TABLE 1.
Different mechanisms of cancer cells to block or suppress PCD
Cancer type | Targeted PCD | Mechanism of suppression | Reference |
---|---|---|---|
Colorectal, breast, lung | Apoptosis | MOMP impairment and cytochrome c inactivation | [69] |
Lymphoma, colorectal, breast, ovarian, prostate, lung | Apoptosis | Overexpression of Bcl‐2 anti‐apoptotic members | [67] |
Colorectal, gastric, breast | Apoptosis/pyroptosis | Low expression of NLRs | [77] |
Myeloma, glioma, gastric, breast, ovarian, prostate | Apoptosis | Overexpression of G1P3 | [74, 75, 76] |
Non‐small‐cell lung carcinoma | Necroptosis | Low expression of CALR | [105] |
Breast carcinoma | Necroptosis | Low expression of HMGB1 | [106] |
Leukaemia, colorectal, breast | Necroptosis | Low expression of RIPK3 | [107, 108, 109] |
Gastric | Pyroptosis | Low expression of GSDMD | [118] |
Melanoma | Pyroptosis | Low expression of GSDME | [120] |
Breast, ovarian, prostate | Autophagic cell death | Low Beclin 1 expression | [135] |
Head and neck squamous cell carcinoma, gastric | Autophagic cell death | Upregulation of G9a | [138, 139] |
Abbreviations: Bcl‐2, B‐cell lymphoma 2; Beclin 1, an autophagy‐related protein; CALR, calreticulin; G1P3, an IFN‐stimulated product; G9a, a histone methyltransferase;GSDMD/E, Gasdermin D/E; HMGB1, high‐mobility group box 1; MOMP, Mitochondrial outer membrane permeabilization; NLRs, Nod‐like receptors; RIPK3, receptor‐interacting protein kinase 3.