ABCA1 Exerts Tumor-Suppressor Function in Myeloproliferative Neoplasms

Viaud, Manon; Abdel‐Wahab, Omar; Gall, Julie; Ivanov, Stoyan; Guinamard, Rodolphe; Sore, Sophie; Merlin, Johanna; Ayrault, Marion; Guilbaud, Emma; Jacquel, Arnaud; Auberger, Patrick; Wang, Nan; Levine, Ross L.; Tall, Alan R.; Yvan‐Charvet, Laurent

doi:10.1016/j.celrep.2020.02.056

Cited by 18 publications

(14 citation statements)

References 55 publications

(118 reference statements)

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“…(3) ABCA1 is known to suppress hematopoietic cell proliferation. Somatic ABCA1 mutations found in chronic myelomonocytic leukemia patients were found to impair cholesterol efflux and increase cell proliferation by enhancing the cholesterol-dependent IL3-receptor β pathway, which activates and protein-tyrosine kinase Janus kinase 2 (JAK2) and mitogen-activated protein kinase (MAPK) signaling [309] ( Figure 3). In contrast, other studies proposed mechanisms associated with ABCA1 activity in favor of cell cancer proliferation.…”

Section: Abca1 In Cancermentioning

confidence: 99%

“…On one hand, diminished ABCA1 expression in neoplastic breast and prostate tissue was associated with an increased rate of cancer cell proliferation [ 303 , 304 ]. Likewise, ABCA1 downregulation caused by ABCA1 promoter hypermethylation, miR-183 degradation or loss of function mutations, led to elevated cholesterol levels in cancer cells, enhanced cell proliferation and inhibited apoptosis [ 305 , 306 , 307 , 308 , 309 ]. On the other hand, ABCA1 has been classified as a member of a lipid metabolism gene expression signature (ColoLipidGene) related to poor prognosis in patients with colorectal cancer (CRC).…”

Section: Abca1 In Cancermentioning

confidence: 99%

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The Role of the ATP-Binding Cassette A1 (ABCA1) in Human Disease

Jacobo-Albavera

Domínguez‐Pérez

Medina-Leyte

et al. 2021

IJMS

100

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Cholesterol homeostasis is essential in normal physiology of all cells. One of several proteins involved in cholesterol homeostasis is the ATP-binding cassette transporter A1 (ABCA1), a transmembrane protein widely expressed in many tissues. One of its main functions is the efflux of intracellular free cholesterol and phospholipids across the plasma membrane to combine with apolipoproteins, mainly apolipoprotein A-I (Apo A-I), forming nascent high-density lipoprotein-cholesterol (HDL-C) particles, the first step of reverse cholesterol transport (RCT). In addition, ABCA1 regulates cholesterol and phospholipid content in the plasma membrane affecting lipid rafts, microparticle (MP) formation and cell signaling. Thus, it is not surprising that impaired ABCA1 function and altered cholesterol homeostasis may affect many different organs and is involved in the pathophysiology of a broad array of diseases. This review describes evidence obtained from animal models, human studies and genetic variation explaining how ABCA1 is involved in dyslipidemia, coronary heart disease (CHD), type 2 diabetes (T2D), thrombosis, neurological disorders, age-related macular degeneration (AMD), glaucoma, viral infections and in cancer progression.

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Section: Abca1 In Cancermentioning

confidence: 99%

Section: Abca1 In Cancermentioning

confidence: 99%

The Role of the ATP-Binding Cassette A1 (ABCA1) in Human Disease

Jacobo-Albavera

Domínguez‐Pérez

Medina-Leyte

et al. 2021

IJMS

100

View full text Add to dashboard Cite

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“…ABCA1 was identified as a tumor suppressor, as it favors the execution of cell death programs via mitochondrial pathways and limits AKT signaling by regulating the lipid composition in the plasma membrane [48]. In line with this, missense mutations in ABCA1 conferring a proliferative advantage have been identified in patients with chronic myelomonocytic leukemia [49]. On the other hand, cancer cells can modulate ABCA1 expression in tumor infiltrating immune cells.…”

Section: Abc Transporters In Immune Cells During Cancermentioning

confidence: 90%

ABC Transporters in T Cell-Mediated Physiological and Pathological Immune Responses

Thurm

Schraven

Kahlfuß

2021

IJMS

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ATP-binding cassette (ABC) transporters represent a heterogeneous group of ATP-dependent transport proteins, which facilitate the import and/or export of various substrates, including lipids, sugars, amino acids and peptides, ions, and drugs. ABC transporters are involved in a variety of physiological processes in different human tissues. More recent studies have demonstrated that ABC transporters also regulate the development and function of different T cell populations, such as thymocytes, Natural Killer T cells, CD8+ T cells, and CD4+ T helper cells, including regulatory T cells. Here, we review the current knowledge on ABC transporters in these T cell populations by summarizing how ABC transporters regulate the function of the individual cell types and how this affects the immunity to viruses and tumors, and the course of autoimmune diseases. Furthermore, we provide a perspective on how a better understanding of the function of ABC transporters in T cells might provide promising novel avenues for the therapy of autoimmunity and to improve immunity to infection and cancer.

