Oncomir

The dysregulation of certain microRNAs (oncomirs) has been associated with specific cancer forming (oncogenic) events.

[5] The first link between miRNA and the growth of cancer was reported in 2002 when researchers observed a down-regulation of miR-15a and miR-16-1 in B-cell chronic lymphocytic leukemia patients.

[6] The term is a portmanteau, derived from "oncogenic" + "miRNA", coined by Scott M. Hammond in a 2006 paper characterizing OncomiR-1.

The study analyzed RNA from biopsied pancreatic cysts to identify deviations in expression of miRNAs.

It has been shown that miRNA's from the OncomiR-1 line inhibit cell death, thus increased expression of oncomir-1 leads to the development of tumors.

miR-19 has been shown to downregulate phosphatase and tensin homolog (PTEN) effectively increasing activity of the cellular survival-promoting signal pathway PI3K-Akt.

In human breast cancer, it has been identified to target the gene which encodes for a protein called suppressor of cytokine signaling 1 (SOCS1).

Recent research suggests that miR-155 negatively regulates SOCS1, but may be a feasible target in breast cancer therapy.

Altered expression of the miR-569 gene has been demonstrated to affect growth and proliferation of breast epithelial cells.

In comparison to normal tissues and less malignant tumors, TP53INP1 occurs at lower levels in more invasive cancers, presumably in part due to the role played by miR-569.

Other anti-oncomirs, including miR-143 and miR-145, have been shown to down-regulate a wide range of human cancer cell lines.

As an avenue of therapeutic research, chemical devitalization (i.e., artificial modification) of miR-143 and miR-145 may prove to be more effective version of their natural counterparts.