STK33 plays an important positive role in the development of human large cell lung cancers with variable metastatic potential Ping Wang, Hongzhong Cheng, Jianqiang Wu, Anrun Yan and Libin Zhang Acta Biochim Biophys Sin 2015, 47: 214–223; doi: 10.1093/abbs/gmu136 Department of Thoracic Surgery, First People's Hospital of Yunnan Province, Kunming 650031, China Serine/threonine kinase 33 (STK33) is a novel protein that has attracted considerable interest in recent years. Previous research has revealed that STK33 expression plays a special role in cancer cell proliferation. However, the mechanisms of STK33 induction of cancer cells remain largely unknown. In this study, it is demonstrated that STK33 expression varies in NL9980 and L9981 cells which are homogeneous cell lines with similar genetic backgrounds. STK33 can promote cell migration and invasion and suppress p53 gene expression in the NL9980 and L9981 cells. In addition, this protein also promotes epithelial–mesenchymal transition (EMT). Moreover, STK33 knockdown decreases tumor-related gene expression and inhibits cell migration, invasion, and EMT, suggesting that STK33 may be a mediator of signaling pathways that are involved in cancer. In conclusion, our results suggest that STK33 may be an important prognostic marker and a therapeutic target for the metastatic progression of human lung cancer. 图例: STK33诱导Snail、Slug、Twist、FoxC2基因的表达 全文: http://abbs.oxfordjournals.org/content/47/3/214.full.pdf+html
ERK1/2 mediates lung adenocarcinoma cell proliferation and autophagy induced by apelin-13 Li Yang, Tao Su, Deguan Lv, Feng Xie, Wei Liu, Jiangang Cao, Irshad Ali Sheikh, Xuping Qin, Lanfang Li and Linxi Chen Acta Biochim Biophys Sin 2014, 46: 100–111; doi: 10.1093/abbs/gmt140 Learning Key Laboratory for Pharmaco-proteomics, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001, China The aim of this study was to investigate the role of apelin in the cell proliferation and autophagy of lung adenocarcinoma. The over-expression of APJ in lung adenocarcinoma was detected by immunohistochemistry, while plasma apelin level in lung cancer patients was measured by enzyme-linked immunosorbent assay. Our findings revealed that apelin-13 significantly increased the phosphorylation of ERK1/2, the expression of cyclin D1, microtubule-associated protein 1 light chain 3A/B (LC3A/B), and beclin1, and confirmed that apelin-13 promoted A549 cell proliferation and induced A549 cell autophagy via ERK1/2 signaling. Moreover, there are pores on the surface of human lung adenocarcinoma cell line A549 and apelin-13 causes cell surface smooth and glossy as observed under atomic force microscopy. These results suggested that ERK1/2 signaling pathway mediates apelin-13-induced lung adenocarcinoma cell proliferation and autophagy. Under our experimental condition, autophagy associated with 3-methyladenine was not involved in cell proliferation. 图例: Apelin信号通路 全文: http://abbs.oxfordjournals.org/content/46/2/100.full 相关论文: 1 The novel peptide apelin lowers blood pressure via a nitric oxide-dependent mechanism 2 Pharmacological and immunohistochemical characterization of the APJ receptor and its endogenous ligand apelin 3 Emerging roles of apelin in biology and medicine 4 The effects of centrally administered apelin - 13 on food intake, water intake and pituitary hormone release in rats 5 Modification of the terminal residue of apelin - 13 antagonizes its hypotensive action 6 Intracerebroventricular injection of apelin - 13 reduces food