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“… mmu-miR-6392-5p, mmu-miR-5622-3p, mmu-miR-708-5p, mmu-miR-28a-5p, mmu-miR-5621-5p Tg Hu ApoA1 mice (stock No. 001927) [ 53 ] HD-5 (NM_021010) Cytotoxic/ antimicrobial protein involved in host defense against pathogens. mmu-miR-3074-5p, mmu-miR-7240-5p, mmu-miR-3473a, mmu-miR-185-5p, mmu-miR-1933-3p, mmu-miR-882, mmu-miR-145a-3p, mmu-miR-203b-3p, mmu-miR-7217-3p, mmu-miR-1264-5p, mmu-miR-7229-3p, mmu-miR-881-5p, mmu-miR-691, mmu-miR-7216-5p, mmu-miR-539-5p, mmu-miR-1897-5p, mmu-miR-12186-5p, mmu-miR-665-3p, mmu-miR-6338, mmu-miR-29b-2-5p HD-5 transgenic mice [ 40 ] HOXD3 (NM_006898) Transcription factor that plays a regulatory role in morphogenesis.…”

Section: Discussionmentioning

confidence: 99%

Inadvertent nucleotide sequence alterations during mutagenesis: highlighting the vulnerabilities in mouse transgenic technology

Ghosh

Chakrabarti

Shukla

2021

Journal of Genetic Engineering and Biotechnology

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In the last three decades, researchers have utilized genome engineering to alter the DNA sequence in the living cells of a plethora of organisms, ranging from plants, fishes, mice, to even humans. This has been conventionally achieved by using methodologies such as single nucleotide insertion/deletion in coding sequences, exon(s) deletion, mutations in the promoter region, introducing stop codon for protein truncation, and addition of foreign DNA for functional elucidation of genes. However, recent years have witnessed the advent of novel techniques that use programmable site-specific nucleases like CRISPR/Cas9, TALENs, ZFNs, Cre/loxP system, and gene trapping. These have revolutionized the field of experimental transgenesis as well as contributed to the existing knowledge base of classical genetics and gene mapping. Yet there are certain experimental/technological barriers that we have been unable to cross while creating genetically modified organisms. Firstly, while interfering with coding strands, we inadvertently change introns, antisense strands, and other non-coding elements of the gene and genome that play integral roles in the determination of cellular phenotype. These unintended modifications become critical because introns and other non-coding elements, although traditionally regarded as “junk DNA,” have been found to play a major regulatory role in genetic pathways of several crucial cellular processes, development, homeostasis, and diseases. Secondly, post-insertion of transgene, non-coding RNAs are generated by host organism against the inserted foreign DNA or from the inserted transgene/construct against the host genes. The potential contribution of these non-coding RNAs to the resulting phenotype has not been considered. We aim to draw attention to these inherent flaws in the transgenic technology being employed to generate mutant mice and other model organisms. By overlooking these aspects of the whole gene and genetic makeup, perhaps our current understanding of gene function remains incomplete. Thus, it becomes important that, while using genetic engineering techniques to generate a mutant organism for a particular gene, we should carefully consider all the possible elements that may play a potential role in the resulting phenotype. This perspective highlights the commonly used mouse strains and the most probable associated complexities that have not been considered previously, resulting in possible limitations in the currently utilized transgenic technology. This work also warrants the use of already established mouse lines in further research.

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ABCA1 Exerts Tumor-Suppressor Function in Myeloproliferative Neoplasms

Cited by 18 publications

References 55 publications

The Role of the ATP-Binding Cassette A1 (ABCA1) in Human Disease

The Role of the ATP-Binding Cassette A1 (ABCA1) in Human Disease

ABC Transporters in T Cell-Mediated Physiological and Pathological Immune Responses

Inadvertent nucleotide sequence alterations during mutagenesis: highlighting the vulnerabilities in mouse transgenic technology

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