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Tumours
Published in Ashley W. Blom, David Warwick, Michael R. Whitehouse, Apley and Solomon’s System of Orthopaedics and Trauma, 2017
Jonathan Stevenson, Michael Parry
While the patho-aetiology remains unclear in the majority of cases of bone and soft-tissue sarcoma, certain DNA mutations or genetic associations are seen. In the case of osteosarcoma, 70% will demonstrate mutations in DNA helices or tumour suppressor genes. Such tumours are more common in patients with Li–Fraumeni syndrome, involving the p53 suppressor gene, and those with retinoblastoma, involving the Rbl gene. In the case of Ewing’s sarcoma, more than 95% of tumours demonstrate EWS-ETS fusion gene rearrangements, most commonly the result of translocations between chromosome 22 and chromosome 11 (t22;11(q24;q12) translocation) or 21 (t21;22(q22;q12)). The ETS transcription factor family is responsible for regulating cellular differentiation, the cell cycle, cell migration and apoptosis. Therefore mutations will result in deregulation of programmed cell death and disruption of cell-cycle control.
Transcription factor ETV1-induced lncRNA MAFG-AS1 promotes migration, invasion, and epithelial–mesenchymal transition of pancreatic cancer cells by recruiting IGF2BP2 to stabilize ETV1 expression
Published in Growth Factors, 2023
Hanqin Weng, Weijian Feng, Fengling Li, Dong Huang, Liangyi Lin, Zaiguo Wang
The ETS-transcription factor family is involved in tumor progression and is divided into nine subfamilies (Heeg et al. 2016). Among them, ETS-translocation variant 1 (ETV1) and ETV5 belong to the polyoma enhancer activator protein 3 subgroup, which has been identified to promote the metastasis progression of various human cancers (Kar and Gutierrez-Hartmann 2013; Oh, Shin, and Janknecht 2012). In prostate cancer, ETV1 plays a carcinogenic role by up-regulating MMP7gene expression (Shin et al. 2013). The upregulation of ETV1 in gastrointestinal stromal tumors is shown to be associated with activation of mutations in the proto-oncogene KIT, and activated KIT can further regulate the transcriptional program of ETV1, prolong the stability of ETV1 protein, and cooperate with ETV1 to promote tumorigenesis (Chi et al. 2010). Meanwhile, ETV1 is crucial in the interstitial expansion and metastasis of PC in mice, and its function is mediated in part through regulation of the downstream secreted protein acidic and rich in cysteine (Sparc) and hyaluronan synthase 2 (Has2) (Heeg et al. 2016). To date, whether ETV1 can regulate the EMT and promote the development of PC by regulating lncRNAMAFG-AS1 has not been reported. This study was intended to explore the expression of ETV1/lncRNA-MAFG-AS1 in PC and its mechanism in the regulation of EMT in PC, so as to find targets or biomarkers for treating PC from a new perspective.
PU.1 interaction with p50 promotes microglial-mediated inflammation in secondary spinal cord injury in SCI rats
Published in International Journal of Neuroscience, 2023
Mingchen Yu, Yiqing Ou, Hongmei Wang, Weidong Gu
When SCI occurs, the microglia hyperactivate and release a large number of inflammatory factors which are involved in the pathological process of secondary SCI [6,7]. Activated microglia can induce neuroinflammation through the nuclear factor (NF)-κB (p65/p50) pathway, promoting interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and other inflammatory factors. TNF-α and IL-lβ products can further activate microglia and the NF-κB pathway to increase neuronal damage and apoptosis [8,9]. Thus, NF-κB uses a complex regulatory loop that amplifies and perpetuates the inflammatory response. The transcription factor PU.1 is a member of the erythroblast transformation specific (ETS) transcription factor family and plays a central role in the inflammatory response [10,11]. It has been reported that PU.1 regulates a large number of microglial cells and nerve inflammation-related gene expression such as TNF-α, IL-1β, IL-12, and IL-18 [11–13].
Inhibition of ELF3 confers synthetic lethality of PARP inhibitor in non-small cell lung cancer
Published in Journal of Receptors and Signal Transduction, 2021
Yan Wang, Min Zuo, Hongtao Jin, Meina Lai, Jinfeng Luo, Zhiqiang Cheng
E74 Like ETS transcription factor 3 (ELF3), located in the human chromosome 1q32.2 region, is a new member of the ETS transcription factor family [6]. It has been widely known that ELF3 functions as a sequence-specific DNA binding transcription factor, and plays an important role in tumor differentiation, progression and embryonic development in recent years [7]. Interestingly, ELF3 plays a different role in different types of cancer. In prostate cancer [8], colorectal cancer [9] and breast cancer [10], ELF3 has been confirmed as an oncogene to promote tumor progression. In contrast, ELF3 has been shown to be an inhibitor of ovarian cancer [11] and oral squamous cell carcinoma [12]. More recently, ELF3 has been shown to promote the growth and metastasis of NSCLC [13].