MicroRNAs (miRNAs) are tiny, endogenously expressed noncoding RNAs (18-25 nucleotides in length) that act as crucial posttranscriptional regulators of gene expression [
1‐
3]. For several miRNAs, their participation in essential biological processes has been proved, such as in cell proliferation control, cell lineage fate decision, cell survival, tissue patterning for development, and cell metabolism [
4]. Cancer is a very complex genetic disease characterized by alterations in genes encoding oncogenic and tumor-suppressor proteins [
5]. Recently, it has been noted that the expression profiles of miRNAs can be used for classification, diagnosis, and prognosis of human malignancies; and the deletion or amplification of the locus encoding an miRNA in a variety of cancers has been reported. Altered patterns of miRNA expression may affect cell-cycle and survival programs and be involved in tumor initiation and progression. We previously found that
microRNA-143 (
miR-143) and -
145 (
miR-145) were down-regulated in colon cancers [
6,
7], gastric cancers [
8], chronic lymphocytic leukemias, and B cell lymphomas [
9], and in several human cancer cell lines [
7]. Several groups also reported the down-regulation of both of these miRNAs in many other types of cancers, such as bladder cancers and their cell lines [
10,
11], cervical cancers and their cell lines [
12], colorectal cancers [
13‐
16], nasopharyngeal carcinoma [
17], and prostate cancer [
18]. Furthermore, such abnormal expression was found not only in malignant cells but also in cells in premalignant stages such as colon adenoma cells [
13,
19]. The introduction of the mature type of either
miR-143 or -
145 into colon cancer cells [
6,
7,
20], B cell lymphoma [
9], and gastric cancer cells [
8,
21] results in a significant growth inhibition that occurs in a dose-dependent manner; and the target genes,
ERK5[
22] and
KRAS[
20] for
miR-143 and
IRS-1[
23] and
c-myc[
21] for
miR-145, were posttranscriptionally down-regulated. Taken together, these findings suggest that
miR-143 and -
145 act as tumor suppressors and provide an important clue in the study of the mechanism of tumor initiation and progression involving miRNAs.