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‘Mir’ roles for miR-302 in cell cycle and tumorigenesis suppression



From Cancer Research

The microRNA miR-302 is implicated in the regulation of stemness and pluripotency, somatic cell reprogramming and more recently the global DNA demethylation and histone methylation which occurs during somatic cell reprogramming (see Splitting hairs: Follicking about with mir-302)1. Results from the same group in California now published in Cancer Research go on to reveal more about the action of this small, non-coding RNA – this time, its role in suppressing the human stem cell cycle and tumorigenicity2. One observation in miR-302-reprogrammed human hair follicle cells (hHFCs) is that they show an attenuated cell cycle. In their new study Lin et al. examine whether this then implicates a role for miR-302 in tumorigenesis. They report that induced expression of miR-302 family members in various cancer cell types effectively inhibited cell proliferation and induced widespread apoptosis and, importantly, the invasion capability of the tumor cells was completely halted. They go on to show the mechanisms by which miR-302 mediates these effects; by co-suppression of G1-phase cell cycle checkpoint regulators CDK2 (cyclin dependent kinase 2), cyclin D1 and 2, and also via the BMI-1 polycomb ring finger oncogene. Impressively, injected delivery of a miR-302 expression vector in close proximity to embryonal carcinoma cell-derived teratomas in immunodeficient mice significantly inhibited teratoma growth and tumor size, yet did not affect the pluripotent nature of teratoma-derived cells. This exciting work has clear implications for miR-302 as an important agent in cancer research, alongside its more defined roles in pluripotency and somatic cell reprogramming.



1. Lin et al. (2010) Regulation of somatic cell reprogramming through inducible mir-302 expression. Nucleic Acids Research 1-12. doi:10.1093/nar/gkq850.

2. Lin et al. (2010) MicroRNA miR-302 Inhibits the Tumorigenecity of Human Pluripotent Stem Cells by Coordinate Suppression of the CDK2 and CDK4/6 Cell Cycle Pathways’ Cancer Res. 2010 Nov 9.