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1.
Life Sci ; 278: 119613, 2021 Aug 01.
Article in English | MEDLINE | ID: mdl-34000263

ABSTRACT

AIMS: SLC9A1 plays an important role in the growth, differentiation and glycolysis of tumor cells. The present study aimed to elucidate the correlation between SLC9A1 and tumor immune infiltration. MAIN METHODS: Expression level of SLC9A1 gene in tumors was identified in GEPIA. The correlation between SLC9A1 and survival in various types of cancers was analyzed by the PrognoScan. SLC9A1 immune infiltration levels and clinical correlation analysis was generated via TIMER and TIMER2.0. KEGG enrichment analysis of SLC9A1 expression was evaluated via STRING. KEY FINDINGS: We found that, in cancers such as liver hepatocellular carcinoma (LIHC), the expression of SLC9A1 was significantly higher in tumor tissues compared with normal tissues, and was significantly associated with poor prognosis. Further analysis showed that SLC9A1 expression in LIHC was significantly positively correlated with immune cell infiltration, and the correlation was the highest for LIHC among 40 cancers. The expression of SLC9A1 is significantly correlated with the immune marker set of most immune cells in LIHC. Furthermore, we found that the expression level of TGF-ß (TGFB1) in Tregs showed the highest correlation with the expression of SLC9A1 in LIHC. SIGNIFICANCE: The increased expression of SLC9A1 is positively correlated with the prognosis of cancer and the level of immune infiltration. Therefore, SLC9A1 is an important prognostic factor for immunotherapy against hepatocellular carcinoma.


Subject(s)
Carcinoma, Hepatocellular/immunology , Liver Neoplasms/immunology , Sodium-Hydrogen Exchanger 1/immunology , Carcinoma, Hepatocellular/diagnosis , Carcinoma, Hepatocellular/genetics , Gene Expression Regulation, Neoplastic , Humans , Liver Neoplasms/diagnosis , Liver Neoplasms/genetics , Prognosis , Sodium-Hydrogen Exchanger 1/genetics , Transcriptome
2.
Proc Natl Acad Sci U S A ; 117(4): 2108-2112, 2020 01 28.
Article in English | MEDLINE | ID: mdl-31964810

ABSTRACT

Avian leukosis virus subgroup J (ALV-J) is an important concern for the poultry industry. Replication of ALV-J depends on a functional cellular receptor, the chicken Na+/H+ exchanger type 1 (chNHE1). Tryptophan residue number 38 of chNHE1 (W38) in the extracellular portion of this molecule is a critical amino acid for virus entry. We describe a CRISPR/Cas9-mediated deletion of W38 in chicken primordial germ cells and the successful production of the gene-edited birds. The resistance to ALV-J was examined both in vitro and in vivo, and the ΔW38 homozygous chickens tested ALV-J-resistant, in contrast to ΔW38 heterozygotes and wild-type birds, which were ALV-J-susceptible. Deletion of W38 did not manifest any visible side effect. Our data clearly demonstrate the antiviral resistance conferred by precise CRISPR/Cas9 gene editing in the chicken. Furthermore, our highly efficient CRISPR/Cas9 gene editing in primordial germ cells represents a substantial addition to genotechnology in the chicken, an important food source and research model.


Subject(s)
Avian Leukosis Virus/genetics , Avian Leukosis/immunology , Avian Proteins/genetics , Poultry Diseases/immunology , Sodium-Hydrogen Exchanger 1/genetics , Animals , Animals, Genetically Modified/genetics , Animals, Genetically Modified/immunology , Animals, Genetically Modified/virology , Avian Leukosis/genetics , Avian Leukosis/virology , Avian Leukosis Virus/classification , Avian Leukosis Virus/physiology , Avian Proteins/immunology , CRISPR-Cas Systems , Chickens , Disease Resistance , Female , Gene Editing , Male , Poultry Diseases/genetics , Poultry Diseases/virology , Sodium-Hydrogen Exchanger 1/immunology
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