scholarly journals Downregulation of MicroRNA-130a Inhibits Oral Squamous Cell Carcinoma Proliferation and Metastasis via the Hippo-YAP Pathway

2021 ◽  
Vol Volume 13 ◽  
pp. 4829-4840
Author(s):  
Yiran Peng ◽  
Shoushan Hu ◽  
Kun Zhang ◽  
Yuru Wang ◽  
Maierdanjiang Rouzi ◽  
...  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yingyi Ma ◽  
Haiye Wang

AbstractOral squamous cell carcinoma (OSCC) is the most common malignant epithelial neoplasm of the head and neck, with poorer prognosis. There is lack of specific targets for diagnosis and treatment of OSCC at present. Annexin A2 (ANXA2) is involved in cell angiogenesis, invasion, proliferation and metastasis. In this study, the significance and effect of ANXA2 on OSCC and OSCC cells were explored from the clinical and basic study. First, ANXA2 expression in OSCC tissues and adjacent non-cancer tissues of 124 patients were detected, and the correlation between ANXA2 expression and clinical parameters were analyzed. The results found that ANXA2 was highly expressed in OSCC tissues, and was associated with the TNM stage, tumor differentiation, lymph node metastasis and poor survival of OSCC patients. The expression of ANXA2 in OSCC cells were higher than the normal oral cells. And knockdown of ANXA2 by transfecting ANXA2-siRNA could suppress the proliferation, migration, and invasion abilities of OSCC cells. Overall, ANXA2 expression is correlated with poor survival of OSCC patients, and silencing of ANXA2 suppress the proliferation, migration and invasion of OSCC cells.


2021 ◽  
Vol 11 (8) ◽  
pp. 1571-1575
Author(s):  
Guowu Ma ◽  
Jia Hou ◽  
Jiezi Qiu ◽  
Jianlin Fan ◽  
Jianxin Yang

Oral squamous cell carcinoma (OSCC) had the poor prognosis. miR-155 was involved in some diseases. However, whether BMSCs with high expression miR-155 affect the proliferation and metastasis of OSCC is unclear. Our study aims to assess BMSCs’ effect on OSCC cells. miR-155 level in OSCC tumor tissues was analyzed. BMSCs were transfected with miR-155 followed by analysis of cell proliferation by MTT assay, cell apoptosis and migration, and MMP-9 level by ELISA and PTEN12 level. In the tumor tissue, miR-155 level was significantly increased (P <0.05). Co-culture of BMSCs with high expression miR-155 with OSCC cells could significantly promote OSCC cell proliferation and reduced cell apoptotic activity, increased cell migration and MMP-9 secretion as well as downregualted PTEN12 expression (P <0.05). In conclusion, miR-155 was increased in the OSCC patients and BMSCs of high expression miR-155 could promote the proliferation and metastasis of OSCC by regulating PTEN12.


2020 ◽  
Vol 12 (7) ◽  
pp. 946-952
Author(s):  
Fengping Mou ◽  
Li Xiao ◽  
Yuanqin Xu

This study aims to investigate the therapeutic effect of a paclitaxel-loaded nano-drug (PTX-mPEGPLA) on oral squamous cell carcinoma (OSCC). PTX-mPEG-PLA nanoparticle (NP) was prepared by loading paclitaxel into the mPEG-PLA nanoparticle and purified by a thin-film hydration method. C57BL/6 mice were used to establish a murine OSCC model. The mice were treated with saline control (G1), paclitaxel (G2), or PTX-mPEG-PLA NPs (G3). After 4 weeks of differential treatment, the saliva of mice in the G1, G2, and G3 groups was collected to detect the concentration of protein markers of OSCC. Also, venous blood and cancer tissues of mice in the three groups were collected for drug concentration measurements. The paclitaxel concentration and retention in G3 mice were significantly higher and more prolonged than those in G2 mice, respectively (P < 0.05). Compared to the level of OSCC protein markers in the saliva of mice in G1 and G2 that in G3 was the lowest. PTX-mPEG-PLA NPs demonstrates effective targeting in the treatment of oral squamous cell carcinoma in mice. It can deliver the drug to the cancerous tissues, increase the drug retention in the same tissues, and effectively inhibit the proliferation and metastasis of malignant tumors.