intake in the rat 7 Apelin peptides block the entry of human immunodeficiency virus (HIV) 8 Apelin - 13 Identified as the Predominant Apelin Isoform in the Human Heart Vasoactive Mechanisms and Inotropic Action in Disease 9 Apelin -induced vascular smooth muscle cell proliferation: the regulation of cyclin D1 10 Structural and functional study of the apelin - 13 peptide, an endogenous ligand of the HIV-1 coreceptor, APJ 11 PI3K/Akt signaling transduction pathway is involved in rat vascular smooth muscle cell proliferation induced by apelin - 13
很多实验证明hsa-miR-126(miR-126)在非小细胞肺癌(NSCLC)细胞系中表达被下调。补回miR-126能通过特定的分子能抑制肿瘤细胞的增殖、迁移、侵袭和存活 。本文 报道了miR-126参与调控NSCLC细胞对化疗的反应。 用miR-126类似物或抑制剂 转染A549细胞导致 miR-126水平是显著升高、阿霉素和长春新碱的半抑制浓度降低、 阿霉素累积增加， 血管内皮生长因子A(VEGFA)和多药耐药相关蛋白1(MRP1)均下调，并且Akt信号通路失活。 此外，miR-126表达上升抑制了A549异种移植的生长。 miR-126通过与VEGFA 3'-非翻译区相互作用有效地下调VEGFA的表达，而补回VEGFA可以部分地削减miR-126对MRP1的抑制。 PI3K/Akt信号传导途径的抑制剂 LY294002能够消除miR-126的这种效果， 这表明miR-126对非小细胞肺癌作用主要是 通过对VEGF/PI3K/Akt/MRP1信号传导途径的负调控来实现的。 图例: 小鼠模型中miR-126类似物抑制肿瘤生长 miR-126 enhances the sensitivity of non-small cell lung cancer cells to anticancer agents by targeting vascular endothelial growth factor A Xiaolan Zhu, Hao Li, Lulu Long, Lulu Hui, Haining Chen, Xuefeng Wang, Huiling Shen, and Wenlin Xu The Affiliated People's Hospital, Jiangsu University, Zhenjiang 212001, China. Increasing evidence suggests that hsa-miR-126 (miR-126) is down-regulated in non-small cell lung cancer (NSCLC) cell lines and the restoration of miR-126 impairs tumor cell proliferation, migration, invasion, and survival by targeting specific molecules. Here, we reported for the first time that miR-126 was involved in regulating the response of NSCLC cells to cancer chemotherapy. After transfected A549 cells with miR-126 mimic or inhibitor, we found that an elevated level of miR-126 was significantly associated with a decreased half maximal inhibitory concentration of adriamycin (ADM) and vincristine, an increased accumulation of ADM, down-regulation of vascular endothelial growth factor A (VEGFA) and multidrug resistance-associated protein 1 (MRP1), and inactivation of the Akt signaling pathway. Furthermore, enhanced expression of miR-126 suppressed the growth of A549 xenograft and inhibited the expression of VEGFA and MRP1. miR-126 could efficiently down-regulate VEGFA expression through the interaction with the VEGFA 3'-untranslated region, whereas restoration of VEGFA could partially attenuate the suppression of MRP1 by miR-126. However, LY294002, an inhibitor of the PI3K/Akt signaling pathway, diminished this effect, suggesting that enhanced expression of miR-126 increased the sensitivity of NSCLC cells to anticancer agents through negative regulation of a VEGF/PI3K/Akt/MRP1 signaling pathway. Acta Biochim Biophys Sin (Shanghai). 2012 Jun;44(6):519-26. doi: 10.1093/abbs/gms026. 全文: http://abbs.oxfordjournals.org/content/44/6/519.full.pdf+html
What's new for 'lung cancer and radiotherapy' in PubMed 发件人： My NCBI efback@mail.nih.gov ; 时 间： 2010年5月21日 18:40 (星期五) 收件人： xupeiyang@vip.163.com ; xupeiyang@vip.163.com ; This message contains My NCBI what's new results from the National Center for Biotechnology Information ( NCBI ) at the U.S. National Library of Medicine ( NLM ). Do not reply directly to this message. Sender's message: Sent on Friday, 2010 May 21 Search lung cancer and radiotherapy Click 点这里看文献 here to view complete results in PubMed. (Results may change over time.) To unsubscribe from these e-mail updates click here .
标签: lung
