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1.
Methods Mol Biol ; 2024 Mar 06.
Article in English | MEDLINE | ID: mdl-38441720

ABSTRACT

In this chapter, we provide a method to purify and culture embryonic melanocytic stem cells that express green fluorescent protein in a cell-type specific manner. Isolation of melanocytic lineage cell populations that are >98% pure is accomplished through the use of GFP-based fluorescence activated cell sorting. We also provide a method to culture the purified melanoblasts and to analyze their proliferation, apoptosis, and motility properties.

2.
Bio Protoc ; 13(17): e4805, 2023 Sep 05.
Article in English | MEDLINE | ID: mdl-37719067

ABSTRACT

In this article, we provide a method to isolate embryonic melanoblasts from reporter mouse strains. The mice from which these cells are isolated are bred into the ROSA26mT/mG reporter background, which results in green fluorescent protein (GFP) expression in the targeted melanoblast population. These cells are isolated and purified by fluorescence-activated cell sorting using GFP fluorescence. We also provide a method to culture the purified melanoblasts for further analysis. This method yields > 99% purity melanoblasts specifically targeted, and can be used for a variety of studies, including gene expression, clonogenic experiments, and biological assays, such as viability, capacity for directional migration, or differentiation into melanin-producing melanocytic cells.

4.
AIDS Res Hum Retroviruses ; 37(11): 852-861, 2021 11.
Article in English | MEDLINE | ID: mdl-34002626

ABSTRACT

With obesity on the rise among people living with HIV (PLWH), there is growing concern that weight gain may result as an undesired effect of antiretroviral therapy (ART). This analysis sought to assess the association between ART regimens and changes in body mass index (BMI) among ART-experienced, virologically suppressed PLWH. ART-experienced, virologically suppressed PLWH ≥18 years of age in the Observational Pharmacoepidemiology Research and Analysis (OPERA) cohort were included for analysis if prescribed a new regimen containing one of the following core agents: dolutegravir (DTG), elvitegravir/cobicistat (EVG/c), raltegravir (RAL), rilpivirine (RPV), or boosted darunavir (bDRV), for the first time between August 1, 2013 and December 31, 2017. Multivariable linear regression was used to assess the association between regimen and mean changes in BMI at 6, 12, and 24 months after switch. In unadjusted analyses, BMI increases ranged from 0.30 kg/m2 (bDRV) to 0.83 kg/m2 (RPV) at 24 months following switch, but gains were observed with every regimen. In adjusted analyses, compared to DTG, only bDRV was associated with a smaller increase in BMI at all time points, while EVG/c and RAL were associated with smaller increases in BMI at 6 months only. Overall, results were consistent in analyses stratified by baseline BMI category. BMI increases were relatively small but followed an upward trend over time in this cohort of treatment-experienced, suppressed PLWH. Gains were attenuated with a longer period of follow-up. BMI gains did not differ by regimens, except for bDRV regimens, which were consistently associated with smaller BMI increases than DTG.


Subject(s)
Anti-HIV Agents , HIV Infections , Anti-HIV Agents/therapeutic use , Anti-Retroviral Agents/therapeutic use , Body Mass Index , Darunavir/therapeutic use , HIV Infections/drug therapy , Heterocyclic Compounds, 3-Ring/therapeutic use , Humans , Oxazines/therapeutic use , Rilpivirine/therapeutic use , United States/epidemiology
5.
Mol Biol Cell ; 31(8): 768-781, 2020 04 01.
Article in English | MEDLINE | ID: mdl-32049584

ABSTRACT

Melanosomes are melanin-containing organelles that provide pigmentation and protection from solar UV radiation to the skin. In melanocytes, melanosomes mature and traffic to dendritic tips, where they are transferred to adjacent epidermal keratinocytes through pathways that involve microtubule networks and the actin cytoskeleton. However, the role of scaffold proteins in these processes is poorly understood. Integrin-linked kinase (ILK) is a scaffold protein that regulates microtubule stability and F-actin dynamics. Here we show that ILK is necessary for normal trafficking of melanosomes along microtubule tracks. In the absence of ILK, immature melanosomes are not retained in perinuclear regions, and mature melanosome trafficking along microtubule tracks is impaired. These deficits can be attenuated by microtubule stabilization. Microtubules are also necessary for the formation of dendrites in melanocytes, and Ilk inactivation reduces melanocyte dendricity. Activation of glycogen synthase kinase-3 (GSK-3) interferes with microtubule assembly. Significantly, inhibition of GSK-3 activity or exogenous expression of the GSK-3 substrate collapsin response mediator protein 2 (CRMP2) in ILK-deficient melanocytes restored dendricity. ILK is also required for normal melanin transfer, and GSK-3 inhibition in melanocytes partially restored melanin transfer to neighboring keratinocytes. Thus, our work shows that ILK is a central modulator of melanosome movements in primary epidermal melanocytes and identifies ILK and GSK-3 as important modulators of melanin transfer to keratinocytes, a key process for epidermal UV photoprotection.