2019 ◽  
Author(s):  
Deyu LIU ◽  
xinchun jian ◽  
PU XU ◽  
Rong ZHU ◽  
Yuan WANG

Abstract Background Mounting studies demonstrate long non-coding RNAs (lncRNAs) play an important role in tumor progression. However, the potential biological functions and clinical importance of linc01234 in oral squamous cell carcinoma (OSCC) still remain unclear. Methods Two OSCC cells were transfected with siRNAs targeting linc01234, and RT-qPCR, CCK-8, EDU, wound healing and Transwell and western blot assays were performed to analyze the effect of linc01234 on cell proliferation, migration and invasion. Bioinformatic analysis, luciferase assays and RT-qPCR identified a competitive endogenous RNAs (ceRNAs) among linc01234, miR-433-3p and PAK4. Results We found that linc01234 was significantly upregulated in OSCC tissues and cell lines and positively associated with T stage, lymphnode metastasis, differentiation. Kaplan-Meier analysis of OSCC reveals a positive correlation between linc01234 and the overall survival. Following the linc01234 deletion, the cell proliferation and metastasis abilities in CAL27 and SCC25 cells were found to be extremely reduced. Mechanism studies indicated that linc01234 located in cytoplasm and shared microRNA (miRNA) response elements with miR-433-3p. Luciferase assays indicated that miR-433-3p bind to the 3′-UTR of PAK4. Conclusions Our results indicated that linc01234 functioned as an oncogene in OSCC and might be a potential therapeutic target for OSCC.


Oral Oncology ◽  
2003 ◽  
Vol 39 (3) ◽  
pp. 240-247 ◽  
Author(s):  
Natsuyo Noguchi ◽  
Shuichi Kawashiri ◽  
Akira Tanaka ◽  
Koroku Kato ◽  
Hiromitsu Nakaya

2019 ◽  
Author(s):  
Deyu LIU ◽  
xinchun jian ◽  
PU XU ◽  
Rong ZHU ◽  
Yuan WANG

Abstract Background: Mounting studies demonstrate long non-coding RNA s ( lncRNAs ) play an important role in tumor progression. However, the potential biological functions and clinical importance of Linc01234 in oral squamous cell carcinoma ( OSCC ) still remain unclear. Methods: We evaluated the expression profile and prognostic values of Linc01234 in OSCC tissues via RT-qPCR. Then, functional experiments in vitro were performed to investigate the effects of Linc01234 on tumor growth, migration and invasion in OSCC. Mechanistically, RT-qPCR, bioinformatic analysis and dual luciferase reporter assays were performed to identify a competitive endogenous RNA s ( ceRNA s) among Linc01234, miR-433-3p and PAK4. Results: We found that Linc01234 was evidently upregulated in OSCC tissues and cell lines, and its level was positively associated with T stage, lymphnode metastasis, differentiation and poor prognosis of patients with OSCC. Our results found that Linc01234 inhibited cell proliferation and metastasis abilities in CAL27 and SCC25 cells following its deletion. Mechanistic analysis indicated that Linc01234 may act as a ceRNA (competing endogenous RNA) of miR-433-3p to relieve the repressive effect of miR-433-3p on its target PAK4. Conclusions: Our results indicated that Linc01234 promotes OSCC progression through Linc01234/miR-433/PAK4 axis and might be a potential therapeutic target for OSCC.


2019 ◽  
Author(s):  
Deyu LIU ◽  
xinchun jian ◽  
PU XU ◽  
Rong ZHU ◽  
Yuan WANG

Abstract Background: Mounting studies demonstrate long non-coding RNA s ( lncRNAs ) play an important role in tumor progression. However, the potential biological functions and clinical importance of Linc01234 in oral squamous cell carcinoma ( OSCC ) still remain unclear. Methods: We evaluated the expression profile and prognostic values of Linc01234 in OSCC tissues via RT-qPCR. Then, functional experiments in vitro were performed to investigate the effects of Linc01234 on tumor growth, migration and invasion in OSCC. Mechanistically, RT-qPCR, bioinformatic analysis and dual luciferase reporter assays were performed to identify a competitive endogenous RNA s ( ceRNA s) among Linc01234, miR-433-3p and PAK4. Results: We found that Linc01234 was evidently upregulated in OSCC tissues and cell lines, and its level was positively associated with T stage, lymphnode metastasis, differentiation and poor prognosis of patients with OSCC. Our results found that Linc01234 inhibited cell proliferation and metastasis abilities in CAL27 and SCC25 cells following its deletion. Mechanistic analysis indicated that Linc01234 may act as a ceRNA (competing endogenous RNA) of miR-433-3p to relieve the repressive effect of miR-433-3p on its target PAK4. Conclusions: Our results indicated that Linc01234 promotes OSCC progression through Linc01234/miR-433/PAK4 axis and might be a potential therapeutic target for OSCC.


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