AFAP1
- Known as:
- AFAP1
- Catalog number:
- 001261A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AFAP1
Related genes to: AFAP1
- Gene:
- AFAP1 NIH gene
- Name:
- actin filament associated protein 1
- Previous symbol:
- -
- Synonyms:
- AFAP-110, AFAP
- Chromosome:
- 4p16.1
- Locus Type:
- gene with protein product
- Date approved:
- 2007-02-07
- Date modifiied:
- 2016-10-05
- Gene:
- AFAP1-AS1 NIH gene
- Name:
- AFAP1 antisense RNA 1
- Previous symbol:
- AFAP1AS, AFAP1-AS
- Synonyms:
- MGC10981
- Chromosome:
- 4p16.1
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2010-07-08
- Date modifiied:
- 2016-11-24
Related products to: AFAP1
Related articles to: AFAP1
- Generated from macrophages, long non-coding RNAs (lncRNAs) are increasingly recognized as imperative in influencing cancer immune evasion, microenvironment alteration, and therapy sensitivity. Together with tumor-associated macrophages (TAMs), this detailed investigation investigates the several roles of lncRNAs derived from M1 and M2 macrophage subtypes in regulating tumor progression. In contrast to the cancer-promoting effect of M2-based derived lncRNAs, such as H19, AFAP1-AS1, and CRNDE, which stimulate tumor proliferation, metastases, and chemoresistance through a variety of cascades, M1-based derived lncRNAs, such as HOTTIP and NBR2, exhibit tumor-suppressive roles in augmenting inflammatory signals and inhibiting epithelial-mesenchymal transition. Other than their involvement in the development of cancer, macrophage-derived lncRNAs have important immune control effects based on macrophage polarization, cytokine production, and immune checkpoints. Recent progress in single-cell RNA sequencing and the CRISPR-based functional studies also now provides new lncRNA targets and improved accuracy of diagnostics and optimization of therapy approaches. It marks a new step in personalized cancer immunotherapy: our research focuses on the possibilities of macrophage-derived lncRNAs as biomarkers and treatment options. - Source: PubMed
Publication date: 2026/04/28
Ramalingam Prasanna SrinivasanHussain Md SadiqueKhan YumnaMaqbool MudasirAgrawal MohitDh Haleema ShahinPrabhu AshwiniAshique SumelKalra Jyoti MaithaniKalra KapilBalakrishnan PurushothamanArumugam Sivakumar - Multiple sclerosis (MS) is a chronic inflammatory autoimmune disease of the central nervous system. It is characterized by inflammation, areas of demyelination and axonal loss called plaques, recruitment of lymphocytes and monocytes, and bursts of focal blood-brain barrier leakage. Treatment strategies for MS focus on delaying disease progression and increasing patients' quality of life. However, most therapies have inconsistent efficacies and are associated with various side effects. Recently, long non-coding RNAs have been found to play a major role in the pathogenesis and development of several diseases. Several long non-coding RNAs have been correlated with MS. We focus on the role of AFAP1-AS1 in regulating the function of M2 macrophages, one of the immune cells believed to attenuate MS. Assessing this long non-coding RNA will improve our understanding of the molecular mechanics of immune cells in MS. We observe the impact of AFAP1-AS1 silencing in M2 macrophages on essential effector and regulatory proteins like MMP9, CCL5 and CXCL10 in MS patients receiving different treatments (Fingolimod, Interferon beta-1a, Interferon beta-1b, Teriflunomide or Dimethyl fumarate). Our results reported an upstream regulatory effect of AFAP1-AS1 on MMP9, CCL5, and CXCL10 in differently treated patients. By measuring the levels of proteins upon silencing of AFAP1-AS1, it was confirmed that this lncRNA has varying effects on the expression of these proteins depending on the treatment the patient is undergoing. These data shed light on the potential role of manipulating the anti-inflammatory activity of M2 cells making it a possible therapeutic target for certain MS patients. - Source: PubMed
