Cellular Oncology最新文献_第10页

Apo10 and TKTL1 in blood macrophages as biomarkers for differentiating lung cancer from benign lung lesions: a comparative study with conventional biomarkers. 血巨噬细胞中Apo10和TKTL1作为鉴别肺癌与肺良性病变的生物标志物:与常规生物标志物的比较研究

IF 6.6 2区医学

Cellular Oncology Pub Date : 2023-12-01 Epub Date: 2023-06-28 DOI: 10.1007/s13402-023-00838-1

Chuanbo Xie, Shuqing Wang, Chi Guo, Yuying Liu, Musheng Zeng

引用次数: 1

Clostridium butyricum and its metabolite butyrate promote ferroptosis susceptibility in pancreatic ductal adenocarcinoma. 丁酸梭菌及其代谢物丁酸盐促进胰腺导管腺癌中铁下垂的易感性。

IF 6.6 2区医学

Cellular Oncology Pub Date : 2023-12-01 Epub Date: 2023-06-01 DOI: 10.1007/s13402-023-00831-8

Xiaotong Yang, Zhengyan Zhang, Xuqing Shen, Junyi Xu, Yawen Weng, Wei Wang, Jing Xue

{"title":"Clostridium butyricum and its metabolite butyrate promote ferroptosis susceptibility in pancreatic ductal adenocarcinoma.","authors":"Xiaotong Yang, Zhengyan Zhang, Xuqing Shen, Junyi Xu, Yawen Weng, Wei Wang, Jing Xue","doi":"10.1007/s13402-023-00831-8","DOIUrl":"10.1007/s13402-023-00831-8","url":null,"abstract":"Purpose: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive disease with limited therapeutic options. The diversity and composition of the intratumoral microbiota are associated with PDAC outcomes, and modulating the tumor microbiota has the potential to influence tumor growth and the host immune response. Here, we explore whether intervention with butyrate-producing probiotics can limit PDAC progression.Methods: Based on the TCGA (PAAD) database, we analyzed the differential communities of intratumoral microbiota in PDAC patients with long survival and short survival and explored the relevant mechanisms of Clostridium butyricum and its metabolite butyrate in the treatment of PDAC. Treatment with Clostridium butyricum or butyrate in combination with the ferroptosis inducer RSL3 in a PDAC mouse model has an inhibitory effect on PDAC progression. The potential molecular mechanisms were verified by flow cytometry, RNA-seq, Western blotting, qRT‒PCR and immunofluorescence.Results: We found that the tumoral butyrate-producing microbiota was linked to a better prognosis and less aggressive features of PDAC. Intervention with Clostridium butyricum or its metabolite butyrate triggered superoxidative stress and intracellular lipid accumulation, which enhanced ferroptosis susceptibility in PDAC.Conclusion: Our study reveals a novel antitumor mechanism of butyrate and suggests the therapeutic potential of butyrate-producing probiotics in PDAC.","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"1645-1658"},"PeriodicalIF":6.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9554560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Retraction Note: IFIT1 modulates the proliferation, migration and invasion of pancreatic cancer cells via Wnt/β-catenin signaling. 退缩注：IFIT1通过Wnt/β-catenin信号调节胰腺癌症细胞的增殖、迁移和侵袭。

IF 6.6 2区医学

Cellular Oncology Pub Date : 2023-12-01 DOI: 10.1007/s13402-023-00897-4

Tian-Hao Li, Bang-Bo Zhao, Cheng Qin, Yuan-Yang Wang, Ze-Ru Li, Hong-Tao Cao, Xiao-Ying Yang, Xing-Tong Zhou, Wei-Bin Wang

引用次数: 0

Triggering pyroptosis enhances the antitumor efficacy of PARP inhibitors in prostate cancer. 触发焦亡可增强PARP抑制剂对前列腺癌的抗肿瘤作用。

IF 6.6 2区医学

Cellular Oncology Pub Date : 2023-12-01 Epub Date: 2023-08-23 DOI: 10.1007/s13402-023-00860-3

