MiR-139-5p inhibits the tumorigenesis and progression of oral squamous carcinoma cells by targeting HOXA9.

Our study sought to clarify the effects of microRNA-139-5p (miR-139-5p) in the tumorigenesis and progression of oral squamous cell carcinoma (OSCC) by regulating HOXA9. MiR-139-5p and HOXA9 expression in OSCC tissues, tumour adjacent tissues, OSCC cells and normal cells were tested by qRT-PCR. SAS and CAL-27 cell lines were selected in among four OSCC cell lines and then transfected with miR-139-5p mimics, pEGFP-HOXA9 and cotransfected with miR-139-5p mimics + pEGFP-HOXA9. We used MTT, colony formation, transwell and wound healing assays to analyse cell viability, proliferation, invasion and migration. The target relationship between miR-139-5p and HOXA9 was verified by luciferase reporter assay and Western blot, respectively. MiR-139-5p was down-regulated, whereas HOXA9 was up-regulated in OSCC tissues and cells. The proliferation, invasion and migration ability of SAS and CAL-27 cells in miR-139-5p mimics group were significantly weaker than those in the control group and the miR-NC group (P < 0.01). MiR-139-5p can negatively regulate HOXA9. The proliferation, invasion and migration of SAS and CAL-27 cells in the miR-139-5p mimics + pEGFP-HOXA9 group were not significantly different from those in the blank control and negative control groups (P > 0.05). Our results indicated that miR-139-5p could directly inhibit HOXA9, which might be a potential mechanism in inhibiting the proliferation, invasiveness and migration of OSCC cells.

Wang K ，Jin J ，Ma T ，Zhai H ... -  《-》

MiR-376c-3p regulates the proliferation, invasion, migration, cell cycle and apoptosis of human oral squamous cancer cells by suppressing HOXB7.

To test the influence of miR-376c-3p on the proliferation, invasion, migration, cell cycle and apoptosis of human oral squamous cancer cells (OSCC) and the relevant mechanism. We applied qRT-PCR and Western blot to compare the expression level of miR-376c-3p and HOXB7 in SCC-4, SCC-9, SCC-15, SCC-25 OSCC cell lines and 49 paired OSCC and normal oral epithelial tissue specimens were included in our present study. Also we analyzed the relative relationship of expression level between miR-376c-3p and HOXB7 in cancer tissues. Luciferase assay was used to confirm the target relationship between miR-376c-3p and HOXB7. Besides, MTT, Transwell, wound healing, colony formation and flow cytometer experiments were applied to evaluate the proliferation, cell viability, apoptosis, invasion and migration of transfected OSCC. MiR-376c-3p was down-regulated while HOXB7 was up-regulated in OSCC tissues and cells than the normal ones. MiR-376c-3p directly targeted HOXB7 and reduced the expression of HOXB7. Overexpression of miR-376c-3p attenuated proliferation of SCC-9, SCC-15, SCC-24 and SCC-25 cells. Moreover, miR-376c-3p suppressed proliferation, viability, migration and invasion and induced G1/G0 arrest and cell apoptosis of SCC-25 cells. Besides, overexpression of HOXB7 efficiently abrogates these influences caused by overexpression of miR-376c-3p. MiR-376c-3p suppresses the fission, proliferation, migration and invasion and induces cell apoptosis of OSCC via targeting HOXB7.

Wang K ，Jin J ，Ma T ，Zhai H ... -  《-》

microRNA-188 is downregulated in oral squamous cell carcinoma and inhibits proliferation and invasion by targeting SIX1.

Wang L ，Liu H 《-》

MicroRNA-129-5p represses the growth and aggressiveness of oral squamous cell carcinoma via suppressing HMGB1.

Recent investigations have suggested that microRNA-129-5p (miR-129-5p) is commonly dysregulated in multiple types of malignancies. Nevertheless, the roles of miR-129-5p in human oral squamous cell carcinoma (OSCC) are not well explored. Herein, we demonstrated that miR-129-5p was down-expressed in OSCC cells and tissues. Moreover, miR-129-5p overexpression restrained the growth, migration ability, and invasiveness of OSCC cells. Notably, high-mobility group box 1 protein (HMGB1) was identified as a downstream target of miR-129-5p. Additional, knockdown of HMGB1 suppressed the growth and aggressive phenotypes of human OSCC cells. Importantly, re-expression of HMGB1 impaired the inhibitory impacts of miR-129-5p on the metastasis of OSCC cells. Altogether, these results implied that miR-129-5p restrained the aggressiveness of OSCC cells through modulating HMGB1.

Song CP ，Cong JK ，Wang MZ 《-》

miR-182-5p Promotes Growth in Oral Squamous Cell Carcinoma by Inhibiting CAMK2N1.

Emerging evidence suggests that the propagation of oral squamous cell carcinoma (OSCC) is influenced by the abnormal expression of microRNAs (miRNAs). This study aimed to characterize the involvement of miR-182-5p in OSCC by targeting the calcium/ calmodulin-dependent protein kinase II inhibitor CAMK2N1. miR-182-5p expression was quantified in OSCC tissues and cell lines with reverse transcription polymerase chain reaction (RT-PCR). Cell colony formation, Cell Counting Kit-8 (CCK-8), Ki-67, and nude mouse xenograft assays were used to characterize the role of miR-182-5p in the proliferation of OSCC. A miR-182-5p target gene was identified with western blotting, RT-PCR, and luciferase activity assays. OSCC patient survival based on CAMK2N1 expression was also analyzed. miR-182-5p was up-regulated in in vitro cell lines and in vivo clinical OSCC samples. CCK-8, colony formation, and Ki-67 assays revealed that miR-182-5p promoted the growth and proliferation of OSCC cells. miR-182-5p directly targeted CAMK2N1, as evidenced by luciferase assays and target prediction algorithms. CAMK2N1 operated as a tumor suppressor gene in patients with OSCC. Down-regulating miR-182-5p expression in the CAL-27 cell line restored CAMK2N1-mediated OSCC cell proliferation. miR-182-5p expression inhibited the activation of AKT, ERK1/2, and NF-κB. Mice injected with CAL-27 cells transfected with miR-182-5p-inhibitor demonstrated a significant increase in tumor size and weight and increased CAMK2N1 mRNA and protein expression compared with the miR-negative control group. The miR-182-5p-CAMK2N1 pathway can be potentially targeted to regulate the proliferation of OSCC cells.

Li N ，Nan CC ，Zhong XY ，Weng JQ ，Fan HD ，Sun HP ，Tang S ，Shi L ，Huang SX ... -  《-》