Tumor metastasis is the major cause of death in CC patients. miRNAs are small non-coding RNAs, which bind to specific complementary sequences in the 3’UTR of target mRNAs and induce their degradation or block the translation of the encoded protein. This raises the possibility that an entire pathway/process may be controlled at several levels through a single miR. With the diverse abilities, reducing of their expression has might been associated with promoting or suppressing tumor metastasis, providing a new perspective on the metastatic process. miR–135a is encoded by two genes localized on different chromosomes, producing an identical and active sequence. Recent reports have shown that the effects of miR–135a on cancer progression are contradictory. As is well-known, miRNAs could promote or inhibit various traits related to tumor aggressiveness such as proliferation, cell migration and invasion in various cancer cell lines. Previous researches showed that the expression of miR–135a decreased in human gastric cancer, the proliferation of gastric cancer cells was repressed while the apoptosis was promoted .On the other hand, miR–135a showed a inhibitive role during the migration and invasion of lung cancer cells by targeting a transcription factor .However, the functions and mechanisms of miR–135a are largely unknown[20–23].Recent studies have demonstrated that miR–135a is upregulated in CC cell lines SW480 and SW620, while in our study, the expression levels of miR–135a were significantly increased in CC tissues, which was in accordance with previous studies. Besides, miR–135a were different in lymph node involvement group and tumor stage group, they were positively related. These results support the hypothesis that miR–135a is involved in CC progression, which may function as an oncogenic factor.
BACH1, a member of the basic leucine zipper transcription factor family, is a critical participant in the regulation of oxidative stress.Recent researches demonstrated that BACH1 is a widely expressed transcriptional repressor, which takes part in cell cycle progression, apoptosis, and the hypoxia response negatively through the targeted genes[25–28].As one of them, heme-oxygenase–1 (HO–1) might be significant in induction of the tumorigenic pathway. The expression of HO–1 increases significantly in various types of cancer, which is proved to promote tumor growth and metastasis and suppress the apoptosis of tumor cells. Furthermore, BACH1 is recognized to inhibit growth and survival of acute myeloid leukemia (AML) cells by downregulation of HO–1 expression. Despite of the mechanisms by which BACH1 plays a role in renal cancer development have not been established, there is a research showing that BACH1 functions as a repressor of HO–1 in human cells[17,29].In additional, the up-regulation of HO–1 might inhibits apoptosis of renal cancer cells via activation of the nuclear factor (erythroid-derived 2)-like 2(Nrf2) pathway.[29,30]. Our results show that the expression of BACH1 significantly decreased with the development of colorectal cancer, these data combined with our findings indicate that BACH1 might play a inhibition role during the development of CC. Additionally, Bach1 and miR–135a were negatively correlated. Thus, BACH1 might be one of targets of miR–135a, miR–135a might play an oncogenic role in CC, at least partially, through down-regulation of BACH1. However, our study indicated the potential role of miR–135a and BACH1, further research should be needed to explore the exact signal pathway between them during the development of CC.