8 ± 2.2%) was significantly higher than that of tumors developed from A549/miR-NC cells (9.6 ± 1.5%) following DDP treatment (P < 0.05; Figure 7C). Like the results observed from in vitro experiments, upregulation of miR-451 could also increase in vivo chemosensitivity of A549 cells to DDP by inducing apoptosis enhancement. Figure 7 Effect of miR-451 upregulation on https://www.selleckchem.com/products/wortmannin.html the in vivo sensitivity of A549 cells to DDP. A. Growth of tumors in the mice injected with A549/miR-451 or A549/miR-451 with or without DDP treatement. The inoculation was performed in eight mice. B. Average tumor volume at day 28 after the inoculation of A549/miR-NC or A549/miR-451 cells with or without DDP treatment

(n = 8/group). C. TUNEL staining analysis of apoptosis in tumor tissues at day 28 after the inoculation of A549/miR-NC or A549/miR-451 cells with or without DDP treatment (n = 8/group). Discussion https://www.selleckchem.com/products/bv-6.html miRNAs are a growing class of small, noncoding RNAs (17-27 nucleotides) that regulate gene expression by targeting mRNAs for translational repression, degradation, or both. Increasing evidence suggests that deregulation of miRNAs has been frequently observed in tumor tissues. These miRNAs SRT2104 chemical structure have regulatory roles in the pathogenesis of cancer in humans, through the suppression of genes involved in cell proliferation, differentiation, apoptosis,

metastasis and resistance [15–18]. Recently, many studies have shown that miRNAs play an important role in malignant transformation. It is likely, therefore, that they can also modulate sensitivity and resistance to anticancer drugs in substantial ways. The mechanisms responsible for chemotherapy resistance by miRNAs have not been clearly identified. Current published data on the association of miRNAs with chemoresistance are limited. While altered expression of miRNAs Niclosamide in primary human NSCLCs has been used for tumor diagnosis and prognosis [19], the potential involvement of miRNAs in induction of drug resistance, particularly, in cisplatin resistance has not been explored. Here, we showed that miR-451 is frequently downregulated in human NSCLC tissues compared with corresponding

noncancerous lung tissues, which is consistent with the results of Gao’et al [20]. It was also reported that microRNA-451 could regulate macrophage migration inhibitory factor production and proliferation of gastrointestinal cancer cells [21]. Nan and his colleagues revealed that miR-451 impacts glioblastoma cell proliferation, invasion and apoptosis, perhaps via regulation of the PI3K/AKT signaling pathway [22]. Thus, miR-451 was proposed as a tumor-suppressor of human cancers. In other reports, Godlewski and his colleagues showed that miRNA-451 regulates LKB1/AMPK signaling and allows adaptation to metabolic stress in glioma cells, which represents a fundamental mechanism that contributes to cellular adaptation in response to altered energy availability [23].