MicroRNAs are a family of non-coding RNAs, *22 nt in
length, which repress gene expression by pairing to the 30
-
untranslated regions of target mRNAs [1]. Aberrant
expression of microRNAs in tumor cells contributes to
tumor growth by the activation of cell proliferation, the
induction of resistance to apoptosis and other related
pathological process [2]. Using anti-miR oligonucleotides to
inhibit onco-miRs has shown efficacies in tumor xenograft
models and thus has great potential in cancer therapy [3].
Emerging evidence indicates that miR-494 plays a
critical role in cancer development. The level of miR-494
was higher in a number of cancers such as classical
Hodgkin’s lymphoma [4] and oral squamous cell carcinoma
[5]. Anti-miR-494 treatment significantly diminished
tumor size in mice with primary myc-driven liver tumor
[6]. Recently, it was reported that knockdown of miR-494
in myeloid-derived suppressor cells, one of the most
important cell types in tumor microenvironment, inhibited
the growth of mouse breast cancer [7], indicating that miR-
494 may also promote cancer progression by modulating
tumor microenvironment. Angiogenesis is an essential
component in microenvironment to tumor growth and
metastasis, whereas inhibiting angiogenesis has become a
promising strategy for cancer therapy [8]. It has been
reported that tumors can promote angiogenesis through
different extracellular pathways, including cellular factors
and microRNAs [9]. Therefore, we sought to examine a
role of miR-494 in the tumor angiogenesis and demonstrated
that miR-494 is a novel tumor-derived paracrine signal to promote angiogenesis and tumor growth under
hypoxic condition.