Subject(s)
Melanins/metabolism , Melanocytes/metabolism , Melanosomes/metabolism , Protein Serine-Threonine Kinases/physiology , Animals , Cells, Cultured , Dendrites/ultrastructure , Genes, Reporter , Glycogen Synthase Kinase 3/antagonists & inhibitors , Glycogen Synthase Kinase 3/metabolism , Intercellular Signaling Peptides and Proteins/metabolism , Keratinocytes/metabolism , Melanocytes/ultrastructure , Mice , Microtubules/metabolism , Microtubules/ultrastructure , Nerve Tissue Proteins/metabolism , Protein Serine-Threonine Kinases/deficiency , Protein Serine-Threonine Kinases/genetics , Recombinant Proteins/metabolism , rab GTP-Binding Proteins/metabolism , rab7 GTP-Binding Proteins
6.
J Invest Dermatol ; 140(2): 425-434.e10, 2020 02.
Article in English | MEDLINE | ID: mdl-31330146

ABSTRACT

Melanocytes are pigment-producing cells found in the skin and other tissues. Alterations in the melanocyte lineage give rise to a plethora of human diseases, from neurocristopathies and pigmentation disorders to melanoma. During embryogenesis, neural crest cell subsets give rise to two waves of melanoblasts, which migrate dorsolaterally, hone to the skin, and differentiate into melanocytes. However, the mechanisms that govern colonization of the skin by the first wave of melanoblasts are poorly understood. Here we report that targeted inactivation of the integrin-linked kinase gene in first wave melanoblasts causes defects in the ability of these cells to form long pseudopods, to migrate, and to proliferate in vivo. As a result, integrin-linked kinase-deficient melanoblasts fail to populate normally the developing epidermis and hair follicles. We also show that defects in motility and dendricity occur upon integrin-linked kinase gene inactivation in mature melanocytes, causing abnormalities in cell responses to the extracellular matrix substrates collagen I and laminin 332. Significantly, the ability to form long protrusions in mutant cells in response to collagen is restored in the presence of constitutively active Rac1, suggesting that an integrin-linked kinase-Rac1 nexus is likely implicated in melanocytic cell establishment, dendricity, and functions in the skin.


Subject(s)
Cell Differentiation/physiology , Embryonic Stem Cells/physiology , Melanocytes/physiology , Neural Crest/physiology , Protein Serine-Threonine Kinases/metabolism , Animals , Cell Line , Cell Movement/physiology , Embryo, Mammalian , Extracellular Matrix/metabolism , Hair Follicle/cytology , Hair Follicle/embryology , Hair Follicle/metabolism , Mice , Mice, Knockout , Neuropeptides/metabolism , Primary Cell Culture , Protein Serine-Threonine Kinases/genetics , Pseudopodia/metabolism , rac1 GTP-Binding Protein/metabolism
8.
Methods Mol Biol ; 1879: 243-256, 2019.
Article in English | MEDLINE | ID: mdl-29582376

ABSTRACT

In this article, we provide a method to isolate primary epidermal melanocytes from reporter mice, which also allow targeted gene inactivation. The mice from which these cells are isolated are bred into a Rosa26mT/mG reporter background, which results in GFP expression in the targeted melanocytic cell population. These cells are isolated and cultured to >95% purity. The cells can be used for gene expression studies, clonogenic experiments, and biological assays, such as capacity for migration. Melanocytes are slow moving cells, and we also provide a method to measure motility using individual cell tracking and data analysis.


