Immunogenetics最新文献_第9页

Tumor necrosis factor-α induces proliferation and reduces apoptosis of colorectal cancer cells through STAT3 activation. 肿瘤坏死因子-α通过激活STAT3诱导结直肠癌细胞增殖并减少凋亡。

IF 3.2 4区医学

Immunogenetics Pub Date : 2023-04-01 DOI: 10.1007/s00251-023-01302-y

Wei Wei, Juanhong Wang, Pu Huang, Siqi Gou, Daihua Yu, Lei Zong

{"title":"Tumor necrosis factor-α induces proliferation and reduces apoptosis of colorectal cancer cells through STAT3 activation.","authors":"Wei Wei, Juanhong Wang, Pu Huang, Siqi Gou, Daihua Yu, Lei Zong","doi":"10.1007/s00251-023-01302-y","DOIUrl":"https://doi.org/10.1007/s00251-023-01302-y","url":null,"abstract":"Tumor necrosis factor-alpha (TNF-α) is a potent pro-inflammatory factor that plays an important role in establishing a complicated connection between inflammation and cancer. TNF-α promotes tumor proliferation, migration, invasion, and angiogenesis according to numerous studies. Studies have shown the significant role of STAT3, a downstream transcription factor of another important inflammatory cytokine, IL-6 in the development and progression of different tumors especially colorectal cancer. In the present study, we investigated whether TNF-α has a role in proliferation and apoptosis of colorectal cancer cells through STAT3 activation. HCT116 cell line as human colorectal cancer cells was used in this study. Major assays were MTT assay, reverse transcription-PCR (RT-PCR), flow cytometric analysis, and ELISA. Results showed that TNF-α significantly increased the phosphorylation of STAT3 and expression of all the STAT3 target genes related to cell proliferation, survival, and metastasis compared with control. Moreover, our data showed that the STAT3 phosphorylation and expression of its target genes significantly were reduced in the presence of TNF-α + STA-21 compared with TNF-α-treated group demonstrating that the increase in genes expression partially was due to the TNF-α-induced STAT3 activation. On the other hand, STAT3 phosphorylation and mRNA levels of its target genes were partially decreased in the presence of TNF-α + IL-6R supporting the indirect pathway of STAT3 activation by TNF-α through inducing IL-6 production in cancer cells. Given the growing evidence for STAT3 as a key mediator of inflammation-induced colon cancer, our findings support further investigation of STAT3 inhibitors as potential cancer therapies.","PeriodicalId":13446,"journal":{"name":"Immunogenetics","volume":"75 2","pages":"161-169"},"PeriodicalIF":3.2,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9197211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Assessment of regulatory T cells (Tregs) and Foxp3 methylation level in chronic myeloid leukemia patients on tyrosine kinase inhibitor therapy. 评估接受酪氨酸激酶抑制剂治疗的慢性髓性白血病患者的调节性 T 细胞（Tregs）和 Foxp3 甲基化水平。

IF 3.2 4区医学

Immunogenetics Pub Date : 2023-04-01 Epub Date: 2022-12-26 DOI: 10.1007/s00251-022-01291-4

Shahla'a Fadhil Sabir, Bassam Francis Matti, Wifaq Mahmood Ali Alwatar

{"title":"Assessment of regulatory T cells (Tregs) and Foxp3 methylation level in chronic myeloid leukemia patients on tyrosine kinase inhibitor therapy.","authors":"Shahla'a Fadhil Sabir, Bassam Francis Matti, Wifaq Mahmood Ali Alwatar","doi":"10.1007/s00251-022-01291-4","DOIUrl":"10.1007/s00251-022-01291-4","url":null,"abstract":"The key cell population permits cancer cells to avoid immune-surveillance is regulatory T cells (Tregs). This study evaluates the level of Tregs in chronic myeloid leukemia (CML) patients and the effect of Tyrosine kinase inhibitor (TKI) on Treg levels, as a pathway to understand the immune response and behavior among advance stage and optimal response CML patients using imatinib therapy. Blood samples were collected from 30 CML patients (optimal response to TKI), 30 CML patients (failure response to TKI), and 30 age- and gender-matched controls. Analysis involved measuring percentages of Tregs (CD4 + CD25 + FOXP3 +) by flow cytometer and demethylation levels of FOXP3 Treg-specific demethylated region (TSDR) by PCR. The data revealed that Tregs and the FOXP3-TSDR demethylation percentages significantly increased in failure response group in comparison to the optimal response and control groups, while no significant difference between optimal response and control groups. Tregs and FOXP3 TSDR demethylation percentages showed high sensitivity and specificity, suggesting powerful discriminatory biomarkers between failure and optimal groups. An assessment of the Tregs and demethylation percentage among different BCR-ABL levels of CML patients on TKI revealed no significant differences in parameter percentage in the optimal response to TKI patients with different molecular responses (log 3 reduction or other deeper log 4.5 and 5 reduction levels). Our findings demonstrate an effective role of functional Tregs among different CML stages. Also, the study suggests that the major molecular response to therapy at level 0.1% of BCR-ABL transcript could be enough to induce immune system restoration in patients.","PeriodicalId":13446,"journal":{"name":"Immunogenetics","volume":"75 2","pages":"145-153"},"PeriodicalIF":3.2,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9196806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