Ao Tian, Tingyu Wu, Yanshuang Zhang, Jiachen Chen, Jianjun Sha, Weiliang Xia

{"title":"Triggering pyroptosis enhances the antitumor efficacy of PARP inhibitors in prostate cancer.","authors":"Ao Tian, Tingyu Wu, Yanshuang Zhang, Jiachen Chen, Jianjun Sha, Weiliang Xia","doi":"10.1007/s13402-023-00860-3","DOIUrl":"10.1007/s13402-023-00860-3","url":null,"abstract":"Purpose: PARP inhibitors have revolutionized the treatment landscape for advanced prostate cancer (PCa) patients who harboring mutations in homologous recombination repair (HRR) genes. However, the molecular mechanisms underlying PARP inhibitors function beyond DNA damage repair pathways remain elusive, and identifying novel predictive targets that favorably respond to PARP inhibitors in PCa is an active area of research.Methods: The expression of GSDME in PCa cell lines and human PCa samples was determined by western blotting. Targeted bisulfite sequencing, gene enrichment analysis (GSEA), clone formation, construction of the stably transfected cell lines, lactate dehydrogenase (LDH) assay, western blotting as well as a mouse model of subcutaneous xenografts were used to investigate the role of GSDME in PCa. The combinational therapeutic effect of olaparib and decitabine was determined using both in vitro and in vivo experiments.Results: We have found low expression of GSDME in PCa. Interestingly, we demonstrated that GSDME activity is robustly induced in olaparib-treated cells undergoing pyroptosis, and that high methylation of the GSDME promoter dampens its activity in PCa cells. Intriguingly, genetically overexpressing GSDME does not inhibit tumor cell proliferation but instead confers sensitivity to olaparib. Furthermore, pharmacological treatment with the combination of olaparib and decitabine synergistically induces GSDME expression and cleavage through caspase-3 activation, thus promoting pyroptosis and enhancing anti-tumor response, ultimately resulting in tumor remission.Conclusion: Our findings highlight a novel therapeutic strategy for enhancing the long-term response to olaparib beyond HRR-deficient tumors in PCa, underscoring the critical role of GSDME in regulating tumorigenesis.","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"1855-1870"},"PeriodicalIF":6.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10043015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

TGF-β-p-STAT1-LAIR2 axis has a "self-rescue" role for exhausted CD8⁺ T cells in hepatocellular carcinoma. TGF-β-p-STAT1-LAIR2轴对肝癌中耗尽的CD8+ T细胞具有“自救”作用。

IF 6.6 2区医学

Cellular Oncology Pub Date : 2023-12-01 Epub Date: 2023-05-24 DOI: 10.1007/s13402-023-00830-9

Banglun Pan, Zengbin Wang, Yuxin Yao, Xiaoling Ke, Shuling Shen, Weihong Chen, Xiaoxia Zhang, Jiacheng Qiu, Xiaoxuan Wu, Nanhong Tang

{"title":"TGF-β-p-STAT1-LAIR2 axis has a \"self-rescue\" role for exhausted CD8+ T cells in hepatocellular carcinoma.","authors":"Banglun Pan, Zengbin Wang, Yuxin Yao, Xiaoling Ke, Shuling Shen, Weihong Chen, Xiaoxia Zhang, Jiacheng Qiu, Xiaoxuan Wu, Nanhong Tang","doi":"10.1007/s13402-023-00830-9","DOIUrl":"10.1007/s13402-023-00830-9","url":null,"abstract":"Background: TGF-β is related to the function of T cells in the tumor microenvironment. However, the characteristics of TGF-β affecting the function of CD8+ T cells in hepatocellular carcinoma (HCC) have not been clearly resolved.Methods: In this study, flow cytometry, mass cytometry, immunohistochemistry, RNA-seq, single-cell RNA-seq, assay for transposase-accessible chromatin with high throughput sequencing, chromatin immunoprecipitation, and dual-luciferase reporter gene assay were used to study the regulatory effect and molecular mechanism of TGF-β on HCC infiltrating CD8+ T cells.Results: Here, we demonstrated that the overall effect of TGF-β on CD8+ T cells in HCC was to activate p-p38 to induce exhaustion, but it also initiated cell-intrinsic resistance mechanisms: 1) TGF-β upregulated the levels of p-STAT1 (S727) and promoted LAIR2 secretion; 2) the TGF-β-p-STAT1-LAIR2 axis relieved CD8+ T cells from exhaustion, which we called \"self-rescue\"; 3) this \"self-rescue\" behavior showed time and dose limitations on TGF-β stimulation, which was easily masked by stronger inhibitory signals; 4) the function of CD8+ T cells was improved by using TAK-981 to amplify \"self-rescue\" signal.Conclusion: Our study describes a \"self-rescue\" mechanism of CD8+ T cells in HCC against exhaustion and the good effects from amplifying this signal.","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"1625-1644"},"PeriodicalIF":6.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9517230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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: 2

CircGLIS3 inhibits thyroid cancer invasion and metastasis through miR-146b-3p/AIF1L axis. cirglis3通过miR-146b-3p/AIF1L轴抑制甲状腺癌的侵袭转移。

IF 6.6 2区医学

Cellular Oncology Pub Date : 2023-12-01 Epub Date: 2023-08-23 DOI: 10.1007/s13402-023-00845-2

