2, generating ROS causing oxidative stress and potential cell death | Noguchi et al[2] |
bax | BCL-2-associated X | Excessive ATP triggers BAX activation, mitochondrial dysfunction, and apoptotic cell death | Wen et al[43] |
MLC | Myosin Light Chain | ATP depletion hampers muscle contraction, affecting myosin function and cellular viability | Hwang et al[44] |
ROCK I | Rho-associated, coiled-coil containing protein kinase 1 | ATP activates P2X7 receptors, inducing apoptosis via the Rho/ROCK pathway, potentially involving ROCK I | Hwang et al[44] |
ERK1/2 | Extracellular signal-regulated kinase 1 and 2 | ERK1/2 promotes cell survival or antagonizes apoptosis, but prolonged activation may lead to cell death. Activates the ERK1/2 pathway, affecting cell fate | Tsukimoto et al[45] |
P2RX6 | P2X purinoceptor 6 | Activation may raise calcium levels, potentially triggering cell death | [46] |
CYTC | Cytochrome c | Cytochrome c released by mitochondria during cell stress triggers cell apoptosis | Sadatomi et al[37] |
TNF-α | Tumor necrosis factor alpha | ATP induces cell death, activating TNF-α and triggering apoptosis or necroptosis pathways. Immune cells produce TNF-α in response to ATP, amplifying the cellular response | Hide et al[47] |
P2RY5 | P2R purinoceptor 5 | NA | Yoon et al[39] |
P2RY14 | P2R purinoceptor14 | NA | Ohishi et al[38] |
P2RY13 | P2R purinoceptor 13 | P2Y13 may play a role in ADP receptors, involved in ATP homeostasis | Ohishi et al[38] |
P2RY12 | P2R purinoceptor 12 | P2Y12 may play a role in ADP receptors, involved in ATP homeostasis | Ohishi et al[38] |
P2RY6 | P2R purinoceptor 6 | P2Y6 may be involved in calcium signaling leading to cell death | Yoon et al[39] |
P2RY4 | P2R purinoceptor 4 | P2Y6 may be involved in calcium signaling leading to cell death | Ohishi et al[38] |
P2RY2 | P2R purinoceptor 2 | ATP binding triggers intracellular signaling pathways that may lead to cell death | Ohishi et al[38] |
ANO6 | Anoctamin-6 | As a calcium-activating channel and superburning enzyme, it may influence cell death pathways | Ousingsawat et al[48] |
cyclinE2 | Cyclin E2 | NA | Wang et al[49] |
cyclinD2 | Cyclin D2 | NA | Wang et al[49] |
Number | Species | miRNA | Genes |
MIRT134791 | Homo sapiens | hsa-miR-765 | CCND2 |
MIRT064764 | Homo sapiens | hsa-miR-665 | CCND2 |
MIRT040184 | Homo sapiens | hsa-miR-615-3p | CCND2 |
MIRT064762 | Homo sapiens | hsa-miR-610 | CCND2 |
MIRT732948 | Homo sapiens | hsa-miR-574-3p | Ccnd2 |
MIRT535518 | Homo sapiens | hsa-miR-548n | PANX1 |
MIRT535500 | Homo sapiens | hsa-miR-548d-5p | PANX1 |
MIRT064724 | Homo sapiens | hsa-miR-520c-3p | CCND2 |
MIRT064723 | Homo sapiens | hsa-miR-520b | CCND2 |
MIRT064719 | Homo sapiens | hsa-miR-519c-3p | CCND2 |
MIRT064722 | Homo sapiens | hsa-miR-519b-3p | CCND2 |
MIRT042101 | Homo sapiens | hsa-miR-484 | CASP7 |
MIRT337453 | Homo sapiens | hsa-miR-4306 | CCND2 |
MIRT038097 | Homo sapiens | hsa-miR-423-5p | CCND2 |
MIRT043702 | Homo sapiens | hsa-miR-342-3p | CCND2 |
MIRT042861 | Homo sapiens | hsa-miR-324-3p | CCND2 |
MIRT044790 | Homo sapiens | hsa-miR-320a | CCND2 |
MIRT113093 | Homo sapiens | hsa-miR-3163 | CCND2 |
MIRT064741 | Homo sapiens | hsa-miR-3125 | CCND2 |
MIRT007217 | Homo sapiens | hsa-miR-206 | CCND2 |
MIRT021301 | Homo sapiens | hsa-miR-125a-5p | PANX1 |
- Citation: Zhang HL, Doblin S, Zhang ZW, Song ZJ, Dinesh B, Tabana Y, Saad DS, Adam Ahmed Adam M, Wang Y, Wang W, Zhang HL, Wu S, Zhao R, Khaled B. Elucidating the molecular basis of ATP-induced cell death in breast cancer: Construction of a robust prognostic model. World J Clin Oncol 2024; 15(2): 208-242
- URL: https://www.wjgnet.com/2218-4333/full/v15/i2/208.htm
- DOI: https://dx.doi.org/10.5306/wjco.v15.i2.208