scholarly journals CCL2/EGF positive feedback loop between cancer cells and macrophages promotes cell migration and invasion in head and neck squamous cell carcinoma

Oncotarget ◽  
2016 ◽  
Vol 7 (52) ◽  
pp. 87037-87051 ◽  
Author(s):  
Lu Gao ◽  
Feng-qin Wang ◽  
Hui-min Li ◽  
Jie-gang Yang ◽  
Jian-Gang Ren ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Migration ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Cancer Cells ◽  
Squamous Cell ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Migration And Invasion ◽  
Positive Feedback Loop

scholarly journals THAP9-AS1/miR-133b/SOX4 positive feedback loop facilitates the progression of esophageal squamous cell carcinoma

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Jiwei Cheng ◽  
Haibo Ma ◽  
Ming Yan ◽  
Wenqun Xing
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Malignant Tumors ◽  
Migration And Invasion ◽  
Positive Feedback Loop

AbstractEsophageal squamous cell carcinoma (ESCC) is one of the most common malignant tumors in the digestive system with a high incidence and poor prognosis. Long non-coding RNAs (LncRNA) have been reported to be closely associated with the occurrence and development of various human cancers. Data from GSE89102 shows an increase of THAP9-AS1 expression in ESCC. However, its functions and mechanisms underlying ESCC progression remain to be investigated. In this study, we found that THAP9-AS1 was overexpressed in ESCC tissues and cells. High THAP9-AS1 expression was positively correlated with tumor size, TNM stage, lymph node metastasis, and worse prognosis. Functionally, depletion of THAP9-AS1 suppressed cell proliferation, migration, and invasion, while enhanced apoptosis in vitro. Consistently, knockdown of THAP9-AS1 inhibited xenograft tumor growth in vivo. Mechanistically, THAP9-AS1 could serve as a competing endogenous RNA (ceRNA) for miR-133b, resulting in the upregulation of SOX4. Reciprocally, SOX4 bound to the promoter region of THAP9-AS1 to activate its transcription. Moreover, the anti-tumor property induced by THAP9-AS1 knockdown was significantly impaired due to miR-133b downregulation or SOX4 overexpression. Taken together, our study reveals a positive feedback loop of THAP9-AS1/miR-133b/SOX4 to facilitate ESCC progression, providing a potential molecular target to fight against ESCC.

scholarly journals A positive feedback loop involving EGFR/Akt/mTORC1 and IKK/NF-κB regulates head and neck squamous cell carcinoma proliferation

Oncotarget ◽  
2016 ◽  
Vol 7 (22) ◽  
pp. 31892-31906 ◽  
Author(s):  
Zhipeng Li ◽  
Zejia Yang ◽  
Antonino Passaniti ◽  
Rena G. Lapidus ◽  
Xuefeng Liu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Neck Squamous Cell Carcinoma ◽  
Positive Feedback Loop

scholarly journals Epigenetic Activation of AP1 Promotes Squamous Cell Carcinoma Metastasis

2013 ◽  
Vol 6 (273) ◽  
pp. ra28-ra28 ◽  
Author(s):  
Xiangming Ding ◽  
Hongya Pan ◽  
Jiong Li ◽  
Qi Zhong ◽  
Xiaohong Chen ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Lymph Node ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Positive Feedback ◽  
Messenger Rna ◽  
Feedback Loop ◽  
Invasive Growth ◽  
Positive Feedback Loop ◽  
Genes Encoding

The transcription factor AP1 (activating protein 1), a heterodimer of the JUN and FOS proteins, promotes the invasive growth and metastasis of various tumors such as squamous cell carcinoma (SCC), breast cancer, and melanoma. AP1 activity is transcriptionally induced through a positive feedback loop. We identified the histone demethylase KDM4A (lysine-specific demethylase 4A) as a key epigenetic priming factor in this positive feedback loop. KDM4A contributed to the induction of genes encoding the AP1 transcription factors and the invasive growth and metastasis of SCC. KDM4A knockdown decreased the growth factor–induced messenger RNA expression and protein abundance of AP1 family members, including JUN and FOSL1. Mechanistically, histone demethylation by KDM4A facilitated the binding of the AP1 complex to the promoters of JUN and FOSL1, thereby promoting the positive feedback loop that maintains activation of AP1. In a mouse model of SCC, KDM4A knockdown inhibited lymph node metastasis. Moreover, the abundance of KDM4A correlated with the abundance of JUN and FOSL1 in human SCC tissues, and KDM4A expression was increased in human lymph node metastases. Our studies provide insights into the epigenetic control of AP1 and tumor invasion and suggest that KDM4A could be an important therapeutic target for inhibiting invasive SCC growth and metastasis.

scholarly journals CCR7 Regulates Cell Migration and Invasion through JAK2/STAT3 in Metastatic Squamous Cell Carcinoma of the Head and Neck

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Fa-Yu Liu ◽  
Jawad Safdar ◽  
Zhen-Ning Li ◽  
Qi-Gen Fang ◽  
Xu Zhang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Migration ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Migration And Invasion ◽  
Signal Pathways ◽  
Invasion And Migration ◽  
Stat3 Phosphorylation ◽  
And Migration

Squamous cell carcinoma of the head and neck (SCCHN) frequently involves metastasis at diagnosis. Our previous research has demonstrated that CCR7 plays a key role in regulating SCCHN metastasis, and this process involves several molecules, such as PI3K/cdc42, pyk2, and Src. In this study, the goals are to identify whether JAK2/STAT3 also participates in CCR7’s signal network, its relationship with other signal pathways, and its role in SCCHN cell invasion and migration. The results showed that stimulation of CCL19 could induce JAK2/STAT3 phosphorylation, which can be blocked by Src and pyk2 inhibitors. After activation, STAT3 was able to promote low expression of E-cadherin and had no effect on vimentin. This JAk2/STAT3 pathway not only mediated CCR7-induced cell migration but also mediated invasion speed. The immunohistochemistry results also showed that the phosphorylation of STAT3 was correlated with CCR7 expression in SCCHN, and CCR7 and STAT3 phosphorylation were all associated with lymph node metastasis. In conclusion, JAk2/STAT3 plays a key role in CCR7 regulating SCCHN metastasis.

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