scholarly journals IRF2‑induced Claudin‑7 suppresses cell proliferation, invasion and migration of oral squamous cell carcinoma

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Xin Li ◽  
Weidong Yang
2020 ◽  
Vol 19 ◽  
pp. 153303382096074
Author(s):  
Daoyong Hu ◽  
Tian Zhong ◽  
Qun Dai

Objective: Emerging studies have identified that long non-coding RNAs (lncRNAs) play critical roles in cancer development. This study aims to explore the mechanism of NF-KappaB (NF-κB) interacting lncRNA (NKILA) in the pathological process of oral squamous cell carcinoma (OSCC). Methods: NKILA expression in OSCC tissues, paracancerous tissues, and normal human oral keratinocytes and OSCC cell lines was detected using RT-qPCR. KB cells were selected for the follow-up experiments. The role of NKILA in cell proliferation, migration, invasion, and NF-κB signaling pathway was identified using the gain- and loss-of function of NKILA in OSCC cells. Additionally, the role of NKILA in vitro was determined by inducing xenograft tumors in nude mice. Results: NKILA was poorly expressed in OSCC tissues and cells. Cell proliferation, invasion and migration, tumor volume and weight were significantly suppressed in cells with overexpressed NKILA, while silencing NKILA led to opposite trends. Moreover, the protein levels of p-IκBα and nuclear-p65 were markedly decreased, while the levels of IκBα and cytoplasm-p65 were enhanced in cells with overexpressed NKILA. Conclusion: This study provided evidence that NKILA could reduce proliferation, invasion and migration of OSCC cells through inhibiting the NF-κB signaling pathway. The findings may offer new insights for OSCC prevention and treatment.


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.


2017 ◽  
Vol 352 (2) ◽  
pp. 357-363 ◽  
Author(s):  
Toshikazu Takahara ◽  
Atsushi Kasamatsu ◽  
Masanobu Yamatoji ◽  
Manabu Iyoda ◽  
Hiroki Kasama ◽  
...  

2020 ◽  
Vol 27 (1) ◽  
Author(s):  
Fei Le ◽  
Yangqian Ou ◽  
Ping Luo ◽  
Xiaoming Zhong

Abstract Background Oral squamous cell carcinoma (OSCC) at early stages can be misdiagnosed as an oral ulcer (OU) due to similar symptoms, such as chronic and indurated ulcer. LncRNA NCK1-AS1 has been characterized as a key player in cervical cancer, while its role in OSCC is unknown. Methods All participants were selected at Jiangxi Province Tumor Hospital from December 2016 to December 2018. Expression levels of NCK1-AS1 and miR-100 in plasma from both OSCC and OU patients were measured by RT-qPCR. Diagnostic analysis was performed through ROC curve. Potential interactions between NCK1-AS1 and miR-100 were detected by cell transfection experiments. Cell invasion and migration were assessed by Transwell assays. Results The expression of NCK1-AS1 was upregulated in early-stage OSCC patients but not in OU patients. Upregulation of NCK1-AS1 distinguished OSCC patients from OU patients. The expression of miR-100 was inversely correlated with the expression of NCK1-AS1. Overexpression of NCK1-AS1 was followed by promoted OSCC cell invasion and migration. Overexpression of miR-100 did not affect the expression of NCK1-AS1 but inhibited the role of NCK1-AS1. Conclusions Therefore, NCK1-AS1 may promote the metastasis of OSCC by downregulating miR-100.


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