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- Table of Contents
Facts about Actin filament-associated protein 1.
May function as an adapter molecule that links other proteins, such as SRC and PKC to the actin cytoskeleton. Seems to play a role in the development and progression of prostate adenocarcinoma by regulating cell-matrix adhesions and migration in the cancer cells.
Human | |
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Gene Name: | AFAP1 |
Uniprot: | Q8N556 |
Entrez: | 60312 |
Belongs to: |
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No superfamily |
actin filament associated protein 1; AFAP; AFAP1; AFAP-110; FLJ56849
Mass (kDA):
80.725 kDA
Human | |
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Location: | 4p16.1 |
Sequence: | 4; NC_000004.12 (7758713..7939926, complement) |
Low expression in normal breast epithelial cell line MCF-10A and in tumorigenic breast cancer cell lines MCF- 7, T-47D and ZR-75-1. Highly expressed in the invasive breast cancer cell lines MDA-MB-231 and MDA-MB-435. Overexpressed in prostate carcinoma.
Cytoplasm, cytoskeleton, stress fiber.
This article explains the role of AFAP1-AS1 in lung cancer cell migration and invasion. We will discuss the role of SNIP1 in AFAP1 expression, and show you how to use an ISH experiment and ELISA kit to detect AFAP1 expression in lung cancer. If you have questions about how these markers can be used in research, please contact Boster Bio.
The role of AFAP1-AS1 in lung cancer metastasis and invasion was recently investigated. This molecule is a receptor for the c-Myc protein. AFAP1-AS1 promotes ZEB1 and ZEB2 genes as well as SNAIL. AFAP1 overexpression is related to lung cancer metastasis and invasion.
AFAP1-AS1 is a long non-coding RNA that is overexpressed in many types of cancer. It was investigated whether AFAP1-AS1 promotes lung cancer cell migration and invasion by assessing its expression in paraffin-embedded lung tumors. Moreover, it was examined to determine whether AFAP1-AS1 expression correlates with poor prognosis.
In a previous study, AFAP1-AS1 expression was positively correlated with distant metastasis in lung adenocarcinoma patients, but not in lung squamous cell carcinoma patients. The authors performed correlation regression analyses on 86 lung adenocarcinoma and 88 lung squamous cell carcinoma tumor tissues.
AFAP1-AS1 inhibits lung cancer cell growth in mice when knocked down. They also found that AFAP1-AS1 regulates miR-545-3p expression, which in turn is involved in lung cancer cell migration and invasion. Ultimately, the study shows that AFAP1-AS1 knockdown suppresses lung cancer cell proliferation, migration, and apoptosis in mice.
The AFAP1-AS1 protein interacts with the SNIP1 gene in the ubiquitination-proteasome degradation pathway. It inhibits c-Myc degradation by binding to SNIP1 protein. Knockdown of AFAP1-AS1 completely abolishes the effect of SNIP1 on c-Myc transcription.
The role of AFAP1-AS1 in lung cancer cell migration and invasion was revealed in a study using mice with a mutant form of the gene. The gene inhibits the ubiquitin-mediated degradation of c-Myc by interacting with the SNIP1 protein. The results suggest that AFAP1-AS1 regulates c-Myc in lung cancer cells.
The study was conducted on two human cell lines, A549 and H3122, and GC cells. Total RNA was isolated using a RNA extraction kit. The resulting cDNA was analyzed using a qRT-PCR to determine the presence of AFAP1-AS1 or NC. Among the two groups, AFAP1-AS1 was overexpressed in GC cells.
In this study, we found that AFAP1-AS1 promotes lung cancer cell migration and invasion. We also found that AFAP1-AS1 mediates the binding of SNIP1 to c-Myc. This finding offers a novel therapeutic target for lung cancer. Here, we used in situ hybridization to study the expression of AFAP1-AS1 in 36 samples of lung cancer tissues and 187 samples of normal lung epithelial tissue.
AFAP1-AS1 is expressed in both A549 and PC9 cells. The main binding region of AFAP1-AS1 is located between 1-3492 nt. The SNIP1 protein is necessary for AFAP1-AS1 expression in Boster Bio. AFAP1-AS1 is required for the expression of GAPDH.
