ABSTRACT
circular RNA ciRS-7 (ciRS-7) is a type of endogenous circular RNA (circRNA) with a closed circular structure. Since Hansen first demonstrated that ciRS-7 could serve as a microRNA sponge in 2013, researchers have paid increased attention to this circRNA. ciRS-7 plays a crucial role in regulating RNA transcription, downstream gene expression, and protein production. Moreover, ciRS-7 acts as an oncogene and promotes tumor progression through competitively inhibiting miR-7 in various types of cancers. ciRS-7 has been identified to be closely associated with breast cancer, nasopharyngeal carcinoma, lung cancer, hepatocellular carcinoma, cervical cancer, osteosarcoma, melanoma, colorectal cancer, esophageal squamous cell carcinoma, gastric cancer, pancreatic cancer, laryngeal squamous cell carcinoma, and cholangiocarcinoma. In this review, we summarize the biological characteristics, molecular mechanisms, and future challenges of ciRS-7 in multiple tumors.
Subject(s)
Neoplasms/genetics , Oncogenes , RNA, Long Noncoding/genetics , Humans , Neoplasms/metabolism , RNA, Long Noncoding/metabolismABSTRACT
After entering tissues, monocytes differentiate into cells that share functional features with either macrophages or dendritic cells (DCs). How monocyte fate is directed toward monocyte-derived macrophages (mo-Macs) or monocyte-derived DCs (mo-DCs) and which transcription factors control these differentiation pathways remains unknown. Using an in vitro culture model yielding human mo-DCs and mo-Macs closely resembling those found in vivo in ascites, we show that IRF4 and MAFB were critical regulators of monocyte differentiation into mo-DCs and mo-Macs, respectively. Activation of the aryl hydrocarbon receptor (AHR) promoted mo-DC differentiation through the induction of BLIMP-1, while impairing differentiation into mo-Macs. AhR deficiency also impaired the in vivo differentiation of mouse mo-DCs. Finally, AHR activation correlated with mo-DC infiltration in leprosy lesions. These results establish that mo-DCs and mo-Macs are controlled by distinct transcription factors and show that AHR acts as a molecular switch for monocyte fate specification in response to micro-environmental factors.
Subject(s)
Dendritic Cells/metabolism , Macrophages/metabolism , Monocytes/metabolism , Receptors, Aryl Hydrocarbon/metabolism , Animals , Ascites , Cells, Cultured , Cluster Analysis , Cytokines/metabolism , Cytokines/pharmacology , Dendritic Cells/cytology , Dendritic Cells/drug effects , Dendritic Cells/immunology , Female , Gene Expression Profiling , Gene Expression Regulation , Humans , Interferon Regulatory Factors/metabolism , Leprosy/immunology , Leprosy/metabolism , Leprosy/microbiology , Macrophages/cytology , Macrophages/drug effects , Macrophages/immunology , MafB Transcription Factor/metabolism , Male , Mice , Mice, Knockout , Monocytes/cytology , Monocytes/drug effects , Monocytes/immunology , Neoplasms/genetics , Neoplasms/metabolism , Positive Regulatory Domain I-Binding Factor 1 , Receptors, Aryl Hydrocarbon/genetics , Repressor Proteins/metabolism , TranscriptomeABSTRACT
Paraneoplastic dermatoses comprise a heterogeneous group of noninherited skin conditions that manifest internal malignancy. Familiarity with paraneoplastic dermatoses is important to both clinician and pathologist alike, as recognition of such a condition offers opportunity for early diagnosis and treatment of internal malignancy; monitoring for tumor recurrence; and insight into pathophysiology which may yield possible clues to treatment. Herein are reviewed 16 of the best established paraneoplastic dermatoses that display distinctive clinical and pathologic findings. LEARNING OBJECTIVE: At the conclusion of this leaning activity, participants should be able to recognize, diagnose, and describe the clinical and pathologic findings of paraneoplastic dermatoses...
Subject(s)
Humans , Neoplasms/complications , Neoplasms/diagnosis , Neoplasms/physiopathology , Neoplasms/genetics , Neoplasms/mortality , Neoplasms/rehabilitation , Neoplasms/therapy , Neoplasm Recurrence, Local/complications , Neoplasm Recurrence, Local/physiopathology , Neoplasm Recurrence, Local/genetics , Skin Diseases/complicationsABSTRACT
The identification of factors causing complex diseases contributes to the understanding of their pathophysiology and provides new diagnostic methods and potentially new prevention and treatment strategies. Polymorphic genes functioning in innate and acquired immune mechanisms participate in interindividual and interpopulational differences of susceptibility to many diseases of complex etiology and pathogenesis. Numerous studies have related especially the HLA genes to pathologic autoimmunity, and to the pathogenesis of infectious diseases and cancer. In recent years, the search for additional susceptibility genes has been facilitated by the resources and information generated by genome mapping and diversity analysis. Genes involved in immunity are being identified at an accelerating rate, and the investigation of implications of their variability regarding disease pathogenesis is beginning. Studies of Brazilian populations have especially contributed to recognition of genes modulating susceptibility to infections and their clinical outcome. Since genetic polymorphism differs between populations, the heterogeneity of the Brazilian populations, if properly explored, will add valuable information to the understanding of causes of complex diseases. Conversely, disease studies contribute to knowledge of the evolution and functional implications of genetic polymorphism.