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. Author manuscript; available in PMC: 2019 Mar 1.
Published in final edited form as: Wiley Interdiscip Rev RNA. 2018 Jan 11;9(2):10.1002/wrna.1462. doi: 10.1002/wrna.1462

Table 1. Roles of CIRP as a Tumor Suppressor.

Role Possible Mechanisms/Conclusions Experimental Model(s) References
Slows cell growth via prolonging G1 phase Possible interaction with G1 regulators Mouse Fibroblasts (BALB/3T3 Cells) (Nishiyama et al., 1997)
Inhibits proliferation through its function as a stress-induced RBP Binds and increases translational efficiency of DNA damage response genes ATR, Trx-1, RPA2 via 3′ UTR binding Human Rectal carcinoma cells (RKO cells) (R. Yang et al., 2006; R. Yang et al., 2010)
Inversely correlates with proliferation/reduced in endometrial cancer compared to normal endometrium Maintains normal endometrial function, aside from its role as a stress response protein Human Normal Endometrium and Endometrial Carcinoma Tissues (Hamid et al., 2003)
Slows doubling time in ovarian cancer cells/reduced in malignant compared to benign ovarian tumors Prevents malignancy in ovarian tumors Human Malignant and Benign Ovarian Tumors, Ovarian Cancer Cells (Biade et al., 2006)
Decreases proliferation during mammary gland development Halts proliferation when it is no longer needed during development Transgenic mice expressing hCIRP in mammary glands (Lujan et al., 2016)
Part of transcriptomic signature for parity Breast differentiation leads to transcriptomic changes that decrease the lifetime risk for breast cancer in parous women Human breast biopsies (Suraj Peri et al., 2012)