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miR-31 functions as an oncomir during human pulmonary carcinogenesis.
Many studies have shown that miR-21 functions as an oncomiR.
Our findings indicate that miR-210-3p miR-210-3p miR-210-3piR in GBM.
These results suggest that miR-20b functions as an oncomir by contributing to breast tumorigenesis partly via regulating PTEN expression at the posttranscriptional level.
Our study indicated that overexpression of miR-1269 promotes cell proliferation in HCC through directly suppressing FOXO1, and functions as an oncomiR in HCC.
Their data show that miR-31 functions as an oncomir by directly repressing the tumour suppressors LATS2 and PPP2R2A (Liu et al, 2010).
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Some miRNAs may function as an oncomiR, having either a tumor suppressive or an oncogenic role [ 17- 20].
miR-103 has been described to function as an oncomiR in colorectal cancer and breast cancer [ 22, 27].
miR-494 has been reported to function as an oncomiR in colorectal cancer and non-small cell lung cancer [ 23, 24], and as a tumor suppressor in cholangiocarcinoma and gastrointestinal stromal tumors [ 25, 28].
Yu BL et al. reported that repressing TOB2 expression would cause miR-378 to function as an oncomiR in nasopharyngeal carcinoma [ 23]; miR-378/ATP also binds Cassette Transporter G1-Signaling pathway [ 24].
This study supports the role of miR-510 functioning as an "oncomir", causing increased migration, invasion and colony formation of non-transformed breast and non-invasive breast cancer cells in vitro and promoting breast tumor growth in vivo.
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