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. 2015 Jun 19;36(Suppl 1):S2–S18. doi: 10.1093/carcin/bgv028

Table 3.

Roles of selected mediators of growth suppression in the cancer hallmarks of replicative immortality, sustained proliferation, invasion and metastasis, inflammation and tumor microenvironment

Target Replicative immortality Sustained proliferation Invasion and metastasis Inflammation Microenvironment
p53 p53 inhibits replicative immortality (193–195) p53 inactivation is associated with sustained proliferative signaling (196) p53 inactivation is associated with invasion and metastasis (197) p53 promotes inflammatory processes (198) p53 maintains the tumor microenvironment (199)
pRB pRb inhibits replicative immortality (200,201) pRb inhibits sustained proliferation (202) Inactivation of pRb is associated with invasion and metastasis (203) pRb promotes inflammatory processes (204) pRb maintains the tumor microenvironment (205).
TGF beta TGF-beta inhibits replicative immortality (206) TGF-beta promotes sustained proliferation (202) TGF-beta promotes invasion and metastasis (207,208) TGF-beta promotes inflammatory processes (209) TGF-beta maintains the tumor microenvironment (210)
LKB1 Unestablisheda LKB1 promotes sustained proliferation (211,212) LKB1 inhibits invasion and metastasis (213,214) LKB1 promotes inflammatory processes (215) LKB1 maintains the tumor microenvironment (216)
Connexins Unestablished Connexins inhibit sustained proliferation (217) Connexins have been shown to inhibit and activate invasion and metastasis depending on the cell model (218–220) Connexins promote inflammatory processes (221) Connexins maintain the tumor microenvironment (222)
Contact inhibition Unestablished Contact inhibition suppresses sustained proliferation (223) Contact inhibition inhibits invasion and metastasis (224) Contact inhibition promotes inflammatory processes (225) Contact inhibition has an inhibitory role in maintenance of the tumor microenvironment (222)

We searched PubMed to determine if the listed growth-inhibitory molecular target had roles in other cancer hallmarks. We combined the name of the target listed in the far-left column with the word ‘cancer’ and the name of each of the specific cancer hallmarks that appear in the top row (e.g. ‘p53 cancer replicative immortality’, ‘p53 cancer sustained proliferation’, etc.).

aIf no literature support was found to document the role of a specific molecular target in a particular hallmark, we stated that the target has an ‘unestablished’ role in that hallmark.