STAT3Modulates Expression Of MiRNA-21in Tongue Squamous Cell Carcinoma

Oral and Maxillofacial-Head and neck cancer is the sixth most common cancer in the world, and tongue cancer is the most common malignant tumors in the oral cancer, squamous cell carcinoma accounts for more than80%of the pathological types of tongue cancer, thus, elucidate the pathogenesis of tongue squamous cell carcinoma to find more effective treatment is still hot point in tongue cancer research field.The current study confirmed miRNA (microRAN) expression is associated with a variety of cancers. Abnormal expression of miRNAs play a key role such as oncogenes or tumor suppressor genes in the development and progression of cancer. The study found that a variety of miRNA expression in tongue cancer disorders and closely contacts with tongue cancer development and prognosis. miR-21is found in human cells or tissues earlier, there is one of the more widely miRNA. Early studies confirmed miR-21expression was elevated in glioma, lung cancer, breast cancer and other malignant tumors; and modutes tumor procession by inhibiting PTEN, PDCD4, TIMP3, TIMP-1, RECK, p53tumor suppressor gene that involved in the regulation of varies of malignant tumors. A miRNA expression profile results suggests that miR-21highly expressed in head and neck squamous cell carcinoma and esophageal squamous cell carcinoma cell lines. Another tongue cancer miRNA expression profiling study also showed that miR-21in103patients with squamous cell carcinoma is high expressiond and antisense miR-21can inhibit tongue cancer cell lines SCC-15and CAL27growth. My team preliminary studies demonstrated that transfecting with miR-21, antisense oligonucleotides, TB3.1tongue cancer cell’s proliferation and invasion ability is suppressed. The results of the study indicates that miR-21may affect the incidence and progress of tongue cancer, as a proto-oncogene.Signal transducer and activator of transcription3(Signal Transducers and Activators of transcription3, STAT3) is an important member of the family of signal transduction and activator of transcription. STAT3plays an important role in maintaining normal physiological.its activation state is short and it is precisely regulated in normal cells and tissues. Sustained activation of STAT3can lead to abnormal cell proliferation and malignant transformation. Study confirmed that STAT3involves in a variety of malignant tumors such as breast cancer, head and neck squamous cell carcinoma, colorectal cancer, ovarian cancer, multiple myeloma, leukemia.It is over-expressed and affects tumor growth, differentiation and metastasis. STAT3may be activated by a variety of cytokines (IL-6), the receptor tyrosine kinase (EGFR) and non-receptor tyrosine kinases (JAK, Src, Abl, etc.). STAT3is the focus of the oncogenic tyrosine kinase signaling channel. Two activated STAT3interacts to form a dimer of homologous or heterologous transferred to the nucleus, affecting the transcription of target genes that regulated tumor cell’s proliferation, apoptosis, metastasis-related. Studies have shown that in patients with head and neck squamous cell carcinoma, epithelial tumor and normal tissues of STAT3expression levels were higher than non-cancer patients with normal epithelial. Prompted a sustained activation of STAT3plays an important role in the progression and invasion of human tongue squamous cell carcinoma.The research of relationship between miRNA and STAT family members in recent years, in particular, the interaction of miR-21and STAT3has been initially elaborated. It’s predicted miR-21encoding gene promoter region of STAT3binding sites via Bioinformatics. Encoding miR-21gene regulatory region is located in the transmembrane domain49gene intron, and be regulated by upstream enhancer, the enhanced promoter regulation sequence containing two binding sites Stat3.Some one speculated IL-6/Stat3anti apoptosis signal pathway is potential miRNA-21regulatory mechanism. In myeloma cells, the transcription of miR-21may be regulated directly by upstream enhancer that contains2STAT3binding sites. Knockdown STAT3can block the IL-6-mediated expression of miR-21.The transcriptional regulation relationship between STAT3and miR-21in tongue cancer has not yet been described. we use a large number of in vitro and in vivo experiments to study molecular mechanisms of the STAT3modutes the expression of miR-21.