ELF1

Official Full Name

E74 like ETS transcription factor 1

Organism

Homo sapiens

GeneID

1997

Background

This gene encodes an E26 transformation-specific related transcription factor. The encoded protein is primarily expressed in lymphoid cells and acts as both an enhancer and a repressor to regulate transcription of various genes. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Feb 2009]

Synonyms

RIA1; EFTUD1;

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Detailed Information

The ELF1 (E74-like factor 1) gene is a T cell-specific transcription factor in the Ets family, most representative of which has been found to be highly active in many human tumors. Ets (erythroblast transformation specific) gene is a type of oncogene composed of a series of highly conserved homologous sequences involved in the regulation of tumor invasion and metastasis. More than 20 members have been found.

ELF1 Figure 1. The role of ELF1 in the development of lupus T cells. (Mak, et al. 2016)

Expression of ELF1 in Tumors

Breast cancer is the most common malignant tumor in women's life in developed countries. Kalet et al. found that ELF1 promotes breast cancer progression in four ERA (estrogen receptor A)-positive breast cancer cell lines. The proliferation, migration and invasion characteristics of ELF1 transcription factors were verified in MCF7 clonal cells. The growth rate of MCF7 tumor cells with high expression of ELF1 was significantly increased, while the control group was lower. Tumors with high expression of ELF1 showed a large central necrosis and increased apoptosis of apoptosis.

Pancreatic cancer is one of the ten common malignant tumors. It is difficult to find in the early stage. After the diagnosis is clear, it is most advanced and the prognosis is poor. Li et al. studied the role of ELF1 in epithelial-mesenchymal transition (EMT) and found that ELF1 gene expression was positively correlated with N-cadherin and negatively correlated with E-cadherin mRNA. To further study the role of ELF1, short hairpin constructs carrying ELF1 ribose acid (shRNA) expression of the green fluorescent protein, and the plasmid was transfected into pancreatic cancer cells. Studies have found that knocking out ELF1 in this pancreatic cancer cell line attenuates the effects of EMT. A decrease in cell migration and adhesion and a decrease in metastasis rate were observed in these cells, further indicating that the gene is involved in the development of pancreatic cancer.

RhoC is a member of the Rho family of Ras superfamily homologous gene families and has been shown to be involved in tumorigenesis and tumor progression. Hepatitis B virus proteins play an important role in the development and progression of hepatocellular carcinoma (HCC). Qin et al. have shown that high expression of ELF1 up-regulates RhoC promoter activity and mRNA and protein levels. Hepatitis B virus-adenovirus recombinant virus infection can lead to up-regulation of ELF1, which in turn leads to tumorigenesis.

ELF1 Promotes Tumorigenesis and Development

Survivin is the strongest inhibitor of apoptosis in the current inhibitor of apoptosis protein (IAP). It has been reported that the expression of ELF1 in non-small cell lung cancer is positively correlated with survivin. The researchers used immunohistochemistry and in situ end labeling (TUNEL) to demonstrate that ELF1 expression was negatively correlated with tumor cell apoptosis in non-small cell lung cancer tissues. The degradation of most regulatory proteins in eukaryotic cells is through the ubiquitin-proteasome pathway, which regulates the ubiquitin-proteasome pathway and regulates cell apoptosis and growth.

Ki-67 antigen is involved in cell division and proliferation. The marker index of Ki-67 can reliably and rapidly reflect the proliferation rate of malignant tumors, which is related to the development, metastasis, and prognosis of various malignant tumors. Kong et al. used tissue microarray and immunohistochemistry to find that the expression of ELF1 and Ki-67 protein in 64 lung cancer tissues was significantly higher than that in 10 normal lung tissues, and the expression level was related to tumor differentiation, clinical stage, and lymph node metastasis. At the same time, it was found that ELF1 was positively correlated with Ki-67 expression. Subsequently, Furlan et al also found a positive correlation between the ratio of Etf-1 and Ki67-positive cells in breast cancer tumorigenic models, which promoted tumor growth and inhibited tumor growth and metastasis after knocking out the gene. Studies have shown that Etf-1 expression is associated with cancer invasion and prognosis.

References:

Pali-Schöll, I., & Jensen-Jarolim, E. (2016). The concept of allergen-associated molecular patterns (aamp). Current Opinion in Immunology, 42, 113-118.
Yin, Y., Sanders, A. J., Feng, L., & Jiang, W. G. (2014). Knockdown of aamp impacts on hecv cell functions in vitro and affects the expression of ve-cadherin. Angiology, 2(2), 1000125.
Kalet, B. T., Anglin, S. R., Handschy, A., O’Donoghue, L. E., Halsey, C., & Chubb, L., et al. (2013). Transcription factor ets1 cooperates with estrogen receptor α to stimulate estradiol-dependent growth in breast cancer cells and tumors. Plos One, 8(7), e68815.
Chunyan, L. I., Wang, Z., Chen, Y., Zhou, M., Zhang, H., & Chen, R., et al. (2015). Transcriptional silencing of ets-1 abrogates epithelial-mesenchymal transition resulting in reduced motility of pancreatic cancer cells. Oncology Reports, 33(2), 559-565.
Qin, D., Li, K., Qu, J., Wang, S., Zou, C., & Sheng, Y., et al. (2013). Hbx and hbs regulate rhoc expression by upregulating transcription factor ets-1. Archives of Virology, 158(8), 1773-1781.
Kong, L., Zhang, H., Ma, Y., Hu, J., & Yang, D. (2009). Expression of elf-1 and its relationship with survivin and ki-67 in non-small-cell lung cancer. Modern Journal of Integrated Traditional Chinese & Western Medicine.
Furlan, A., Vercamer, C., Bouali, F., Damour, I., Chotteau-Lelievre, A., & Wernert, N., et al. (2015). Ets-1 controls breast cancer cell balance between invasion and growth. International Journal of Cancer, 135(10), 2317-2328.
Mak, A., & Kow, N. Y. (2014). The pathology of t cells in systemic lupus erythematosus. Journal of Immunology Research,2014,(2014-4-23), 2014(22), 419029.

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