Subject(s)
Cell Movement/physiology , Epidermal Cells/metabolism , Epidermal Cells/physiology , Gene Expression/physiology , Green Fluorescent Proteins/metabolism , Melanocytes/metabolism , Melanocytes/physiology , Animals , Biological Assay/methods , Cell Tracking/methods , Mice
11.
Nat Commun ; 8(1): 1801, 2017 11 27.
Article in English | MEDLINE | ID: mdl-29180617

ABSTRACT

The transcribed ultraconserved regions (T-UCRs) encode long non-coding RNAs implicated in human carcinogenesis. Their mechanisms of action and the factors regulating their expression in cancers are poorly understood. Here we show that high expression of uc.339 correlates with lower survival in 210 non-small cell lung cancer (NSCLC) patients. We provide evidence from cell lines and primary samples that TP53 directly regulates uc.339. We find that transcribed uc.339 is upregulated in archival NSCLC samples, functioning as a decoy RNA for miR-339-3p, -663b-3p, and -95-5p. As a result, Cyclin E2, a direct target of all these microRNAs is upregulated, promoting cancer growth and migration. Finally, we find that modulation of uc.339 affects microRNA expression. However, overexpression or downregulation of these microRNAs causes no significant variations in uc.339 levels, suggesting a type of interaction for uc.339 that we call "entrapping". Our results support a key role for uc.339 in lung cancer.


Subject(s)
Carcinoma, Non-Small-Cell Lung/genetics , Conserved Sequence/genetics , Lung Neoplasms/genetics , MicroRNAs/genetics , RNA, Long Noncoding/metabolism , Animals , Base Sequence/genetics , Carcinogenesis/genetics , Carcinoma, Non-Small-Cell Lung/pathology , Cell Line, Tumor , Cell Proliferation/genetics , Cyclins/genetics , Cyclins/metabolism , Down-Regulation , Female , Gene Expression Regulation, Neoplastic , Genes, Tumor Suppressor , Humans , Lung/pathology , Lung Neoplasms/pathology , Mice , Mice, Nude , MicroRNAs/metabolism , Up-Regulation , Xenograft Model Antitumor Assays
12.
Tissue Barriers ; 5(4): e1341969, 2017 10 02.
Article in English | MEDLINE | ID: mdl-28665776

ABSTRACT

The skin of mammals and other terrestrial vertebrates protects the organism against the external environment, preventing heat, water and electrolyte loss, as well as entry of chemicals and pathogens. Impairments in the epidermal permeability barrier function are associated with the genesis and/or progression of a variety of pathological conditions, including genetic inflammatory diseases, microbial and viral infections, and photodamage induced by UV radiation. In mammals, the outside-in epidermal permeability barrier is provided by the joint action of the outermost cornified layer, together with assembled tight junctions in granular keratinocytes found in the layers underneath. Tight junctions serve as both outside-in and inside-out barriers, and impede paracellular movements of ions, water, macromolecules and microorganisms. At the molecular level, tight junctions consist of integral membrane proteins that form an extracellular seal between adjacent cells, and associate with cytoplasmic scaffold proteins that serve as links with the actin cytoskeleton. In this review, we address the roles that scaffold proteins play specifically in the establishment and maintenance of the epidermal permeability barrier, and how various pathologies alter or impair their functions.


Subject(s)
Epidermis/metabolism , Membrane Proteins/metabolism , Skin Absorption/physiology , Tight Junctions/metabolism , Animals , Humans , Occludin/metabolism , Permeability , Protein Transport/physiology
13.
J Cancer ; 8(7): 1123-1128, 2017.
Article in English | MEDLINE | ID: mdl-28607585

ABSTRACT

At present, it is unclear if melanocytes contain Cx43 gap junctions and whether Cx43 expression is regulated in melanoma onset and progression. To this end, we cultured pure populations of mouse melanocytes and found that they had no detectable Cx43 and exhibited an inability for dye transfer indicating they were devoid of functional gap junctions. Given the evidence that melanomas acquire the expression of other connexin isoforms during tumor progression, we assessed if Cx43 was also expressed and assembled into gap junctions at any stage of human melanoma onset and progression to distant metastases. Nearly all primary melanomas within the epidermis lacked Cx43. In contrast, nodal metastases expressed low levels of Cx43 which was markedly higher in distant metastases that had invaded vital organs. Importantly, in all stages of melanoma progression, Cx43 could be detected in intracellular compartments but was rarely assembled into gap junctions indicative of functional gap junction channels. Overall, these studies suggest that melanocytes do not form Cx43 homocellular gap junctions and even though Cx43 levels increase during melanoma progression, this connexin rarely assembles into gap junction structures.

