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OncoTargets and Therapy 2020Lung cancer is the most common cause of cancer death worldwide. Tobacco smoking is the most predominant etiology for lung cancer. However, only a small percentage of... (Review)
Review
Lung cancer is the most common cause of cancer death worldwide. Tobacco smoking is the most predominant etiology for lung cancer. However, only a small percentage of heavy smokers develop lung cancer, which suggests that other cofactors are required for lung carcinogenesis. Viruses have been central to modern cancer research and provide profound insights into cancer causes. Nevertheless, the role of virus in lung cancer is still unclear. In this article, we reviewed the possible oncogenic viruses associated with lung cancer.
PubMed: 33116642
DOI: 10.2147/OTT.S263976 -
Journal of Cellular Physiology Nov 2019Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV) are herpesviruses associated with human malignancies. As exosomes can shuttle many... (Review)
Review
Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV) are herpesviruses associated with human malignancies. As exosomes can shuttle many herpesvirus-associated biomolecules from host cells to recipient cells, the exosomal pathway is utilized by herpesviruses to achieve extensive infections and even oncogenesis. In this review, we discuss the oncogenic biomolecules present in exosomes derived from KSHV- and EBV-infected cells. Moreover, oncogenesis via exosomal biomolecules mainly occurs through three processes, including regulation of downstream signals, promotion of immune dysfunction and transformation of cells. Also, the exosomes may provide diagnostic markers and therapeutic targets specific for KSHV- and EBV-associated malignancies.
Topics: Carcinogenesis; Cell Transformation, Neoplastic; Exosomes; Herpesvirus 4, Human; Herpesvirus 8, Human; Humans; Neoplasms
PubMed: 30941765
DOI: 10.1002/jcp.28573 -
Molecular Pharmaceutics Aug 2023Human viral oncogenesis is a complex phenomenon and a major contributor to the global cancer burden. Several recent findings revealed cellular and molecular pathways... (Review)
Review
Human viral oncogenesis is a complex phenomenon and a major contributor to the global cancer burden. Several recent findings revealed cellular and molecular pathways that promote the development and initiation of malignancy when viruses cause an infection. Even, antiviral treatment has become an approach to eliminate the viral infections and prevent the activation of oncogenesis. Therefore, for a better understanding, the molecular pathogenesis of various oncogenic viruses like, hepatitis virus, human immunodeficiency viral (HIV), human papillomavirus (HPV), herpes simplex virus (HSV), and Epstein-Barr virus (EBV), could be explored, especially, to expand many potent antivirals that may escalate the apoptosis of infected malignant cells while sparing normal and healthy ones. Moreover, contemporary therapies, such as engineered antibodies antiviral agents targeting signaling pathways and cell biomarkers, could inhibit viral oncogenesis. This review elaborates the recent advancements in both natural and synthetic antivirals to control viral oncogenesis. The study also highlights the challenges and future perspectives of using antivirals in viral oncogenesis.
Topics: Humans; Epstein-Barr Virus Infections; Herpesvirus 4, Human; Carcinogenesis; Neoplasms; Antiviral Agents
PubMed: 37486263
DOI: 10.1021/acs.molpharmaceut.2c01080 -
Molecular and Cellular Biochemistry Nov 2023Viral infection is a kind of cellular stress that leads to the changes in cellular metabolism. Many metabolic pathways in a host cell such as glycolysis, amino acid and... (Review)
Review
Viral infection is a kind of cellular stress that leads to the changes in cellular metabolism. Many metabolic pathways in a host cell such as glycolysis, amino acid and nucleotide synthesis are altered following virus infection. Both oncogenic and non-oncogenic viruses depend on host cell glycolysis for their survival and pathogenesis. Recent studies have shown that the rate of glycolysis plays an important role in oncolysis as well by oncolytic therapeutic viruses. During infection, viral proteins interact with various cellular glycolytic enzymes, and this interaction enhances the catalytic framework of the enzymes subsequently the glycolytic rate of the cell. Increased activity of glycolytic enzymes following their interaction with viral proteins is vital for replication and to counteract the inhibition of glycolysis caused by immune response. In this review, the importance of host cell glycolysis and the modulation of glycolysis by various viruses such as oncogenic, non-oncogenic and oncolytic viruses are presented.
