Cancer cell & microenvironment最新文献_第4页

Sweet-P inhibition of glucocorticoid receptor β as a potential cancer therapy 糖皮质激素受体β的Sweet-P抑制作为潜在的癌症治疗方法

Cancer cell & microenvironment Pub Date : 2016-07-05 DOI: 10.14800/CCM.1362

Assumpta C. Nwaneri, L. McBeth, T. Hinds

{"title":"Sweet-P inhibition of glucocorticoid receptor β as a potential cancer therapy","authors":"Assumpta C. Nwaneri, L. McBeth, T. Hinds","doi":"10.14800/CCM.1362","DOIUrl":"https://doi.org/10.14800/CCM.1362","url":null,"abstract":"The need for the development of new cancer therapies and push for the design of new targeting techniques is on the rise, and would be useful for cancers that are resistant to current drug treatments. The understanding of the genome has significantly advanced cancer therapy, as well as prevention and earlier detection. This research highlight discusses a potential new type of cancer-targeting molecule, Sweet-P, which is the first of its kind. Sweet-P specifically targets the microRNA-144 binding site in the 3′ untranslated region (3′ UTR) of the human glucocorticoid receptor β (GRβ), which has been demonstrated to increase expression. GRβ has been shown to be highly expressed in cells from solid tumors of uroepithelial carcinomas, gliomas, osteosarcomas, and hepatocellular carcinomas, as well as in liquid tumor cells from leukemia patients. In non-cancerous diseases, GRβ has been shown to be highly expressed in glucocorticoid-resistant asthma. These maladies brought the need for the development of the Sweet-P anti-GRβ molecule. Sweet-P was shown to repress the migration of bladder cancer cells, and may serve as a new therapeutic for GRβ-related diseases.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"19 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79170520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

Versatile activity of the master regulator of the antioxidant response in tumor initiation, progression and metastasis 肿瘤起始、进展和转移中抗氧化反应的主要调节因子的多功能活性

Cancer cell & microenvironment Pub Date : 2016-06-29 DOI: 10.14800/CCM.1355

Takashi Moriguchi

{"title":"Versatile activity of the master regulator of the antioxidant response in tumor initiation, progression and metastasis","authors":"Takashi Moriguchi","doi":"10.14800/CCM.1355","DOIUrl":"https://doi.org/10.14800/CCM.1355","url":null,"abstract":"Oxidative intermediates derived from endogenous metabolism or xenobiotic stimuli are a major cause of cancer initiation. Host defense systems have evolved to cope with these oxidative stresses and prevent carcinogenesis. The basic leucine zipper transcription factor Nrf2 (Nuclear factor-erythroid derived 2-like 2, Nfe2l2) regulates the cellular defense system against oxidative stress, and governs cellular protection against chemical carcinogens. At the same time, Nrf2 enhances anti-cancer immunity in the tumor microenvironment, thereby suppressing growth and metastasis of cancer cells. These beneficial aspects of Nrf2 activities contribute to the prevention of cancer initiation, as well as its subsequent progression. On the other hand, aberrant Nrf2 activation confers malignant properties on cancer cells by enhancing proliferative ability and drug resistance. Thus, Nrf2 contributes to the prevention of carcinogenesis as well as the malignant growth of cancer cells. Increasing numbers of studies have been focusing on elucidating how these contradictory activities of Nrf2 are elicited during the multistep carcinogenic process. In this research highlight, we discuss our current understandings of Nrf2 function in cancer initiation, promotion and metastasis in a murine lung cancer model, and related topics are summarized.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75144960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Stromal cells and myeloid leukemic cells: Are they friends? Or foes? 基质细胞和髓性白血病细胞:它们是朋友吗?还是敌人?