X-linked hyper-immunoglobulin M syndrome harboring a novel CD40-ligand gene mutation: a case report. 携带一种新的cd40配体基因突变的x连锁超免疫球蛋白M综合征:一例报告。

IF 3.2 4区医学

Immunogenetics Pub Date : 2023-04-01 DOI: 10.1007/s00251-022-01289-y

Rahul Ramachandran, Yamini Krishnan, Parminder Singh, Ashok Kumar, Abhishek Mohanty

{"title":"X-linked hyper-immunoglobulin M syndrome harboring a novel CD40-ligand gene mutation: a case report.","authors":"Rahul Ramachandran, Yamini Krishnan, Parminder Singh, Ashok Kumar, Abhishek Mohanty","doi":"10.1007/s00251-022-01289-y","DOIUrl":"https://doi.org/10.1007/s00251-022-01289-y","url":null,"abstract":"The X-linked hyper-IgM syndrome (X-HIGM1) is a rare primary immunodeficiency disorder (PID) caused by mutations in the gene encoding the CD154 protein, also known as CD40 ligand (CD40LG). X-HIGM1 is characterized by normal or elevated serum levels of IgM in association with decreased levels of IgG, IgA, and IgE. The CD40LG protein expressed on activated T cells interacts with its receptor protein, CD40, on B lymphocytes and dendritic cells. Mutations in the CD40LG gene lead to the production of an abnormal CD40L protein that fails to attach to its receptor, CD40 on B cells resulting in failure to produce IgG, IgA, and IgE antibodies. In the present study, we investigated the molecular defects underlying such a PID in a patient presenting with clinical history of pneumonia and acute respiratory distress syndrome (ARDS) at 7 months of age and diagnosed as transient hypogammaglobulinemia with decreased levels of IgG and increased levels of IgM. We have identified a novel and yet to be reported frame shift deletion of a single base pair (c.229delA) in exon 2 (p.Arg77AspfsTer6) of the CD40L gene ensuing the premature truncation of the protein by 6 amino acids by targeted gene sequencing. This frame shift mutation identified as a CD40L variant was found to be pathogenic which was also validated by Sanger sequencing. The in-silico analysis of c.229 del A mutation also predicted the change to be pathological affecting the structure and function of the CD40L (CD40L, CD154) protein and its protein-protein interaction properties.","PeriodicalId":13446,"journal":{"name":"Immunogenetics","volume":"75 2","pages":"191-194"},"PeriodicalIF":3.2,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9201473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Age-dependent effect of the IFIH1/MDA5 gene variants on the risk of critical COVID-19. IFIH1/MDA5基因变异对COVID-19危重症风险的年龄依赖性影响

IF 3.2 4区医学

Immunogenetics Pub Date : 2023-04-01 DOI: 10.1007/s00251-022-01281-6

María G Muñiz-Banciella, Guillermo M Albaiceta, Laura Amado-Rodríguez, Estefanía Salgado Del Riego, Inés López Alonso, Cecilia López-Martínez, Paula Martín-Vicente, Marta García-Clemente, Tamara Hermida-Valverde, Ana I Enríquez-Rodriguez, Cristina Hernández-González, Elías Cuesta-Llavona, Victoria Alvarez, Juan Gómez, Eliecer Coto

