ABSTRACT
Forkhead box protein O1 (FOXO1) has been extensively studied as a tumor suppressor. In oral squamous cell carcinoma, studies have demonstrated that FOXO1 can inhibit tumor cell oxidative stress, stemness and epithelial-mesenchymal transition, and promote tumor cell autophagy and apoptosis. FOXO1 may serve as a potential target for the treatment of oral squamous cell carcinoma.
ABSTRACT
Oral submucous fibrosis (OSF) can cause various oral dysfunctions in patients and can turn into oral cancer. The causes and processes of OSF malignant transformation involve betel nut chewing, vascular atrophy, tissue hypoxia, cell cycle changes, aging, autophagy, and changes in cancer/cancer suppressor genes and microRNAs. It is of great significance to study the causes and process of OSF malignant transformation for the treatment and prevention of OSF malignant transformation.
ABSTRACT
BACKGROUND: Tumor stem cells are a small number of types of tumor cells that have the ability to self-renew and differentiate into different types of tumor cells. Oral squamous cell carcinoma stem cells are highly tumorigenic and play a role in tumor differentiation, treatment resistance, recurrence and metastasis. Simultaneously, tumor stem cells have great similarities with normal stem cells, so it is necessary to establish effective and accurate tumor stem cell identification methods; and corresponding targeted treatment strategies are designed to help the prognosis of patients with oral squamous cell carcinoma. OBJECTIVE: To summarize the current methods used in the literature to identify and isolate oral squamous cell carcinoma stem cells, analyze potential targets for oral squamous cell carcinoma stem cells, and summarize the potential research progress on targets. METHODS: Computers were used to retrieve the CNKI and PubMed databases for relevant literature published since its establishment to 2020. The English key words were “oral squamous cell carcinoma, OSCC, cancer stem cells, HNSCC, head and neck squamous carcinoma cell”. Chinese key words were “oral squamous cell carcinoma stem cells, oral squamous cell carcinoma, tumor stem cells, head and neck squamous cell carcinoma”. Retrieval results were summarized and analyzed to exclude low-relevance, duplicate, and obsolete documents. RESULTS AND CONCLUSION: Targeted intervention of oral squamous cell carcinoma stem cells has important clinical significance. CD44, CD133 and ALDH are currently the most suitable biomarkers for the identification and isolation of oral squamous cell carcinoma stem cells. They are the same as Oct3/4, Nanog, Sox2, Bmi1, EGFR signaling pathway, SHH signaling pathway, Notch signaling pathway, Wnt signaling pathway, Let-7 family, MicroRNA-200 family and natural compounds together as potential targets for targeted therapy of oral squamous cell carcinoma stem cells.
ABSTRACT
Family with sequence similarity 3 (FAM3) gene family is closely related to human tumors, and plays an important role in glucose and lipid metabolism and angiogenesis, and it is related to the occurrence and development of esophageal squamous cell carcinoma, gastric cancer, colon cancer, pancreatic cancer, oral squamous cell carcinoma and breast cancer. Analysis of the role of the FAM3 gene family in glycolipid metabolism and tumors may be of great significance for understanding the occurrence and development of human tumors.
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Objective:To investigate wake-promoting effects of transcranial direct current stimulation (tDCS) on brain injury-induced coma and the possible mechanism.Method:Fifty-four adult SD rats were randomly divided into three groups with 18 rats in each group.They were blank group,traumatic brain injury-induced coma (TBI) group and tDCS group.Using classical free fall method to create brain injury-induced coma and then treated rats with tDCS,consciousness level of rats were assessed at 6h,12h,24h time points.After consciousness level evaluation,rats were put to death and then the prefrontal cortex (PFC) and hippocampus of rats were extracted.Western Blot method was used to determine the expression of brain-derived neurotrophic factor (BDNF) in three groups.Result:Eighteen rats in control group,6 rats in TBI group and 11 rats in tDCS group awakened.BDNF expression in TBI group was higher than that in blank group in PFC and hippocampus.More over,at 12h in PFC and at 6h in hippocampus,BDNF expression in tDCS group was higher than that in TBI group with statistically significant difference(P ＜ 0.05).Conclusion:tDCS can improve the consciousness level of coma rats following TBI and the mechanism may be related to upregulation of BDNF expression in the PFC and hippocampus of rats.
ABSTRACT
Objective To investigate the wake-promoting effect of vagus nerve stimulation (VNS) on coma rats after traumatic brain in-jury (TBI), and the related mechanism. Methods A total of 168 healthy Sprague-Dawley rats were randomly divided into blank group, TBI group, antagonist group and VNS group, 42 rats in each group. The latter three groups were established TBI model with impact, and the rats in coma at least 30 minutes were included. VNS group accepted VNS, the antagonist group were injected intralateroventricularly Orexin A receptor 1 (OXR1) antagonist SB334867, and TBI group accepted sham VNS. Their behaviors were observed to determine the level of con-sciousness six, twelve and 24 hours after intervention, while the expression ofγ-aminobutyric acid b1 receptor (GABAb1R) in prefrontal cortex was detected with immunohistochemistry and Western blotting. Results There were 42 rats in the blank group, 11 rats in TBI group, 13 rats in the antagonist group, and 28 rats in VNS group awakened finally. The expression of GABAb1R in prefrontal cortex ranged as TBI group, antagonist group, blank group and VNS group from more to less twelve and 24 hours after intervention under Western blotting (F>60.412, P<0.001), and it ranged as TBI group, antagonist group, VNS group and blank group under immunohistochemistry (H=15.121, P=0.002), with no significant difference among time points (H=3.028, P=0.220). Conclusion VNS can promote waking from coma in rats after TBI, which may relate with the decrease of GABAb1R in prefrontal cortex that induced by Orexin A.