14.
Biol Open ; 6(8): 1219-1228, 2017 Aug 15.
Article in English | MEDLINE | ID: mdl-28642245

ABSTRACT

Alterations in melanocytic lineage cells give rise to a plethora of distinct human diseases, including neurocristopathies, cutaneous pigmentation disorders, loss of vision and hearing, and melanoma. Understanding the ontogeny and biology of melanocytic cells, as well as how they interact with their surrounding environment, are key steps in the development of therapies for diseases that involve this cell lineage. Efforts to culture and characterize primary melanocytes from normal or genetically engineered mouse models have at times yielded contrasting observations. This is due, in part, to differences in the conditions used to isolate, purify and culture these cells in individual studies. By breeding ROSAmT/mG and Tyr::CreERT2 mice, we generated animals in which melanocytic lineage cells are identified through expression of green fluorescent protein. We also used defined conditions to systematically investigate the proliferation and migration responses of primary melanocytes on various extracellular matrix (ECM) substrates. Under our culture conditions, mouse melanocytes exhibit doubling times in the range of 10 days, and retain exponential proliferative capacity for 50-60 days. In culture, these melanocytes showed distinct responses to different ECM substrates. Specifically, laminin-332 promoted cell spreading, formation of dendrites, random motility and directional migration. In contrast, low or intermediate concentrations of collagen I promoted adhesion and acquisition of a bipolar morphology, and interfered with melanocyte forward movements. Our systematic evaluation of primary melanocyte responses emphasizes the importance of clearly defining culture conditions for these cells. This, in turn, is essential for the interpretation of melanocyte responses to extracellular cues and to understand the molecular basis of disorders involving the melanocytic cell lineage.

16.
PLoS One ; 8(6): e67581, 2013.
Article in English | MEDLINE | ID: mdl-23805317

ABSTRACT

Lung cancer is the leading cause of cancer mortality in the world today. Although some advances in lung cancer therapy have been made, patient survival is still poor. MicroRNAs (miRNAs) can act as oncogenes or tumor-suppressor genes in human malignancy. The miR-34 family consists of tumor-suppressive miRNAs, and its reduced expression has been reported in various cancers, including non-small cell lung cancer (NSCLC). In this study, we found that miR-34a and miR-34c target platelet-derived growth factor receptor alpha and beta (PDGFR-α and PDGFR-ß), cell surface tyrosine kinase receptors that induce proliferation, migration and invasion in cancer. MiR-34a and miR-34c were downregulated in lung tumors compared to normal tissues. Moreover, we identified an inverse correlation between PDGFR-α/ß and miR-34a/c expression in lung tumor samples. Finally, miR-34a/c overexpression or downregulation of PDGFR-α/ß by siRNAs, strongly augmented the response to TNF-related apoptosis inducing ligand (TRAIL) while reducing migratory and invasive capacity of NSCLC cells.


Subject(s)
Apoptosis/drug effects , Carcinogenesis/drug effects , MicroRNAs/metabolism , Receptor, Platelet-Derived Growth Factor alpha/metabolism , Receptor, Platelet-Derived Growth Factor beta/metabolism , TNF-Related Apoptosis-Inducing Ligand/toxicity , 3' Untranslated Regions , Base Sequence , Cell Line, Tumor , Cell Movement , Cell Proliferation/drug effects , Down-Regulation/drug effects , Humans , Lung/metabolism , Lung/pathology , Lung Neoplasms/metabolism , Lung Neoplasms/pathology , MicroRNAs/genetics , RNA Interference , RNA, Messenger/metabolism , RNA, Small Interfering/metabolism , Receptor, Platelet-Derived Growth Factor alpha/antagonists & inhibitors , Receptor, Platelet-Derived Growth Factor alpha/genetics , Receptor, Platelet-Derived Growth Factor beta/antagonists & inhibitors , Receptor, Platelet-Derived Growth Factor beta/genetics , Sequence Alignment
17.
Mol Ther Nucleic Acids ; 2: e84, 2013 Apr 16.
Article in English | MEDLINE | ID: mdl-23591808