Publication date: 2026/04/26
Hegazy Lina NasserElkhodiry Aya AlyRashad Mohamed HamedMoustafa Ramez RedaEl Tayebi Hend Mohamed - Lung cancer is the most common and deadliest malignancy worldwide, with about 85% of cases being non-small cell lung cancer (NSCLC). Although targeting PD-1/PD-L1 with immune checkpoint inhibitors has revolutionized NSCLC treatment, a substantial proportion of patients still experience intrinsic or acquired resistance. Understanding the mechanisms of immune evasion and resistance and identifying novel therapeutic targets remain critical challenges. - Source: PubMed
Publication date: 2026/04/24
Zhang YijieOuyang JiaweiYan QijiaGe JunshangWu PanWang DanLi LvyuanZhang JiarongZhong YuYang LitingShi LeiXiong FangZhou MingXiang BoZeng ZhaoyangChen PanXiong WeiGong Zhaojian - Actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) has been found to be closely associated with the initiation and progression of various tumors; however, its role in oral squamous cell carcinoma (OSCC) remains unclear. AFAP1-AS1 expression in OSCC cells was detected using qRT-PCR. The regulatory effects of AFAP1-AS1 on tumor cell proliferation, migration, and invasive capabilities were systematically evaluated through CCK-8 proliferation, colony formation, wound healing, and Transwell invasion assays. Flow cytometry was employed to quantitatively analyze its impact on cell cycle progression and apoptotic. Based on bioinformatics predictions, a dual-luciferase reporter system was utilized to validate the targeting interactions among AFAP1-AS1, miR-93-3p, and CCND1. Functional rescue experiments were conducted to elucidate the functional regulatory network among them. Furthermore, a xenograft tumor model in nude mice was employed to verify in vivo the promoting effect of AFAP1-AS1 on tumor growth. AFAP1-AS1 was significantly upregulated in OSCC cells. AFAP1-AS1 knockdown inhibited the malignant phenotypes of OSCC cells. Mechanistic studies revealed that AFAP1-AS1 could target miR-93-3p and regulate CCND1 expression, thereby influencing OSCC progression. Subcutaneous tumor model in mice further confirmed the in vivo relevance of the AFAP1-AS1/miR-93-3p/CCND1 axis. AFAP1-AS1 downregulation inhibited OSCC progression through the miR-93-3p/CCND1 axis. - Source: PubMed
Publication date: 2026/04/10
Li KuangzhengLi ChengweiHe QianFan XiaoshengXu LiliJiang Yixia - Radioresistance remains a critical barrier to successful radiotherapy in non-small cell lung cancer (NSCLC). ATMLP, a mitochondrial-localized peptide encoded by lncRNA AFAP1-AS1, has been previously associated with tumor progression. In this study, we uncover a previously unrecognized role of ATMLP in promoting radioresistance by facilitating intracellular lipid droplet (LD) accumulation through AKT pathway activation. Mechanistically, ATMLP reduces radiation-induced reactive oxygen species (ROS) accumulation, thereby relieving ROS-mediated suppression of AKT phosphorylation, which in turn enhances lipid storage and promotes tumor cell survival under ionizing radiation. Genetic knockout of ATMLP leads to excessive ROS generation, impaired AKT activation, and diminished LD accumulation, ultimately sensitizing NSCLC cells to radiation. Conversely, ATMLP overexpression decreases ROS levels, increases post-radiation clonogenicity, and accelerates tumor growth. Inhibition of the AKT pathway abrogates ATMLP-induced lipid accumulation and reverses the radioresistant phenotype. These findings identify ATMLP as a key mediator linking ROS homeostasis and lipid metabolic reprogramming to radiation response, and suggest that targeting the ATMLP-AKT axis may represent a promising therapeutic strategy to enhance radiotherapy efficacy in NSCLC. - Source: PubMed
Publication date: 2026/01/21
Dai YingchuWu WanyiJiao TingyuHou LuLi WanshiLiu JiyuanGu QianjialeSu FengtaoNie JingLi BingyanWang JingPei HailongZhou Guangming