scholarly journals Circular RNA_0001742 has potential to predict advanced tumor stage and poor survival profiles in tongue squamous cell carcinoma management

2020 ◽  
Vol 34 (8) ◽  
Author(s):  
Yuan Yao ◽  
Lei Bi ◽  
Chunguang Zhang
2017 ◽  
Vol 137 (3) ◽  
pp. 775-778 ◽  
Author(s):  
Melody Abikhair ◽  
Nazanin Roudiani ◽  
Hiroshi Mitsui ◽  
James G. Krueger ◽  
Anna Pavlick ◽  
...  

2008 ◽  
Vol 135 (5) ◽  
pp. 703-713 ◽  
Author(s):  
Silvia S. Borkosky ◽  
Mehmet Gunduz ◽  
Hitoshi Nagatsuka ◽  
Levent Bekir Beder ◽  
Esra Gunduz ◽  
...  

2016 ◽  
Vol 273 (12) ◽  
pp. 4515-4524 ◽  
Author(s):  
Miia Seppälä ◽  
Konsta Pohjola ◽  
Jussi Laranne ◽  
Markus Rautiainen ◽  
Heini Huhtala ◽  
...  

2020 ◽  
Author(s):  
Jie Fan ◽  
Yang Yang ◽  
Qigen Fang ◽  
Meng Cui ◽  
Wei Du ◽  
...  

Abstract Objective: To analyze the prognostic value of frequency of heterotypic neutrophil-in-tumor structure(FNiT) in patients with tongue squamous cell carcinoma(TSCC).Methods: In vitro, we cocultured TSCC cell line-CAL33 with neutrophils to form heterotypic neutrophil-in-tumor structures, which were then subject to fluorescence staining. Clinically, 197 patients were enrolled. Information including age, sex, FNiT, ECOG PS(Performance Status), FH (family history) of cancer, complications, and pathological characteristics such as tumor stage, node stage, metastasis, disease stage, lymphovascular invasion, perineural invasion, tumor grade, and follow-up results was extracted and analyzed.Results: Fluorescent staining results of typical heterotypic neutrophil-in-tumor structure showed that well-differentiated CAL-33-2 had stronger ability to internalize more neutrophils than poorly-differentiated CAL-33-1 did, the latter often internalizing only one neutrophil. The mean FNiT was 4.8‰,with a range from 2.1‰ to 8.9‰. The FNiT was significantly associated with tumor stage, disease stage and tumor grade. A total of 119 patients died of the disease, and the 5-year disease-specific survival(DSS) rate was 36%. The median survival time was 52.6 months. In patients with an FNiT<4.8‰, the 5-year DSS rate was 40%; in patients with an FNiT>=4.8‰, the 5-year DSS was 28%, and the difference was significant(P=0.001). Cox model analysis showed that FNiT along with disease stage, lymphovascular invasion and tumor grade was an independent prognostic factor for DSS.Conclusion: The FNiT as a novel predictor is positively correlated with adverse prognosis of patients with TSCC.


2020 ◽  
Vol 48 (9) ◽  
pp. 4858-4876 ◽  
Author(s):  
Yue Wu ◽  
Xue Wang ◽  
Feifei Xu ◽  
Lu Zhang ◽  
Tianjiao Wang ◽  
...  

Abstract High-mobility group AT-hook 2 (HMGA2) is an architectural transcription factor that plays essential roles in embryonic development and cancer progression. However, the mechanism of HMGA2 regulation remains largely uncharacterized. Here, we demonstrate that HMGA2 can be modulated by hepatitis B X-interacting protein (HBXIP), an oncogenic transcriptional coactivator, in esophageal squamous cell carcinoma (ESCC). HMGA2 expression was positively associated with HBXIP expression in clinical ESCC tissues, and their high levels were associated with advanced tumor stage and reduced overall and disease-free survival. We found that oncogenic HBXIP could posttranslationally upregulate HMGA2 protein level in ESCC cells. HBXIP induced HMGA2 acetylation at the lysine 26 (K26), resulting in HMGA2 protein accumulation. In this process, HBXIP increased the acetyltransferase p300/CBP-associated factor (PCAF) phosphorylation and activation via the Akt pathway, then PCAF directly interacted with HMGA2, leading to HMGA2 acetylation in the cells. HMGA2 K26 acetylation enhanced its DNA binding capacity and blocked its ubiquitination and then inhibited proteasome-dependent degradation. Functionally, HBXIP-stabilized HMGA2 could promote ESCC cell growth in vitro and in vivo. Strikingly, aspirin suppressed ESCC growth by inhibiting HBXIP and HMGA2. Collectively, our findings disclose a new mechanism for the posttranslational regulation of HMGA2 mediated by HBXIP in ESCC.


Cancers ◽  
2021 ◽  
Vol 13 (19) ◽  
pp. 4952
Author(s):  
Cristina Mir ◽  
Yoelsis Garcia-Mayea ◽  
Laia Garcia ◽  
Pol Herrero ◽  
Nuria Canela ◽  
...  

To characterize the mechanisms that govern chemoresistance, we performed a comparative proteomic study analyzing head and neck squamous cell carcinoma (HNSCC) cells: CCL-138 (parental), CCL-138-R (cisplatin-resistant), and cancer stem cells (CSCs). Syntenin-1 (SDCBP) was upregulated in CCL-138-R cells and CSCs over parental cells. SDCBP depletion sensitized biopsy-derived and established HNSCC cell lines to cisplatin (CDDP) and reduced CSC markers, Src activation being the main SDCBP downstream target. In mice, SDCBP-depleted cells formed tumors with decreased mitosis, Ki-67 positivity, and metastasis over controls. Moreover, the fusocellular pattern of CCL-138-R cell-derived tumors reverted to a more epithelial morphology upon SDCBP silencing. Importantly, SDCBP expression was associated with Src activation, poor differentiated tumor grade, advanced tumor stage, and shorter survival rates in a series of 382 HNSCC patients. Our results reveal that SDCBP might be a promising therapeutic target for effectively eliminating CSCs and CDDP resistance.


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