ABSTRACT

MicroRNA-29b (miR-29b) expression has been shown to be reduced in non-small-cell lung cancer (NSCLC) tissues. Here, we have identified the oncogene cyclin-dependent protein kinase 6 (CDK6) as a direct target of miR-29b in lung cancer. We hypothesized that in vivo restoration of miR-29b and thus targeting of genes important to tumor initiation and progression may represent an option for lung cancer treatment. We developed a cationic lipoplexes (LPs)-based carrier that efficiently delivered miR-29b both in vitro and in vivo. LPs containing miR-29b (LP-miR-29b) efficiently delivered miR-29b to NSCLC A549 cells, reduced the expression of key targets CDK6, DNMT3B, and myeloid cell leukemia sequence 1 (MCL1), as well as cell growth and clonogenicity of A549 cells. In addition, the IC50 for cisplatin in the miR-29b-treated cells was effectively reduced. In a xenograft murine model, LPs efficiently accumulated at tumor sites. Systemic delivery of LP-miR-29b increased the tumor miR-29b expression by approximately fivefold, downregulated the tumor mRNA expression of CDK6, DNMT3B, and MCL1 by ~57.4, ~40.5, and ~52.4%, respectively, and significantly inhibited tumor growth by ~60% compared with LP-miR-NC (negative control). Our results demonstrate that cationic LPs represent an efficient delivery system that holds great potential in the development of miRNA-based therapeutics for lung cancer treatment.Molecular Therapy-Nucleic Acids (2013) 2, e84; doi:10.1038/mtna.2013.14; published online 16 April 2013.

18.
PLoS One ; 8(1): e53663, 2013.
Article in English | MEDLINE | ID: mdl-23365639

ABSTRACT

Lung cancer is the leading cause of cancer-related deaths worldwide. Lack of early detection and limited options for targeted therapies are both contributing factors to the dismal statistics observed in lung cancer. Thus, advances in both of these areas are likely to lead to improved outcomes. MicroRNAs (miRs or miRNAs) represent a class of non-coding RNAs that have the capacity for gene regulation and may serve as both diagnostic and prognostic biomarkers in lung cancer. Abnormal expression patterns for several miRNAs have been identified in lung cancers. Specifically, let-7 and miR-9 are deregulated in both lung cancers and other solid malignancies. In this paper, we construct a mathematical model that integrates let-7 and miR-9 expression into a signaling pathway to generate an in silico model for the process of epithelial mesenchymal transition (EMT). Simulations of the model demonstrate that EGFR and Ras mutations in non-small cell lung cancers (NSCLC), which lead to the process of EMT, result in miR-9 upregulation and let-7 suppression, and this process is somewhat robust against random input into miR-9 and more strongly robust against random input into let-7. We elected to validate our model in vitro by testing the effects of EGFR inhibition on downstream MYC, miR-9 and let-7a expression. Interestingly, in an EGFR mutated lung cancer cell line, treatment with an EGFR inhibitor (Gefitinib) resulted in a concentration specific reduction in c-MYC and miR-9 expression while not changing let-7a expression. Our mathematical model explains the signaling link among EGFR, MYC, and miR-9, but not let-7. However, very little is presently known about factors that regulate let-7. It is quite possible that when such regulating factors become known and integrated into our model, they will further support our mathematical model.


Subject(s)
Carcinoma, Non-Small-Cell Lung/genetics , Gene Expression Regulation, Neoplastic/drug effects , Lung Neoplasms/genetics , MicroRNAs/genetics , Models, Genetic , Antineoplastic Agents/pharmacology , Carcinoma, Non-Small-Cell Lung/drug therapy , Carcinoma, Non-Small-Cell Lung/metabolism , Carcinoma, Non-Small-Cell Lung/pathology , Cell Line, Tumor , Computer Simulation , Epithelial-Mesenchymal Transition , ErbB Receptors/genetics , ErbB Receptors/metabolism , Gefitinib , Gene Expression Profiling , Humans , Lung Neoplasms/drug therapy , Lung Neoplasms/metabolism , Lung Neoplasms/pathology , MicroRNAs/metabolism , Mutation , Oncogene Protein p21(ras)/genetics , Oncogene Protein p21(ras)/metabolism , Proto-Oncogene Proteins c-myc/genetics , Proto-Oncogene Proteins c-myc/metabolism , Quinazolines/pharmacology , Signal Transduction/drug effects
19.
PLoS One ; 7(11): e50837, 2012.
Article in English | MEDLINE | ID: mdl-23226399

