Oral squamous cell carcinoma (OSCC) is the most common head and neck neoplasm, and the incidence of new cases indicates a continuing rise in developing countries [
1]. Although the clinical outcome of OSCC has gradually improved, the overall 5-year survival rate of patients is still disappointing [
2,
3], reflecting limited advances in our understanding of the pathogenesis of this disease and the molecular events that contributed to its development. Thus, a better understanding of the molecular mechanisms driving oral carcinogenesis may lead to new diagnostic and therapeutic approaches to this disease, and improve the prognosis of OSCC patients.
Like other cancers, oral carcinogenesis involves gradual accumulation of multiple genetic and epigenetic alterations, leading to gain-of-function in oncogenes and loss-of-function in tumor suppressor genes [
4,
5]. MicroRNAs (miRNAs) are a class of small non-coding RNAs, which play an important role in regulating gene function through targeting mRNAs for translational repression or degradation [
6‐
8]. Abnormalities of miRNA have been implicated in the pathogenesis of a variety of human diseases, notably neoplasms [
9‐
11]. Overexpression of oncogenic miRNAs or underexpression of tumor suppressor miRNAs plays a critical role in tumorigenesis. One major tumor suppressor miRNA, miR-145, which plays a crucial role in regulating smooth muscle cell differentiation [
12] and inducing apoptosis [
13], is downregulated in many cancers, including prostate, bladder and colon cancer, as well as B-cell malignancies [
14‐
17]. To date, a cohort of genes related to different cancer pathways have been identified and validated as targeted genes of miR-145, such as
Pai-1,
Fascin1,
Oct-4,
Sox-2,
Klf4,
c-Myc,
IRS1,
Muc1,
Yes,
Stat1, and
p70S6K1[
18‐
25], suggesting that miR-145 is an oncosuppressor and plays an important role in the initiation and progression of tumor, as supported by several direct evidences that the ectopic expression of miR-145 in cancer cells leads to a loss in cell viability and induces cell death [
13,
19,
26]. It has been well known that downregulation of miR-145 is caused by promoter hypermethylation in several cancers [
27,
28]. Additionally, the tumor suppressor gene
p53, which is inactivate in approximately 50% of human cancers, upregulates miR-145 expression, whereas the
Ras oncogene downregulates its expression [
28,
29]. Although downregulation of miR-145 is found in an animal OSCC model [
30], its role in human oral carcinogenesis remains largely unknown.
In the present study, we investigated expression levels of miR-145 in primary OSCCs and adjacent normal oral tissues using reverse transcription quantitative real-time PCR (RT-qPCR). Our data showed that miR-145 was significantly downregulated in OSCCs compared with normal oral tissues. We also demonstrated the miR-145 suppressed OSCC cell growth by targeting c-Myc and Cdk6.