Cyclin-Dependent Kinase Inhibitor 3 Promotes Cancer Cell Proliferation and Tumorigenesis in Nasopharyngeal Carcinoma by Targeting p27.

Nasopharyngeal carcinoma (NPC) is a common malignancy of the head and neck that arises from the nasopharynx epithelium and is highly invasive. Cyclin-dependent kinase inhibitor 3 (CDKN3) belongs to the dual-specificity protein phosphatase family, which plays a key role in regulating cell division. Abnormal expression of CDKN3 has been found in numerous types of cancer. In the current study, we explored the possible role of CDKN3 in cell proliferation, ability to invade, and radiosensitivity in NPC cells. We reported that CDKN3 was upregulated and p27 was downregulated in NPC tissues and is associated with a worse prognosis for patients. In addition, downregulation of CDKN3 and upregulation of p27 decreased cell proliferation, induced cell cycle arrest, increased apoptosis, decreased cell invasion, and enhanced radiosensitivity. Silencing of p27 significantly inhibited the effects of the knockdown of CDKN3. Moreover, downregulation of CDKN3 and upregulation of p27 inhibited the increase in tumor volume and weight in implanted tumors, decreased the phosphorylation of Akt, and increased the expression of cleaved caspase 3 in tumors. CDKN3 expression was also inversely correlated with p27 expression in NPC patients. Knockdown of CDKN3 increased p27 expression. Silencing of p27 markedly inhibited the effects of CDKN3 on cell proliferation, cell cycle progression, apoptosis, invasion, and radiosensitivity. These results demonstrate that upregulation of p27 is involved in the knockdown of CDKN3-induced decrease in cell proliferation, increase in cell cycle arrest and apoptosis, decrease in invasion, and increase in radiosensitivity. The results demonstrate that the CDKN3/p27 axis may be a novel target in the treatment of NPC.

[The expression and clinical significance of MyD88 in laryngeal cancer].

OBJECTIVE: To investigate the myeloid differentiation factor 88 (MyD88) expression in laryngeal carcinoma and its clinical significance. METHOD: Fifty-one patients with laryngeal carcinoma were collected, and all patients were confirmed by pathological diagnosis results. The expression of MyD88 protein was detected by immunohistochemical method in laryngeal cancer and its adjacent tissues to investigate the correlation among MyD88 expression, clinicopathological characteristics and prognosis of patients. RESULT: The positive expression rate of MyD88 in laryngeal cancer tissues was 68.6%, significantly higher than that in normal tissues adjacent to carcinoma of which positive expression rate was 11.8%; MyD88 positive rate had nothing to do with laryngeal cancer patients age, sex, differentiation and tumour location (all P > 0.05), but correlated with clinical stage (P < 0.01) and lymph node metastasis (P < 0.05). In addition, the study also found that the expression of MyD88 quantity was inversely proportional with the five-year survival rate. The survival rate of patients with higher expression of MyD88 was significantly lower than that of patients with lower expression (P < 0.05). CONCLUSION: MyD88 may be an important participant in the pathogenesis of laryngeal carcinoma, MyD88 targeted therapy may improve the prognosis of patients with laryngeal cancer.

[The diagnosis applying effects of ocular vestibular evoked myogenic potentials in BBPV disease].

OBJECTIVE: To investigate the diagnosis applying effects of ocular vestibular evoked myogenic potentials(oVEMP) in peripheral BPPV disease. METHOD: During September 2012 to January 2015, we selected 80 healthy people in our hospital medical center as the control group, choose the same period of primary benign paroxysmal positional vertigo as the observation group of 80 patients. Two groups were carried out fully functional auditory evoked potential analysis, determination of oVEMP and cervical vestibular evoked myogenic potentials (cVEMP) anomaly amplitude threshold, P1 latencies, N1 incubation period. RESULT: The cVEMP abnormal rate in the observation group was 28.8%, the oVEMP abnormal rate was 38.8%, while cVEMP and oVEMP abnormal rates in the control group was 1.3% and 2.5% respectively that compared to significant differences between the two groups (P < 0.05). The oVEMP test amplitude in the observation group was (5.98 ± 2.15) µv, the N1 incubation period was (10.03 ± 0.76)ms, while the control group were (4.09 ± 2.11)µv and (11.67 ± 0.78) ms that compared difference were statistically significant (P < 0.05). The cVEMP test amplitude in the observation group was (154.8 ± 43.9)2 µv, while the control group was (180.49 ± 45.34)µv, compared the difference was statistically significant (P < 0.05). CONCLUSION: Paroxysmal positional vertigo patients ocular vestibular evoked myogenic potentials abnormal rate is relatively high, the utricle dysfunction for more severe than the balloon can be the subject of an objective function of the ear stone judgment, judgment in favor of the disease.

MicoRNA-451 is a novel tumor suppressor via targeting c-myc in head and neck squamous cell carcinomas.

OBJECTIVE: Head and neck squamous cell carcinoma (HNSCC) represents as a common malignancy with increasing incidence in the worldwide. The fact of its poor survival rate urgently requires developing efficient predictive biomarkers for clinical use. MicroRNAs (miRNAs) recently represent as a novel direction for early diagnosis and prognosis prediction in HNSCC therapy. In this study, we comprehensively investigated the function and putative target of miRNA-451 in vitro. METHODS: The expression of miRNA-451 was detected in HNSCC tissues and cell lines by real-time PCR. Forced expression or inhibition of miRNA-451 was done by transient transfection of mimics or inhibitor of miRNA-451 into indicated cells, respectively. Cell proliferation was evaluated by cell counting and crystal staining. Afterwards, we perform western blot to verify the expression of the miRNA-451 predicted target, c-myc, after miRNA-451 was overexpressed. RESULTS: We showed that miRNA-451 was downregulated in paired HNSCC tissues as well as in cell lines. And overexpression of miRNA-451 in cells with low endogenous expression of miRNA-451 accelerated proliferation. To the contrast, knockdown of miRNA-451 in cells with high levels of miRNA-451 significantly reduced cell growth rate. Furthermore, we used bioinformatics and cellular methods to predict and prove that c-myc was targeted by miRNA-451, since forced expression of miRNA-451 leaded to decreased c-myc protein expression in HNSCC cells. CONCLUSION: Our findings identify miRNA-451 as a potential biomarker and suggest a key role of miRNA-451-c-myc pathway in HNSCC cell transformation, which could represent a novel therapeutic strategy in HNSCC treatment.