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Table 4 Synthetic lethal partners with mutp53

From: Targeting mutant p53 for cancer therapy: direct and indirect strategies

Synthetic lethal partner

Mechanism

References

ATR

ATR inhibitors target ATR/CHK1 pathway to suppress G2 arrest in p53-deficient cancers

[68, 69, 177]

CHK1

CHK1 inhibitors target CHK1 to suppress G2 arrest in p53-deficient cancers

[70]

p38MAPK/MK2

MK2 regulates of G2/M and S-phase checkpoint in p53-mutated/p53-deficient cancers in response to DNA damage

[64, 72]

WEE1

WEE1 plays a crucial role in the G2/M transition for p53-mutated cancers

[76, 77]

PLK1

PLK1 is required for mitosis entry by activating CDC25 and inhibiting both WEE1 and PKMYT1

[73, 79]

PIP4K2B

High level of PI5P4Ks promotes glucose uptake to support glucose metabolism and enhances NADPH generation to mediated ROS response in the condition of p53 mutation/deletion

[89]

HK2

HK2 regulates the transform from phosphorylating glucose into glucose-6-phosphate to elevate glycolysis for glycolysis

[88, 178]

mTOR

mTOR-induced inhibition of autophagy prevents mutp53 proteins from autophagy-mediated degradation

[96]

PDGFRβ

PDGFRβ maintains the premetastatic phenotype for pancreatic ductal adenocarcinoma with p53 R172H

[103]

PLA2G16

Mutp53 binds to the promoter of PLA2G16 to promote metastatic phenotype

[104]