scholarly journals Activator protein 2 alpha (AP2α) suppresses 42 kDa C/CAAT enhancer binding protein α (p42C/EBPα) in head and neck squamous cell carcinoma

2009 ◽  
Vol 124 (6) ◽  
pp. 1285-1292 ◽  
Author(s):  
Kristi L. Bennett ◽  
Todd Romigh ◽  
Khelifa Arab ◽  
Rosemary E. Teresi ◽  
Yasuhiro Tada ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Binding Protein ◽  
Neck Squamous Cell Carcinoma ◽  
Activator Protein ◽  
Enhancer Binding Protein ◽  
Activator Protein 2

scholarly journals Alternatively spliced ANLN isoforms synergistically contribute to the progression of head and neck squamous cell carcinoma

2021 ◽  
Vol 12 (8) ◽  
Author(s):  
Erliang Guo ◽  
Xionghui Mao ◽  
Xueying Wang ◽  
Lunhua Guo ◽  
Changming An ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Cell Lines ◽  
Squamous Cell ◽  
Binding Protein ◽  
Neck Squamous Cell Carcinoma ◽  
Alternatively Spliced

AbstractHead and neck squamous cell carcinoma (HNSCC) is a common cancer with high mortality. Anilin actin-binding protein (ANLN) has been reported to be associated with carcinogenesis in multiple tumors. However, the expression pattern and functional effects of ANLN in HNSCC remain to be unclear. Clinical data and online databases were used to analyze the expression of ANLN and its relationship with HNSCC patient survival. Expression of two major splice variants of ANLN was assessed in HNSCC tissues and cell lines. The functional effects and related mechanisms of ANLN isoforms were investigated in HNSCC in vitro and in vivo. Our study showed that patients with high expression of ANLN had a poor prognosis. The two primary isoforms of ANLN transcripts ANLN-201 and ANLN-210 were highly expressed in HNSCC tissues and cell lines. Knockout of ANLN restrained cell proliferation, migration, and invasion of SCC-9 cells. Mechanically, ANLN-201 could interact with c-Myc to keep its protein stability, thereby playing a oncogenic role in HNSCC. ANLN-210 could be transferred to macrophages via exosomes by binding to RNA-binding protein hnRNPC. Exosomal ANLN-210 promoted macrophage polarization via PTEN/PI3K/Akt signaling pathway, thus stimulating tumor growth of HNSCC. ANLN was an independent prognostic factor in patients with HNSCC. Alternatively spliced ANLN isoforms collaboratively promote HNSCC tumorigenesis in vitro and in vivo, which might provide the in-depth role and mechanism of ANLN in HNSCC development.

scholarly journals Alternatively Spliced ANLN Isoforms Synergistically Contribute To The Progression of Head and Neck Squamous Cell Carcinoma

2021 ◽  
Author(s):  
Erliang Guo ◽  
Xionghui Mao ◽  
Lunhua Guo ◽  
Changming An ◽  
Cong Zhang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Cell Lines ◽  
Squamous Cell ◽  
Binding Protein ◽  
Neck Squamous Cell Carcinoma ◽  
Alternatively Spliced

Abstract Background: Head and neck squamous cell carcinoma (HNSCC) is a common cancer with high mortality. Anilin actin binding protein (ANLN) has been reported to be associated with carcinogenesis in multiple tumors. However, the expression pattern and functional effects of ANLN in HNSCC remains to be unclear.Methods: Expression of two major splice variants of ANLN was assessed in HNSCC tissues and cell lines. The functional effects and related mechanisms of ANLN isoforms were investigated in HNSCC in vitro and in vivo.Results: Our results showed that the two primary isoforms of ANLN transcripts ANLN-201 and ANLN-210 were highly expressed in HNSCC tissues and cell lines. Knockout of ANLN restrained cell proliferation, migration and invasion of SCC-9 cells. Mechanically, ANLN-201 could interact with c-Myc to keep its protein stability, thereby playing a oncogenic role in HNSCC. ANLN-210 could be transferred to macrophages via exosomes by binding to RNA binding protein hnRNPC. Exosomal ANLN-210 promoted macrophage polarization via PTEN/PI3K/Akt signaling pathway, thus stimulating tumor growth of HNSCC.Conclusions: Our findings demonstrate that alternatively spliced ANLN isoforms collaboratively promote HNSCC tumorigenesis in vitro and in vivo, which might provide the in-depth role and mechanism of ANLN in HNSCC development.

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