Siting Cao, Yali Yin, Huijuan Hu, Shubin Hong, Weiman He, Weiming Lv, Rengyun Liu, Yanbing Li, Shuang Yu, Haipeng Xiao

{"title":"CircGLIS3 inhibits thyroid cancer invasion and metastasis through miR-146b-3p/AIF1L axis.","authors":"Siting Cao, Yali Yin, Huijuan Hu, Shubin Hong, Weiman He, Weiming Lv, Rengyun Liu, Yanbing Li, Shuang Yu, Haipeng Xiao","doi":"10.1007/s13402-023-00845-2","DOIUrl":"10.1007/s13402-023-00845-2","url":null,"abstract":"Purpose: Studies have shown that circRNA is involved in the occurrence and development of human cancers. However, it remains unclear that the contribution of circRNA in thyroid carcinoma and its role in the process of tumorigenesis.Methods: The expression profile of circRNA-miRNA-mRNA in thyroid carcinoma was detected by RNA sequencing and verified by qRT-PCR. The characteristics of circGLIS3 were verified by RNase R and actinomycin assays, subcellular fractionation, and fluorescence in situ hybridization. The functions of circGLIS3 and AIF1L were detected by wound healing, transwell, 3D culture and Western blot. RNA Immunoprecipitation (RIP), RNA pulldown and dual-luciferase reporter assays were used to verify the target genes of circGLIS3 and downstream miRNAs. Functional rescue experiments were performed by transfecting miRNA mimics or siRNA of target genes. Finally, metastatic mouse models were used to investigate circGLIS3 function in vivo.Results: In this study, we discovered a novel circRNA (has_circ_0007368, named as circGLIS3) by RNA sequencing. CircGLIS3 was down-regulated in thyroid carcinoma tissues and cells line, and was negatively associated with malignant clinical features of thyroid carcinoma. Functional studies found that circGLIS3 could inhibit the migration and invasion of thyroid carcinoma cells, and was related to the EMT process. Mechanistically, circGLIS3 can upregulate the expression of the AIF1L gene by acting as a miR-146b-3p sponge to inhibit the progression of thyroid carcinoma.Conclusion: Our study identified circGLIS3 as a novel tumor suppressor in thyroid cancer, indicating the potential of circGLIS3 as a promising diagnostic and prognostic marker for thyroid cancer.","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"1777-1789"},"PeriodicalIF":6.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10043016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Therapeutic effects against high-grade glioblastoma mediated by engineered induced neural stem cells combined with GD2-specific CAR-NK. 工程诱导神经干细胞联合gd2特异性CAR-NK治疗高级别胶质母细胞瘤的疗效

IF 6.6 2区医学

Cellular Oncology Pub Date : 2023-12-01 Epub Date: 2023-07-07 DOI: 10.1007/s13402-023-00842-5

Weihua Liu, Yu Zhao, Zhongfeng Liu, Guangji Zhang, Huantong Wu, Xin Zheng, Xihe Tang, Zhiguo Chen

{"title":"Therapeutic effects against high-grade glioblastoma mediated by engineered induced neural stem cells combined with GD2-specific CAR-NK.","authors":"Weihua Liu, Yu Zhao, Zhongfeng Liu, Guangji Zhang, Huantong Wu, Xin Zheng, Xihe Tang, Zhiguo Chen","doi":"10.1007/s13402-023-00842-5","DOIUrl":"10.1007/s13402-023-00842-5","url":null,"abstract":"Purpose: High-grade glioblastoma is extremely challenging to treat because of its aggressiveness and resistance to conventional chemo- and radio-therapies. On the contrary, genetic and cellular immunotherapeutic strategies based on the stem and immune cells are emerging as promising treatments against glioblastoma (GBM). We aimed to developed a novel combined immunotherapeutic strategy to improve the treatment efficacy using genetically engineered PBMC-derived induced neural stem cells (iNSCs) expressing HSV-TK and second-generation CAR-NK cells against GBM.Methods: iNSCs cells expressing HSV-TK (iNSCsTK) and GD2-specific CAR-NK92 (GD2NK92) were generated from PBMC-derived iNSCs and NK92 cell lines, respectively. The anti-tumor effect of iNSCsTK and the combinational therapeutics of iNSCsTK and GD2NK92 were evaluated by GBM cell line using in vitro and in vivo experiments.Results: PBMC-derived iNSCsTK possessed tumor-tropism migration ability in vitro and in vivo, which exhibited considerable anti-tumor activity via bystander effect in the presence of ganciclovir (GCV). iNSCsTK/GCV could slow GBM progression and prolong median survival in tumor-bearing mice. However, the anti-tumor effect was limited to single therapy. Therefore, the combinational therapeutic effect of iNSCsTK/GCV and GD2NK92 against GBM was investigated. This approach displayed a more significant anti-tumor effect in vitro and in xenograft tumor mice.Conclusions: PBMC-derived iNSCsTK showed a significant tumor-tropic migration and an effective anti-tumor activity with GCV in vitro and in vivo. In addition, combined with GD2NK92, iNSCsTK therapeutic efficacy improved dramatically to prolong the tumor-bearing animal model's median survival.","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"1747-1762"},"PeriodicalIF":6.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9761816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Correction: Targeting ARHGEF12 promotes neuroblastoma differentiation, MYCN degradation, and reduces tumorigenicity. 更正：靶向ARHGEF12可促进神经母细胞瘤分化、MYCN降解并降低致瘤性。

