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- Table of Contents
Facts about Receptor-binding cancer antigen expressed on SiSo cells.
Human | |
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Gene Name: | EBAG9 |
Uniprot: | O00559 |
Entrez: | 9166 |
Belongs to: |
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No superfamily |
Cancer-associated surface antigen RCAS1; EB9cancer associated surface antigen; estrogen receptor binding site associated, antigen, 9; Estrogen receptor-binding fragment-associated gene 9 protein; RCAS1PDAF; receptor-binding cancer antigen expressed on SiSo cells
Mass (kDA):
24.377 kDA
Human | |
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Location: | 8q23.2 |
Sequence: | 8; NC_000008.11 (109539700..109565996) |
Widely expressed. Expressed in ovary, testis, prostate, thymus, muscle and heart, but not in small intestine, colon, lymph nodes, or peripherical blood lymphocytes. The protein is not detected in any of the above organs.
Golgi apparatus membrane; Single-pass type III membrane protein. According to PubMed:10426319, it also exists as a soluble form which has the same biological activities. The existence of such soluble form is however uncertain.
It's easy to be confused by EBAG9 but it's actually an molecule that promotes tumor growth. It is believed to stimulate the development and distant metastasis in primary 4T1 mammary cancers. This article will examine some of the most effective applications of EBAG9.
The role of EBAG9 in breast cancer metastasis has been explored in various studies. In this study a mouse model of primary 4T1 mammary cancer was injected with siRNA that targeted the EBAG9 gene. The mice were treated with siRNA or an uncontrolled siRNA. The siRNAs had the same sense and antisense strands, and were synthesized in tandem.
Two mouse models were used to examine the effects of EBAG9 on tumor growth. In a murine model, gene silencing of EBAG9 inhibited tumor growth in 4T1 cells, and also increased the infiltration of T cells that are CD8+ into tumor masses. Both mice models survived for 90 days. In the EBAG9 group 50 percent of mice survived, whereas 25 percent of the 4T1-siRNA parental group died by day 50. This study offers insights into the immune system of tumors and suggests a strategy for therapeutic intervention for cancer metastasis.
Numerous studies have revealed that EBAG9 promotes primary and secondary 4T1 mammary cancer growth as in distant metastases. A strong increase in the serum MMP-9 and a moderate rise in VEGF were linked to an increase in the number of metastases that spread to the system in this kind of cancer. This study also demonstrates that the drug has immunomodulatory and anti-tumor effects.
Effective therapeutic intervention of the disease requires EBAG9 to be expressed in cellular and molecular levels. The EBAG9 gene can also trigger the death of T cells. We observed an increase in apoptosis in 4T1 cells treated with mitomycin C (50 Ug/mL) by annexin V as well as propidium Iodide staining. This could be due to the short-term treatment duration of the murine model as well as the absence of apoptosis-associated cell cells inducing cytokine EBAG9 via siRNA.
Furthermore, a new study found that an overexpression of EBAG9 increases the risk of lung metastasis in 4T1 cells carcinoma. The gene silencing EBAG9 significantly reduced the risk of tumor metastasis. The study also suggested that EBAG9 may increase CXCR4 expression. In the end, this study suggests that EBAG9 may be a promising prognostic factor for patients suffering from RCC.
In this study mice were inoculated with 4T1 tumor cells and RAW264.7 macrophages. The primary pattern of metastasis and tumor growth in the treatment group using 4T1 cells and RAW264.7 macrophages were similar. Additionally, both groups showed similar rates of Ki67 tumor cells proliferation and hypoxia-associated CAIX expression.
The study divided female BALB/c mice into MV and non-MV groups. The MV group received MSCs 107 times a week for three weeks and was able to live with normal ovarian function. Mice treated with MVs were at greater risk of developing lung metastases. The MV group however did not receive any chemotherapy.
EBAG9 is a molecule released by cancer-related EVs. EBAG9 is a protein released by cancer-derived EVs. It inhibits tumor cell growth and metastasis as well as immune cell cytotoxicity. These findings offer new insight into the ways that tumors are able to escape immune surveillance. It is possible that EBAG9 could be an effective therapeutic target for advanced cancers. Further studies will be necessary to determine the precise function of EBAG9.
To determine the effect of EBAG9 on metastasis and growth of tumors in cancer, TM9SF1 cell lines and 293T cells were transfected using the appropriate EBAG9 expression genes. The cells were suspended in lysis buffer comprising 20 millimeters of HEPES at pH 7.9 300 mg NaCl, 1M EDTA , and 15% glycerol.
EBAG9 expression in a breast carcinoma 4T1 cell line was linked to an increase in metastasis and tumor growth. Transfection with siRNAs that target EBAG9 and non-silencing siRNAs and GAPDH inhibited metastasis and growth of tumors within the mouse model. Co-culture of EBAG9 overexpressed 4T1 cells and the negative control reduced IFN production, which is an indicator of the immune response.
By using a murine cell-line cDNA encoding EBAG9 could be overexpressed in oocytes of 4T1. The EBAG9 gene that encodes for murine cells was amplified using RT-PCR from total RNA. The products that were ligated were digested with restricted endonucleases EcoRI and BamHI and positive recombinants identified by restriction endonuclease digests, PCR and DNA sequencing.
The findings of this study indicate that the overexpression of EBAG9 hinders tumor growth through reducing the production of IFN-g. The overexpression of EBAG9 in 4T1 cells causes hyporesponsiveness and apoptosis of T cells. Although the impact of EBAG9 on the movement of immune cells is not known, overexpression of this protein might induce apoptosis.
Chu HW and his team have discovered that EBAG9 is a gene that is linked with breast cancer progression, and estrogen receptor status is the subject of ongoing research. This gene also regulates miR-1966a-3p expression. This study has identified two new targets for EBAG9 inhibitors. They have been found to inhibit expression of microRNA 190a in breast cancer cells, a sign of its potential role in the progression of cancer and metastasis.
EBAG9 has also been shown to increase plasma IgG levels. This helps to induce and maintenance of immune system function during the course of tumor development. This effect is mediated by changes in the LN conduits which facilitate the movement of soluble antigens to FDCs in GCs. Additionally, tumor-associated antibodies promote the maturation of B cells associated with tumors.
Interleukin-1 beta converting protein (IL-1 beta) is an enzyme that is associated with tumors and causes cell death through apoptosis. Incredibly, IL-1 beta-converting enzyme is detected in breast cancer and is associated with the grade of tumor. EBAG9 is thought to activate interleukin-1 beta converting enzyme and to regulate the expression on the surface of O-linked glycans that are associated with tumors. It is also linked to increased antigenicity to tumors.
PMID: 10426319 by Nakashima M., et al. Inhibition of cell growth and induction of apoptotic cell death by the human tumor-associated antigen RCAS1.
PMID: 9418891 by Watanabe T., et al. Isolation of estrogen-responsive genes with a CpG island library.