Glutaredoxin 3 promotes migration and invasion via the Notch signalling pathway in oral squamous cell carcinoma

: Cancer, a set of diseases characterized by abnormal cell growth resulting from alteration in the expression pattern of diverse genes, is one of the prominent cause of mortality and morbidity worldwide. This modification of various genes lead to altered signalling cascades and changes in the molecular network. These changes eventually give rise to cellular dysfunction and then to systemic failure causing death. Of the several pathways that are aberrantly activated in cancer, Notch signalling pathway is a prominent one. Notch signalling pathway is a juxtracrine signalling pathway which activates the genes associated with cell proliferation, survival and angiogenesis. Notch signalling pathway components are seen to be upregulated in several types of cancer. Oral squamous cell carcinoma (OSCC) is a predominant category of oral cancer where aberrant activation of Notch signalling causes tumour progression and metastasis. In this review, we discuss the Notch signalling pathway, its components, forms and its role in the progression and metastasis of oral squamous cell carcinoma.

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MicroRNA‐29b‐3p suppresses oral squamous cell carcinoma cell migration and invasion via IL32/AKT signalling pathway

Journal of Cellular and Molecular Medicine ◽

10.1111/jcmm.14794 ◽

2020 ◽

Vol 24 (1) ◽

pp. 841-849 ◽

Cited By ~ 3

Author(s):

Jianya He ◽

Wen Ye ◽

Ni Kou ◽

Kang Chen ◽

Bai Cui ◽

...

Keyword(s):

Squamous Cell Carcinoma ◽

Cell Migration ◽

Oral Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Carcinoma Cell ◽

Signalling Pathway ◽

Migration And Invasion ◽

Squamous Cell Carcinoma Cell ◽

Cell Migration And Invasion

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Cyclosporine A Suppresses the Malignant Progression of Oral Squamous Cell Carcinoma in vitro

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520618666181029170605 ◽

2019 ◽

Vol 19 (2) ◽

pp. 248-255 ◽

Cited By ~ 2

Author(s):

Ling Gao ◽

Jianwei Dong ◽

Nanyang Zhang ◽

Zhanxian Le ◽

Wenhao Ren ◽

...

Keyword(s):

Cell Cycle ◽

Squamous Cell Carcinoma ◽

Oral Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Cyclosporine A ◽

Migration And Invasion ◽

Signal Molecules ◽

Cox 2

Background:The Oral Squamous Cell Carcinoma (OSCC) is one of the most frequent cancer types. Failure of treatment of OSCC is potentially lethal because of local recurrence, regional lymph node metastasis, and distant metastasis. Chemotherapy plays a vital role through suppression of tumorigenesis. Cyclosporine A (CsA), an immunosuppressant drug, has been efficiently used in allograft organ transplant recipients to prevent rejection, and also has been used in a subset of patients with autoimmunity related disorders. The present study aims to investigate novel and effective chemotherapeutic drugs to overcome drug-resistance in the treatment of OSCC.Methods:Cells were incubated in the standard way. Cell viability was assayed using the MTT assay. Cell proliferation was determined using colony formation assay. The cell cycle assay was performed using flow cytometry. Apoptosis was assessed using fluorescence-activated cell sorting after stained by the Annexin V-fluorescein isothiocyanate (FITC). Cell migration and invasion were analyzed using wound healing assay and tranwell. The effect of COX-2, c-Myc, MMP-9, MMP-2, and NFATc1 protein expression was determined using Western blot analysis while NFATc1 mRNA expression was determined by RT-PCR.Results:In vitro studies indicated that CsA inhibited partial OSCC growth by inducing cell cycle arrest, apoptosis, and the migration and invasion of OSCC cells. We also demonstrated that CsA could inhibit the expression of NFATc1 and its downstream genes COX-2, c-Myc, MMP-9, and MMP-2 in OSCC cells. Furthermore, we analyzed the expression of NFATc1 in head and neck cancer through the Oncomine database. The data was consistent with the experimental findings.Conclusion:The present study initially demonstrated that CsA could inhibit the progression of OSCC cells and can mediate the signal molecules of NFATc1 signaling pathway, which has strong relationship with cancer development. That explains us CsA has potential to explore the possibilities as a novel chemotherapeutic drug for the treatment of OSCC.

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Downregulation of ceramide synthase 1 promotes oral cancer through endoplasmic reticulum stress

International Journal of Oral Science ◽

10.1038/s41368-021-00118-4 ◽

2021 ◽

Vol 13 (1) ◽

Author(s):

Wen Chen ◽

Chenzhou Wu ◽

Yafei Chen ◽

Yuhao Guo ◽

Ling Qiu ◽

...