ABSTRACT

The Cystic Fibrosis Transmembrane conductance Regulator (CFTR) is a chloride channel that plays a critical role in the lung by maintaining fluid homeostasis. Absence or malfunction of CFTR leads to Cystic Fibrosis, a disease characterized by chronic infection and inflammation. We recently reported that air pollutants such as cigarette smoke and cadmium negatively regulate the expression of CFTR by affecting several steps in the biogenesis of CFTR protein. MicroRNAs (miRNAs) have recently received a great deal of attention as both biomarkers and therapeutics due to their ability to regulate multiple genes. Here, we show that cigarette smoke and cadmium up-regulate the expression of two miRNAs (miR-101 and miR-144) that are predicted to target CFTR in human bronchial epithelial cells. When premature miR-101 and miR-144 were transfected in human airway epithelial cells, they directly targeted the CFTR 3'UTR and suppressed the expression of the CFTR protein. Since miR-101 was highly up-regulated by cigarette smoke in vitro, we investigated whether such increase also occurred in vivo. Mice exposed to cigarette smoke for 4 weeks demonstrated an up-regulation of miR-101 and suppression of CFTR protein in their lungs. Finally, we show that miR-101 is highly expressed in lung samples from patients with severe chronic obstructive pulmonary disease (COPD) when compared to control patients. Taken together, these results suggest that chronic cigarette smoking up-regulates miR-101 and that this miRNA could contribute to suppression of CFTR in the lungs of COPD patients.


Subject(s)
Cystic Fibrosis Transmembrane Conductance Regulator/genetics , Gene Expression Regulation , Lung/metabolism , MicroRNAs/metabolism , 3' Untranslated Regions/genetics , Air Pollutants/toxicity , Animals , Base Sequence , Bronchi/pathology , Cadmium/toxicity , Cell Line , Cystic Fibrosis Transmembrane Conductance Regulator/metabolism , Epithelial Cells/drug effects , Epithelial Cells/metabolism , Epithelial Cells/pathology , Female , Gene Expression Regulation/drug effects , Humans , Lung/pathology , Mice , Mice, Inbred C57BL , MicroRNAs/genetics , Molecular Sequence Data , Pulmonary Disease, Chronic Obstructive/genetics , Pulmonary Disease, Chronic Obstructive/pathology , Smoking/adverse effects , Smoking/genetics , Up-Regulation/drug effects , Up-Regulation/genetics
20.
Proc Natl Acad Sci U S A ; 109(31): E2110-6, 2012 Jul 31.
Article in English | MEDLINE | ID: mdl-22753494

ABSTRACT

MicroRNAs (miRNAs) are small noncoding RNAs, 19-24 nucleotides in length, that regulate gene expression and are expressed aberrantly in most types of cancer. MiRNAs also have been detected in the blood of cancer patients and can serve as circulating biomarkers. It has been shown that secreted miRNAs within exosomes can be transferred from cell to cell and can regulate gene expression in the receiving cells by canonical binding to their target messenger RNAs. Here we show that tumor-secreted miR-21 and miR-29a also can function by another mechanism, by binding as ligands to receptors of the Toll-like receptor (TLR) family, murine TLR7 and human TLR8, in immune cells, triggering a TLR-mediated prometastatic inflammatory response that ultimately may lead to tumor growth and metastasis. Thus, by acting as paracrine agonists of TLRs, secreted miRNAs are key regulators of the tumor microenvironment. This mechanism of action of miRNAs is implicated in tumor-immune system communication and is important in tumor growth and spread, thus representing a possible target for cancer treatment.


Subject(s)
Membrane Glycoproteins/metabolism , MicroRNAs/blood , Neoplasms/blood , RNA, Neoplasm/blood , Toll-Like Receptor 7/metabolism , Toll-Like Receptor 8/metabolism , Animals , HEK293 Cells , Humans , Inflammation/genetics , Inflammation/metabolism , Inflammation/pathology , Membrane Glycoproteins/genetics , Mice , Mice, Knockout , MicroRNAs/genetics , Neoplasm Metastasis , Neoplasms/genetics , Neoplasms/pathology , Neoplasms/therapy , Paracrine Communication/genetics , RNA, Neoplasm/genetics , Toll-Like Receptor 7/genetics , Toll-Like Receptor 8/genetics
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