IF 6.6 2区医学

Cellular Oncology Pub Date : 2023-12-01 DOI: 10.1007/s13402-023-00890-x

Yi Yang, Siqi Wang, Jiaoyang Cai, Jianwei Liang, Yingwen Zhang, Yangyang Xie, Fei Luo, Jingyan Tang, Yijin Gao, Shuhong Shen, Haizhong Feng, Yanxin Li

引用次数: 0

Targeting nucleolin improves sensitivity to chemotherapy in acute lymphoblastic leukemia. 靶向核蛋白提高急性淋巴细胞白血病化疗敏感性。

IF 6.6 2区医学

Cellular Oncology Pub Date : 2023-12-01 Epub Date: 2023-07-24 DOI: 10.1007/s13402-023-00837-2

Yanxin Chen, Zhengjun Wu, Lingyan Wang, Minhui Lin, Peifang Jiang, Jingjing Wen, Jiazheng Li, Yunda Hong, Xiaoyun Zheng, Xiaozhu Yang, Jing Zheng, Robert Peter Gale, Ting Yang, Jianda Hu

{"title":"Targeting nucleolin improves sensitivity to chemotherapy in acute lymphoblastic leukemia.","authors":"Yanxin Chen, Zhengjun Wu, Lingyan Wang, Minhui Lin, Peifang Jiang, Jingjing Wen, Jiazheng Li, Yunda Hong, Xiaoyun Zheng, Xiaozhu Yang, Jing Zheng, Robert Peter Gale, Ting Yang, Jianda Hu","doi":"10.1007/s13402-023-00837-2","DOIUrl":"10.1007/s13402-023-00837-2","url":null,"abstract":"Purpose: Most patients with acute lymphoblastic leukemia (ALL) are treated with chemotherapy as primary care. Although the treatment response is usually positive, resistance and relapse often occur via unknown mechanisms. The purpose of this study was to identify factors associated with chemotherapy resistance in ALL. Here, we present clinical and experimental evidence that overexpression of nucleolin (NCL), a multifunctional nucleolar protein, is linked to drug resistance in ALL.Methods: NCL mRNA and protein levels were compared between cell lines and patient samples using qRT-PCR and immunoblotting. NCL mRNA levels were compared between patients of different disease stages from our clinic patients' specimens and publicly available ALL patient datasets. Cells and patient-derived xenograft mouse experiments were performed to assess the effect of NCL inhibition on ALL chemotherapy effectiveness.Results: Analysis of patient specimens, and publicly available RNA-sequencing datasets revealed a strong correlation between the abundance of NCL and disease relapse or poor survival in B-ALL. Altering NCL expression results in changes in drug sensitivity in ALL cell lines. High levels of NCL upregulated components of the ATP-binding cassette transporters via activation of the ERK pathway, resulting in a decrease in drug accumulation inside the cells. Targeting NCL with AS1411, an NCL-binding oligonucleotide aptamer, significantly increased the sensitivity of ALL cell lines and cells/patient-derived ALL xenograft mice to chemotherapeutic drugs and prolonged mouse survival.Conclusion: Our results highlight NCL as a prognostic marker in B-ALL and a potential therapeutic target to combat chemotherapy resistance in ALL.","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"1709-1724"},"PeriodicalIF":6.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10216801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Effect of infiltrating immune cells in tumor microenvironment on metastasis of hepatocellular carcinoma. 肿瘤微环境中浸润性免疫细胞对肝癌转移的影响。

IF 6.6 2区医学

Cellular Oncology Pub Date : 2023-12-01 Epub Date: 2023-07-06 DOI: 10.1007/s13402-023-00841-6

Yiwen Chen, Yuhang Zhou, Ziyang Yan, Peilin Tong, Qiang Xia, Kang He

引用次数: 1