Decreased PITX1 gene expression in human cutaneous malignant melanoma and its clinicopathological significance

2013 ◽  
Vol 23 (3) ◽  
pp. 344-349 ◽  
Author(s):  
Mitsuhiko Osaki ◽  
Hikari Chinen ◽  
Yuichi Yoshida ◽  
Takahito Ohhira ◽  
Naohiro Sunamura ◽  
...  
2016 ◽  
Vol 32 (10) ◽  
pp. 494-500 ◽  
Author(s):  
Figen Barut ◽  
Perihan Udul ◽  
Furuzan Kokturk ◽  
Nilufer Onak Kandemir ◽  
Sevinc Hallac Keser ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Baihe Wang ◽  
Yang Li ◽  
Caixia Kou ◽  
Jianfang Sun ◽  
Xiulian Xu

Background. Epithelial splicing regulatory protein 1 (ESRP1) has been described as an RNA-binding protein involved in cancer development. However, the expression and regulatory network of ESRP1 in cutaneous malignant melanoma (CMM) remain unclear. Methods. From the sequencing data of 103 CMM samples in The Cancer Genome Atlas database, the expression level of ESRP1 and its correlation with the clinicopathological characteristics were analyzed using the Oncomine 4.5, Gene Expression Profiling Interactive Analysis (GEPIA), and UALCAN tools, while LinkedOmics was used to identify differential gene expression with ESRP1 and to analyze Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Gene enrichment analysis examined target networks of kinases, miRNAs, and transcription factors. Finally, TIMER was used to analyze the relationship between ESRP1 and tumor immune cell infiltration. Results. We found that ESRP1 was lowly expressed in CMM tissues, and a low level of ESRP1 expression correlated with better overall survival. Expression of this gene was linked to functional networks involving the condensed chromosomes, epidermal development, and translation initiation. Functional network analysis suggested that ESRP1 regulated ribosome metabolism, drug metabolism, and chemical carcinogenesis via pathways involving several cancer-related kinases, miRNAs, and transcription factors. Furthermore, our results suggested that ESRP1 played an important role in regulating tumor-associated macrophage polarization, dendritic cell infiltration, Treg cells, and T cell exhaustion. Conclusion. Our study demonstrates ESRP1 expression, prognostic value, and potential regulatory networks in CMM, thereby shedding light on the clinical significance of ESRP1, and provides a novel biomarker for determining prognosis and immune infiltration in CMM.


2010 ◽  
Vol 130 (1) ◽  
pp. 221-229 ◽  
Author(s):  
Yasufumi Goto ◽  
Kazuo Koyanagi ◽  
Norihiko Narita ◽  
Yutaka Kawakami ◽  
Minoru Takata ◽  
...  

Nature ◽  
2000 ◽  
Vol 406 (6795) ◽  
pp. 536-540 ◽  
Author(s):  
M. Bittner ◽  
P. Meltzer ◽  
Y. Chen ◽  
Y. Jiang ◽  
E. Seftor ◽  
...  

2010 ◽  
Vol 38 (1) ◽  
pp. 76-83 ◽  
Author(s):  
Sachiko NORO ◽  
Naoya YAMAZAKI ◽  
Yukihiro NAKANISHI ◽  
Akifumi YAMAMOTO ◽  
Yuko SASAJIMA ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 605
Author(s):  
Jana Jandova ◽  
Anh B. Hua ◽  
Jocelyn Fimbres ◽  
Georg T. Wondrak

There are two stable isotopes of hydrogen, protium (1H) and deuterium (2H; D). Cellular stress response dysregulation in cancer represents both a major pathological driving force and a promising therapeutic target, but the molecular consequences and potential therapeutic impact of deuterium (2H)-stress on cancer cells remain largely unexplored. We have examined the anti-proliferative and apoptogenic effects of deuterium oxide (D2O; ‘heavy water’) together with stress response gene expression profiling in panels of malignant melanoma (A375V600E, A375NRAS, G361, LOX-IMVI), and pancreatic ductal adenocarcinoma (PANC-1, Capan-2, or MIA PaCa-2) cells with inclusion of human diploid Hs27 skin fibroblasts. Moreover, we have examined the efficacy of D2O-based pharmacological intervention in murine models of human melanoma tumor growth and metastasis. D2O-induction of apoptosis was substantiated by AV-PI flow cytometry, immunodetection of PARP-1, and pro-caspase 3 cleavage, and rescue by pan-caspase inhibition. Differential array analysis revealed early modulation of stress response gene expression in both A375 melanoma and PANC-1 adenocarcinoma cells elicited by D2O (90%; ≤6 h) (upregulated: CDKN1A, DDIT3, EGR1, GADD45A, HMOX1, NFKBIA, or SOD2 (up to 9-fold; p < 0.01)) confirmed by independent RT-qPCR analysis. Immunoblot analysis revealed rapid onset of D2O-induced stress response phospho-protein activation (p-ERK, p-JNK, p-eIF2α, or p-H2AX) or attenuation (p-AKT). Feasibility of D2O-based chemotherapeutic intervention (drinking water (30% w/w)) was demonstrated in a severe combined immunodeficiency (SCID) mouse melanoma metastasis model using luciferase-expressing A375-Luc2 cells. Lung tumor burden (visualized by bioluminescence imaging) was attenuated by D2O, and inhibition of invasiveness was also confirmed in an in vitro Matrigel transwell invasion assay. D2O supplementation also suppressed tumor growth in a murine xenograft model of human melanoma, and median survival was significantly increased without causing adverse effects. These data demonstrate for the first time that systemic D2O administration impairs growth and metastasis of malignant melanoma through the pharmacological induction of deuterium (2H)-stress.


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