MiR‐194 regulates nasopharyngeal carcinoma progression by modulating MAP3K3 expression

Abstract

Despite the recent development of treatment strategies for nasopharyngeal carcinoma, the effective management of this disease remains a challenging clinical problem. A better understanding of the regulatory roles of miR‐194 and mitogen‐activated protein kinase kinase kinase 3 ( MAP 3K3) in the nasopharyngeal‐carcinoma‐related gene network is required to address this issue. Here, we measured relative expression of miR‐194 in human nasopharyngeal carcinoma tissues and normal epithelial tissues by quantitative real time PCR . We transfected cultured CNE ‐1 and C666‐1 cells with miR‐194 mimics, and then examined the effects on cell proliferation, cell migration and invasion. Luciferase reporter assay was used to validate the putative binding between miR‐194 and MAP 3K3. We then examined the effect of knockdown and overexpression of MAP3K3 on cell tumorigenesis. Expression of miR‐194 is significantly down‐regulated in nasopharyngeal carcinoma specimens and tumor cell lines when compared with normal controls. In addition, miR‐194 suppressed tumor cell proliferation and viability, as well as migration and invasion of carcinoma cells. We found that miR‐194 binds the 3′ untranslated region of MAP3K3, and knockdown of miR‐194 inhibited nasopharyngeal carcinoma cell proliferation, migration and invasion. In accordance, overexpression of MAP3K3 reversed the inhibitory effects of miR‐194 in carcinoma cells. This study suggests that expression of miR‐194 is down‐regulated in nasopharyngeal carcinoma, and that miR‐194 can directly target MAP 3K3 to regulate tumor progression. Given the pivotal involvement of MAP 3K3 in nasopharyngeal carcinoma development, targeting miR‐194 may be a novel strategy for the treatment of nasopharyngeal carcinoma.

Serum miR-373-3p and miR-194-5p Are Associated with Early Tumor Progression during FOLFIRINOX Treatment in Pancreatic Cancer Patients: A Prospective Multicenter Study

“…This is in contrast to our findings. However, in multiple different cancer experiments, including gastric cancer, lung cancer, and nasopharyngeal cancer, it is shown that miR-194 suppresses cancer cell proliferation, which is in line with our results [32][33][34]. Additionally, in osteosarcoma and colorectal cancer, low serum miR-194 was associated with poor prognosis, comparable to our findings [35,36].…”

Identification of the Roles of a Stemness Index Based on mRNA Expression in the Prognosis and Metabolic Reprograming of Pancreatic Ductal Adenocarcinoma

“…Some studies have shown that it acts as a tumor suppressor that inhibits Hedgehog pathway-dependent medulloblastoma, and its overexpression in tumor cells and tumor-infiltrating lymphocytes is correlated with favorable lung cancer patient survival (30,31). Some other studies have implied that MAP3K3 is a protumor molecule (32,33).…”

CircSETDB1 knockdown inhibits the malignant progression of serous ovarian cancer through miR-129-3p-dependent regulation of MAP3K3

“…Biochemical researches indicate lots of MAPKs can be activated by MAP3K3, such as ERK1/2, c-Jun N-terminal kinases (JNKs) as well as p38 [ 21 ], suggesting the importance of MAP3K3 in cancers. MAP3K3 acted as a promoter in diverse cancers, including nasopharyngeal carcinoma [ 38 ], lung cancer [ 42 ] and pancreatic cancer [ 32 ]. In this paper, based on its oncogenic role and complementary sites with miR-129-3p, MAP3K3 was also hypothesized to participate in SOC biological functions.…”