{"title":"Age-dependent effect of the IFIH1/MDA5 gene variants on the risk of critical COVID-19.","authors":"María G Muñiz-Banciella, Guillermo M Albaiceta, Laura Amado-Rodríguez, Estefanía Salgado Del Riego, Inés López Alonso, Cecilia López-Martínez, Paula Martín-Vicente, Marta García-Clemente, Tamara Hermida-Valverde, Ana I Enríquez-Rodriguez, Cristina Hernández-González, Elías Cuesta-Llavona, Victoria Alvarez, Juan Gómez, Eliecer Coto","doi":"10.1007/s00251-022-01281-6","DOIUrl":"https://doi.org/10.1007/s00251-022-01281-6","url":null,"abstract":"MDA5, encoded by the IFIH1gene, is a cytoplasmic sensor of viral RNAs that triggers interferon (IFN) antiviral responses. Common and rare IFIH1 variants have been associated with the risk of type 1 diabetes and other immune-mediated disorders, and with the outcome of viral diseases. Variants associated with reduced IFN expression would increase the risk for severe viral disease. The MDA5/IFN pathway would play a critical role in the response to SARS-CoV-2 infection mediating the extent and severity of COVID-19. Here, we genotyped a cohort of 477 patients with critical ICU COVID-19 (109 death) for three IFIH1 functional variants: rs1990760 (p.Ala946Thr), rs35337543 (splicing variant, intron 8 + 1G > C), and rs35744605 (p.Glu627Stop). The main finding of our study was a significant increased frequency of rs1990760 C-carriers in early-onset patients (< 65 years) (p = 0.01; OR = 1.64, 95%CI = 1.18-2.43). This variant was also increased in critical vs. no-ICU patients and in critical vs. asymptomatic controls. The rs35744605 C variant was associated with increased blood IL6 levels at ICU admission. The rare rs35337543 splicing variant showed a trend toward protection from early-onset critical COVID-19. In conclusion, IFIH1 variants associated with reduced gene expression and lower IFN response might contribute to develop critical COVID-19 with an age-dependent effect.","PeriodicalId":13446,"journal":{"name":"Immunogenetics","volume":"75 2","pages":"91-98"},"PeriodicalIF":3.2,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9702716/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9249121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Correction to: Llama peripheral B-cell populations producing conventional and heavy chain-only IgG subtypes are phenotypically indistinguishable but immunogenetically distinct. 修正:产生常规和仅重链IgG亚型的羊驼外周b细胞群在表型上无法区分，但在免疫遗传学上是不同的。

IF 3.2 4区医学

Immunogenetics Pub Date : 2023-04-01 DOI: 10.1007/s00251-023-01299-4

Kevin A Henry, Henk van Faassen, Doreen Harcus, Anne Marcil, Jennifer J Hill, Serge Muyldermans, C Roger MacKenzie

引用次数: 0

Unfavorable immunotherapy plus tyrosine kinase inhibition outcome of metastatic renal cell carcinoma after radical nephrectomy with increased ADAM9 expression. 不良免疫治疗加酪氨酸激酶抑制转移性肾癌根治性肾切除术后ADAM9表达升高的结果。

IF 3.2 4区医学

Immunogenetics Pub Date : 2023-04-01 DOI: 10.1007/s00251-022-01292-3

Xianglai Xu, Ying Wang, Zhaoyi Chen, Yanjun Zhu, Jiajun Wang, Jianming Guo

{"title":"Unfavorable immunotherapy plus tyrosine kinase inhibition outcome of metastatic renal cell carcinoma after radical nephrectomy with increased ADAM9 expression.","authors":"Xianglai Xu, Ying Wang, Zhaoyi Chen, Yanjun Zhu, Jiajun Wang, Jianming Guo","doi":"10.1007/s00251-022-01292-3","DOIUrl":"https://doi.org/10.1007/s00251-022-01292-3","url":null,"abstract":"Immunotherapy plus tyrosine kinase inhibitor (IO-TKI) has become the standard first-line therapy for advanced renal cell carcinoma (RCC). However, the modest response rate of IO-TKI therapy and the absence of biomarkers limited the selection of treatment strategies for RCC patients. There were three cohorts enrolled: two from our facility (ZS-MRCC and ZS-HRRCC) and one from a clinical study (JAVELIN-101). By RNA sequencing, the expression of ADAM9 in each sample was measured. By flow cytometry and immunohistochemistry, immune infiltration and T cell function were examined. Primary outcomes were established as treatment response and progression-free survival (PFS). Patients with low-ADAM9 expression had a higher objective response rate (56.5% vs 13.6%, P = 0.01) and longer PFS in both cohorts. In the ZS-HRRCC cohort, the expression of ADAM9 was associated with increased tumor-infiltrating T cells, which was proved by immunohistochemistry (P < 0.05) and flow cytometry (Spearman's ρ = 0.42, P < 0.001). In the high-ADAM9 group, CD8+ and CD4+ T cells revealed an exhausted phenotype with decreased GZMB (Spearman's ρ = - 0.31, P = 0.05, and Spearman's ρ = - 0.49, P < 0.001, respectively), and fewer Macrophages were identified. A predictive RFscore was further constructed by random forest approach, involving ADAM9 and immunologic genes. Only in the subgroup with the lower RFscore did IO-TKI outperform TKI monotherapy. High-ADAM9 expression was associated with immunosuppression and IO-TKI resistance. Expression of ADAM9 was also associated with the exhaustion and dysfunction of T cells. ADAM9-based RFscore has the potential to be used as a biomarker to distinguish the optimal patient treatment methods between IO-TKI and TKI monotherapy.","PeriodicalId":13446,"journal":{"name":"Immunogenetics","volume":"75 2","pages":"133-143"},"PeriodicalIF":3.2,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9201482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