SNIP1 is necessary for AFAP1-AS1 expression, and c-Myc is regulated by this protein. AFAP1-AS1 acts as a molecular guide for c-Myc. It inhibits the degradation of c-Myc, a signaling protein. The expression of SNIP1-AS1 decreases in Boster Bio cells when AFAP1-AS1 is overexpressed.
AFAP1-AS1 induces ZEB1, ZEB2, and SNAIL expression. Knocking out SNIP1 abolishes these effects, and AFAP1-AS1 and ZEB1-AS1 are upregulated. Furthermore, AFAP1-AS1 and SNIP1 co-regulate c-Myc transcription.
The aim of this study was to identify the gene AFAP1-AS1 in lung cancer tissues. The protein promotes lung cancer cell migration and invasion through its association with c-Myc. Moreover, the gene may have therapeutic potential. To detect this gene in lung cancer tissue, we used in situ hybridization. To this end, we used 187 lung cancer tissue samples and 36 normal lung epithelial tissue samples.
We first examined the expression of AFAP1-AS1 in lung cancer tissues and normal tissue samples. We found that AFAP1-AS1 expression was significantly higher in lung tumor tissues compared to normal tissue. The study also identified a strong correlation between the expression level of AFAP1-AS1 and lymph node metastasis in lung cancer. Further analysis indicated that high expression of AFAP1-AS1 was associated with poor survival in lung cancer patients.
Interestingly, a significant number of lung tumor samples containing AFAP1-AS1 showed overexpression of this gene. Among the overexpressed and knockdown groups, the AFAP1-AS1 group showed larger metastatic tumor areas than the negative control group. The expression of AFAP1-AS1 in lung cancer tumors correlated with both lymph node metastasis and tissue differentiation.
The ISH results also revealed a correlation between AFAP1-AS1 expression and tumor size. The high-expression group exhibited more aggressive disease (intense tumor size, lymph node metastasis, TNM stage, and T2-M3) and worse prognosis. The findings suggest that AFAP1-AS1 might play an oncogene role in lung cancer.
ISH experiments to detect AFAP1-AS1 in lung cancer cells have shown a significant correlation between c-Myc and AFAP1-AS1. Interestingly, AFAP1-AS1 is essential for the regulation of c-Myc and SNIP1.
The knockdown of AFAP1-AS1 in lung cancer cells was effective at reducing the levels of FGF7 and miR-155-5p in GC cells. Further, ISH experiments of lung cancer patients were performed with an eGFP-miR-155-5p reporter assay. These experiments showed that miR-155-5p is associated with AFAP1-AS1 expression, thereby suggesting that this miRNA may have a beneficial impact on the cancer cell growth.
The AFAP1-AS1 gene has been associated with lung cancer. This gene is overexpressed in various lung cancer cell lines and tumor tissues and is related to poor outcomes. In one study, AFAP1-AS1 expression was found to be significantly upregulated in lung cancer cells and tissues associated with poor prognosis. Moreover, the knockdown of AFAP1-AS1 significantly inhibited the migration and invasive capabilities of lung cancer cells.
To validate the ELISA kit, a panel of human lung tumor cells was used. The ELISA kit for lung cancer samples was developed using two NSCLC cell lines provided by the Chinese Academy of Sciences. The cell lines were cultured in M199 medium that contained 10% serum. The cells were incubated at 37degC with 5% CO2 in the presence of a nitrogen source. The highest expression level of AFAP1-AS1 was found in the h2975 cell line.
The ELISA kits contain pre-coated chromatography plates, detection antibodies, diluents, and standards. In the case of lung cancer, a sandwich ELISA kit contains a sample diluent, capture and detection antibodies, and a standard curve. In this manner, the target antigen is directly immobilized in the assay plate.
In addition, the lncGm16410 gene suppresses the expression of PI3K/AKT and SRC. These three proteins interact with one another and regulate the balance of M1/M2 macrophages. Activation of macrophages results in an overproduction of inflammatory factors, including IL-6. As a result, inflammation occurs in the lung.
PMID: 15485829 by Han B., et al. Conversion of mechanical force into biochemical signaling.
PMID: 17520695 by Dorfleutner A., et al. AFAP-110 is required for actin stress fiber formation and cell adhesion in MDA-MB-231 breast cancer cells.