Keyword(s):

Squamous Cell Carcinoma ◽

Endoplasmic Reticulum ◽

Oral Cancer ◽

Oral Squamous Cell Carcinoma ◽

Endoplasmic Reticulum Stress ◽

Cell Carcinoma ◽

Squamous Cell ◽

Migration And Invasion ◽

Ceramide Synthase

AbstractC18 ceramide plays an important role in the occurrence and development of oral squamous cell carcinoma. However, the function of ceramide synthase 1, a key enzyme in C18 ceramide synthesis, in oral squamous cell carcinoma is still unclear. The aim of our study was to investigate the relationship between ceramide synthase 1 and oral cancer. In this study, we found that the expression of ceramide synthase 1 was downregulated in oral cancer tissues and cell lines. In a mouse oral squamous cell carcinoma model induced by 4-nitroquinolin-1-oxide, ceramide synthase 1 knockout was associated with the severity of oral malignant transformation. Immunohistochemical studies showed significant upregulation of PCNA, MMP2, MMP9, and BCL2 expression and downregulation of BAX expression in the pathological hyperplastic area. In addition, ceramide synthase 1 knockdown promoted cell proliferation, migration, and invasion in vitro. Overexpression of CERS1 obtained the opposite effect. Ceramide synthase 1 knockdown caused endoplasmic reticulum stress and induced the VEGFA upregulation. Activating transcription factor 4 is responsible for ceramide synthase 1 knockdown caused VEGFA transcriptional upregulation. In addition, mild endoplasmic reticulum stress caused by ceramide synthase 1 knockdown could induce cisplatin resistance. Taken together, our study suggests that ceramide synthase 1 is downregulated in oral cancer and promotes the aggressiveness of oral squamous cell carcinoma and chemotherapeutic drug resistance.

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SNHG1/miR‐186/FUT8 regulates cell migration and invasion in oral squamous cell carcinoma

Oral Diseases ◽

10.1111/odi.13878 ◽

2021 ◽

Author(s):

Yanxia Zhao ◽

Jun Shi ◽

Yankun Zhao ◽

Zhifang Lu

Keyword(s):

Squamous Cell Carcinoma ◽

Cell Migration ◽

Oral Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Migration And Invasion ◽

Cell Migration And Invasion

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Clinical significance of Annexin A2 expression in oral squamous cell carcinoma and its influence on cell proliferation, migration and invasion

Scientific Reports ◽

10.1038/s41598-021-84675-y ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Yingyi Ma ◽

Haiye Wang

Keyword(s):

Squamous Cell Carcinoma ◽

Oral Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Annexin A2 ◽

Migration And Invasion ◽

Poor Survival ◽

Basic Study ◽

Proliferation And Metastasis ◽

Cancer Tissues

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.

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Knockdown of circ_0011946 targets miR-216a-5p/BCL2L2 axis to regulate proliferation, migration, invasion and apoptosis of oral squamous cell carcinoma cells

BMC Cancer ◽

10.1186/s12885-021-08779-4 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Ying Zhou ◽

Shuhong Zhang ◽

Zhonghan Min ◽

Zhongwei Yu ◽

Huaiwei Zhang ◽

...

Keyword(s):

Cell Proliferation ◽

Squamous Cell Carcinoma ◽

Oral Squamous Cell Carcinoma ◽

Tumor Growth ◽

Cell Carcinoma ◽

Squamous Cell ◽

B Cell Lymphoma ◽

Luciferase Reporter ◽

Migration And Invasion

Abstract Background Circular RNAs (circRNAs) are implicated in the development of oral squamous cell carcinoma (OSCC). The aim of current research is to elucidate the role and mechanism of circ_0011946 in the functional behaviors of OSCC cells. Methods Circ_0011946, microRNA (miR)-216a-5p, B cell lymphoma-2-like 2 protein (BCL2L2) abundances were exposed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) or western blot. Cell proliferation, migration, invasion and apoptosis were detected by MTT, colony formation assay, transwell, wound-healing and flow cytometry assays, respectively. Target correlation was tested by dual-luciferase reporter and RNA pull-down assays. An in vivo xenograft experiment was employed to investigate the function of circ_0011946 on tumor growth in vivo. Results Circ_0011946 and BCL2L2 levels were increased, while miR-216a-5p level was decreased in OSCC tissues and cells. Circ_0011946 knockdown impeded proliferation, migration, and invasion, but promoted apoptosis in OSCC cells. Circ_0011946 functioned as a sponge for miR-216a-5p, and BCL2L2 was targeted by miR-216a-5p. Besides, miR-216a-5p or BCL2L2 knockdown partly attenuated the inhibitory influences of circ_0011946 silence or miR-216a-5p overexpression on OSCC cell progression. Furthermore, circ_0011946 post-transcriptionally regulated BCL2L2 through sponging miR-216a-5p. Moreover, circ_0011946 knockdown constrained OSCC tumor growth in vivo. Conclusion Circ_0011946 silence repressed OSCC cell proliferation, migration, and invasion, but promoted apoptosis through the regulation of the miR-216a-5p/BCL2L2 axis.

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