IL4I1 enhances PD-L1 expression through JAK/STAT signaling pathway in lung adenocarcinoma. IL4I1通过JAK/STAT信号通路增强PD-L1在肺腺癌中的表达。

IF 3.2 4区医学

Immunogenetics Pub Date : 2023-02-01 DOI: 10.1007/s00251-022-01275-4

Jiefei Zhu, Yan Li, Xu Lv

{"title":"IL4I1 enhances PD-L1 expression through JAK/STAT signaling pathway in lung adenocarcinoma.","authors":"Jiefei Zhu, Yan Li, Xu Lv","doi":"10.1007/s00251-022-01275-4","DOIUrl":"https://doi.org/10.1007/s00251-022-01275-4","url":null,"abstract":"Lung adenocarcinoma (LUAD) is the major type of lung cancer and is one of the deadliest cancers worldwide. IL4I1, as a gene associated with unsatisfactory prognosis, is involved in tumor immune escape, but its immune regulatory mechanism in LUAD is limited. Bioinformatics analysis was applied to analyze the differentially expressed mRNAs and enriched signaling pathways in LUAD tissue. Quantitative real-time polymerase chain reaction (qRT-PCR) was manipulated to test IL4I1 expression. We carried out several methods to examine cell functions: CCK-8 to measure LUAD cell proliferation; flow cytometry to determine cell apoptosis; Western blot to assess the expression of JAK/STAT pathway-related proteins and PD-L1; T cell cytotoxicity assay to evaluate the effect of IL4I1 on the immune escape of LUAD cells. Through bioinformatics analysis, IL4I1 was verified to be highly expressed in LUAD tissue, participate in the modulation of JAK/STAT signaling pathway, and be positively associated with CD274 (PD-L1) expression. Cell function experiments indicated that silencing IL4I1 notably repressed LUAD cell proliferation and induced apoptosis. IL4I1 silence would block JAK/STAT signaling pathway, but this effect could be reversed by RO8191 activator treatment. Moreover, IL4I1 silence suppressed PD-L1 expression and facilitated T cell cytotoxicity, while its inhibitory impact on PD-L1 expression and immune escape of LUAD cells could be reversed by atezolizumab treatment. Overall, we confirmed that IL4I1 promoted the malignant cell behaviors and immune escape of LUAD through JAK/STAT signaling pathway. IL4I1 has the potential to be a diagnostic biomarker for LUAD.","PeriodicalId":13446,"journal":{"name":"Immunogenetics","volume":"75 1","pages":"17-25"},"PeriodicalIF":3.2,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10698833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

Functional consequences of allotypic polymorphisms in human immunoglobulin G subclasses. 人类免疫球蛋白 G 亚类异型多态性的功能性后果。

IF 2.9 4区医学

Immunogenetics Pub Date : 2023-02-01 Epub Date: 2022-07-29 DOI: 10.1007/s00251-022-01272-7

Andrew R Crowley, Simone I Richardson, Marina Tuyishime, Madeleine Jennewein, Meredith J Bailey, Jiwon Lee, Galit Alter, Guido Ferrari, Lynn Morris, Margaret E Ackerman

引用次数: 0

Mutated Pkhd1 alone is sufficient to cause autoimmune biliary disease on the nonobese diabetic (NOD) genetic background. 在非肥胖糖尿病（NOD）遗传背景下，仅突变的 Pkhd1 就足以导致自身免疫性胆道疾病。

IF 3.2 4区医学

Immunogenetics Pub Date : 2023-02-01 Epub Date: 2022-09-13 DOI: 10.1007/s00251-022-01276-3

