. Author manuscript; available in PMC: 2016 Dec 1.

Published in final edited form as: Trends Pharmacol Sci. 2015 Oct 17;36(12):858–877. doi: 10.1016/j.tips.2015.08.013

Table 2.

Plks in the development of mouse and human cancers

	Role in tumor	Phenotypes in mouse models		Human cancer association
	Role in tumor	Knock out (−/−)	Haploinsufficient(+/−)	Human cancer association
Plk1	Promoter	Lethal at 4 or 8 cell stage [35]	Develop lymphomas, lung carcinomas, squamous cell carcinomas, and ovarian sarcomas [35] Increased tumor frequency in PLK1+/− TP53−/− cells [35]	Upregulated in breast, oesophageal, lung, and colorectal cancer, gastric, anaplastic thyroid, hepatocellular carcinoma, melanomas and gliomas, non-small cell lung, ovarian, prostate, pancreatic, head and neck cancers [39,40]
Plk2	Suppressor?	Retarded embryonic growth [36]	No apparent phenotype	Downregulated in B cell neoplasias and heptocellular carcinoma [41]
Plk3	Suppressor	Highly vascularized tumors in lung, kidney, liver, and uterus [37]	No apparent phenotype	Downregulated in lung carcinoma, head and neck squamous cell carcinoma, heptocellular carcinoma [41–43]
Plk5	Suppressor?	N/A	N/A	Downregulated in primary brain tumor (astrocytoma and glioblastoma multiforme) [16]
Plk4	Suppressor/promoter	Lethal at E7.5 [14]	Developed in liver and lung cancers [44]	Upregulated in colorectal cancer and poor prognosis breast cancer [45,46] Downregulated in heptocellular carcinoma [41]