Cancer cell & microenvironment Pub Date : 2016-06-21 DOI: 10.14800/CCM.1348

Lingling Yu, Yingmin Zhao, J. F. Wang, Duonan Yu

引用次数: 0

Tumor-targeted costimulation by using bi-specific aptamers. 使用双特异性适配体的肿瘤靶向共刺激。

Cancer cell & microenvironment Pub Date : 2016-06-06 DOI: 10.14800/ccm.1333

Fernando Pastor

引用次数: 2

Potential therapeutic effects of natural extracts in multiple myeloma 天然提取物对多发性骨髓瘤的潜在治疗作用

Cancer cell & microenvironment Pub Date : 2016-06-06 DOI: 10.14800/CCM.1311

Rong Fu, Wen-Cong Lv, Q. Guo, Zhao-Qiu Wu

引用次数: 0

Current trends in oral cancer: A systematic review 口腔癌的当前趋势:一项系统综述

Cancer cell & microenvironment Pub Date : 2016-06-06 DOI: 10.14800/CCM.1332

G. Corso, A. Villa, A. Tarsitano, A. Gohel

引用次数: 8

Therapeutic targeting of methylthioadenosine phosphorylase 甲基硫代腺苷磷酸化酶的治疗靶向性

Cancer cell & microenvironment Pub Date : 2016-06-06 DOI: 10.14800/CCM.1322

Yu-Chan Chang, Chia-Yi Su, M. Hsiao

引用次数: 4

Targeting the glioblastoma-initiating cell-associated antigens 靶向胶质母细胞瘤起始细胞相关抗原

Cancer cell & microenvironment Pub Date : 2016-05-30 DOI: 10.14800/CCM.1329

T. Kondo

引用次数: 1

Highlighting the potential of aptamer-based strategy to treat EGFRvIII-positive glioblastoma 强调基于适配体的策略治疗egfrviii阳性胶质母细胞瘤的潜力

Cancer cell & microenvironment Pub Date : 2016-05-23 DOI: 10.14800/ccm.1314

S. Camorani, L. Cerchia

{"title":"Highlighting the potential of aptamer-based strategy to treat EGFRvIII-positive glioblastoma","authors":"S. Camorani, L. Cerchia","doi":"10.14800/ccm.1314","DOIUrl":"https://doi.org/10.14800/ccm.1314","url":null,"abstract":"Epidermal growth factor receptor variant III (EGFRvIII) is the most common EGFR mutant found in glioblastoma (GBM). Due to a truncation of large portion of the extracellular region, EGFRvIII is unable to bind any ligand and constitutively signals to downstream effector molecules. It is tumor-specific, highly oncogenic and usually co-expressed with EGFR wild type (EGFRwt). EGFR tyrosine kinase inhibitors (TKIs) have proven ineffective in GBM and different mechanisms account for the occurrence of resistance to such inhibitors. Among these, EGFR TKIs induce a switch to platelet-derived growth factor receptor β (PDGFRβ) expression and signaling, thus rendering the tumors addicted to such receptor for continued growth and resistance to treatment. In our recent investigation, we showed the ability of a nuclease-resistant RNA aptamer, named CL4, to bind and inhibit EGFRvIII thus hampering proliferation, migration and invasion of EGFRvIII-positive GBM cells. Importantly, both CL4 and EGFR TKIs cooperate with a previously validated anti-PDGFRβ aptamer in inhibiting cell growth. Here, we highlight the potential of the EGFRvIII aptamer to hamper the EGFRvIII functional interplay with other receptor tyrosine kinases (RTKs) and cell surface proteins responsible for GBM development and progression. The utility of CL4 as targeting ligand for drug-delivery approaches is also discussed. Overall, aptamer-based molecules have significant implications for managing GBM in the near future.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"23 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79299556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

A retrospective review of lip squamous cell carcinoma characteristics as predictors of nodal spread 唇鳞状细胞癌特征作为淋巴结转移预测因子的回顾性研究

Cancer cell & microenvironment Pub Date : 2016-05-23 DOI: 10.14800/CCM.1265

A. Pastuszek

引用次数: 0