David E Adams, Luke S Heuer, Manuel Rojas, Weici Zhang, William M Ridgway

{"title":"Mutated Pkhd1 alone is sufficient to cause autoimmune biliary disease on the nonobese diabetic (NOD) genetic background.","authors":"David E Adams, Luke S Heuer, Manuel Rojas, Weici Zhang, William M Ridgway","doi":"10.1007/s00251-022-01276-3","DOIUrl":"10.1007/s00251-022-01276-3","url":null,"abstract":"We previously reported that nonobese diabetic (NOD) congenic mice (NOD.c3c4 mice) developed an autoimmune biliary disease (ABD) with similarities to human primary biliary cholangitis (PBC), including anti-mitochondrial antibodies and organ-specific biliary lymphocytic infiltrates. We narrowed the possible contributory regions in a novel NOD.Abd3 congenic mouse to a B10 congenic region on chromosome 1 (\"Abd3\") and a mutated Pkhd1 gene (Pkhd1del36-67) upstream from Abd3, and we showed via backcrossing studies that the NOD genetic background was necessary for disease. Here, we show that NOD.Abd3 mice develop anti-PDC-E2 autoantibodies at high levels, and that placing the chromosome 1 interval onto a scid background eliminates disease, demonstrating the critical role of the adaptive immune system in pathogenesis. While the NOD genetic background is essential for disease, it was still unclear which of the two regions in the Abd3 locus were necessary and sufficient for disease. Here, using a classic recombinant breeding approach, we prove that the mutated Pkhd1del36-67 alone, on the NOD background, causes ABD. Further characterization of the mutant sequence demonstrated that the Pkhd1 gene is disrupted by an ETnII-beta retrotransposon inserted in intron 35 in an anti-sense orientation. Homozygous Pkhd1 mutations significantly affect viability, with the offspring skewed away from a Mendelian distribution towards NOD Pkhd1 homozygous or heterozygous genotypes. Cell-specific abnormalities, on a susceptible genetic background, can therefore induce an organ-specific autoimmunity directed to the affected cells. Future work will aim to characterize how mutant Pkhd1 can cause such an autoimmune response.","PeriodicalId":13446,"journal":{"name":"Immunogenetics","volume":"75 1","pages":"27-37"},"PeriodicalIF":3.2,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9468241/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10704640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

SNHG3 regulates NEIL3 via transcription factor E2F1 to mediate malignant proliferation of hepatocellular carcinoma. SNHG3通过转录因子E2F1调控NEIL3介导肝细胞癌恶性增殖。

IF 2.9 4区医学

Immunogenetics Pub Date : 2023-02-01 Epub Date: 2022-09-17 DOI: 10.1007/s00251-022-01277-2

Fabiao Zhang, Jie Lu, Jian Yang, Qiqiang Dai, Xuefeng Du, Yongfu Xu, Caiming Zhang

{"title":"SNHG3 regulates NEIL3 via transcription factor E2F1 to mediate malignant proliferation of hepatocellular carcinoma.","authors":"Fabiao Zhang, Jie Lu, Jian Yang, Qiqiang Dai, Xuefeng Du, Yongfu Xu, Caiming Zhang","doi":"10.1007/s00251-022-01277-2","DOIUrl":"10.1007/s00251-022-01277-2","url":null,"abstract":"The involvement of small nucleolar RNA host gene 3 (SNHG3) in cancer regulation has been reported. This study attempted to deeply investigate the molecular regulatory mechanism of SNHG3 on malignant progression of hepatocellular carcinoma (HCC). According to TCGA analysis, high SNHG3 expression was a risk factor for poor prognosis of HCC patients. Therefore, we further detected the mRNA level of SNHG3 in HCC tissue and cells. It was found that SNHG3 was upregulated in HCC tissue and cells. Afterwards, CCK-8 and flow cytometry assays further proved that silencing SNHG3 inhibited HCC cell proliferation while inducing cell apoptosis and G0/G1 phase arrest. It was also attested in vivo experiments that silencing SNHG3 could reduce the volume and weight of tumors and downregulate the Ki-67 expression to suppress HCC tumor growth. Next, it was discovered that SNHG3 increased the binding of E2F1 and NEIL3 promoter region, thereby activating the transcription feature of NEIL3. Lastly, rescue assays indicated that NEIL3 participated in SNHG3-mediated HCC cell cycle, apoptosis and proliferation. All in all, this study revealed the specific regulatory mechanism of SNHG3 in HCC to enable SNHG3 a hopeful marker for HCC diagnosis and treatment.","PeriodicalId":13446,"journal":{"name":"Immunogenetics","volume":"75 1","pages":"39-51"},"PeriodicalIF":2.9,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10688998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0