PubMed: 36709223
DOI: 10.1007/s11010-023-04669-4 -
International Journal of Molecular... Nov 2022In the multi-factorial etiology of organ-site cancers by suspect human chemical carcinogens, oncogenic virus, activation of RAS, Myc and HER-2 oncogenes, inactivation of...
In the multi-factorial etiology of organ-site cancers by suspect human chemical carcinogens, oncogenic virus, activation of RAS, Myc and HER-2 oncogenes, inactivation of TP53, RB and APC tumor suppressor genes represent early-occurring genetic events [...].
Topics: Humans; Antineoplastic Agents; Oncogenes; Oncogenic Viruses; Carcinogens; Neoplasms
PubMed: 36430932
DOI: 10.3390/ijms232214457 -
Viruses Jul 2021Insulin-like growth factor-1 (IGF-1) and the IGF-1 receptor (IGF-1R) belong to the insulin-like growth factor family, and IGF-1 activates intracellular signaling... (Review)
Review
Insulin-like growth factor-1 (IGF-1) and the IGF-1 receptor (IGF-1R) belong to the insulin-like growth factor family, and IGF-1 activates intracellular signaling pathways by binding specifically to IGF-1R. The interaction between IGF-1 and IGF-1R transmits a signal through a number of intracellular substrates, including the insulin receptor substrate (IRS) and the Src homology collagen (Shc) proteins, which activate two major intracellular signaling pathways: the phosphatidylinositol 3-kinase (PI3K)/AKT and mitogen-activated protein kinase (MAPK) pathways, specifically the extracellular signal-regulated kinase (ERK) pathways. The PI3K/AKT kinase pathway regulates a variety of cellular processes, including cell proliferation and apoptosis. IGF1/IGF-1R signaling also promotes cell differentiation and proliferation via the Ras/MAPK pathway. Moreover, upon IGF-1R activation of the IRS and Shc adaptor proteins, Shc stimulates Raf through the GTPase Ras to activate the MAPKs ERK1 and ERK2, phosphorylate and several other proteins, and to stimulate cell proliferation. The IGF-1 signaling pathway is required for certain viral effects in oncogenic progression and may be induced as an effect of viral infection. The mechanisms of IGF signaling in animal viral infections need to be clarified, mainly because they are involved in multifactorial signaling pathways. The aim of this review is to summarize the current data obtained from virological studies and to increase our understanding of the complex role of the IGF-1 signaling axis in animal virus infections.
Topics: Animals; Humans; Insulin-Like Growth Factor I; Mice; Oncogenic Viruses; Phosphorylation; Receptor, IGF Type 1; Signal Transduction; Virus Diseases
PubMed: 34452353
DOI: 10.3390/v13081488 -
Postepy Biochemii Dec 2020Oncogenic viruses (oncoviruses) are implicated in approximately 12% of all human cancers. Currently, the viruses known to cause human cancer are: Hepatitis B and C...
Oncogenic viruses (oncoviruses) are implicated in approximately 12% of all human cancers. Currently, the viruses known to cause human cancer are: Hepatitis B and C viruses (HBV and HCV), Human Papillomaviruses (HPV), Merkel Cell Polyomavirus (MCV), Human Herpesvirus-8 (HHV-8), Epstein-Barr Virus (EBV) and Human T-cell lymphotropic virus-1 (HTLV-1). However, oncoviruses are not complete carcinogens, need additional factors andisplay different roles in transformation. Oncoviruses can directly disrupt important regulatory cell genes by inserting virus genom into the DNA of the host cell. They also contain their own genes that damage the regulation of the cell. Some viruses have v-onc that cause disregulation of cellular processes and can lead to cancerous growth.
Topics: Hepacivirus; Humans; Neoplasms; Oncogenic Viruses; Retroviridae
PubMed: 33470075
DOI: 10.18388/pb.2020_360 -
Viruses Jun 2022A signature trait of neurotropic α-herpesviruses (α-HV) is their ability to establish stable non-productive infections of peripheral neurons termed latency. This... (Review)
Review
A signature trait of neurotropic α-herpesviruses (α-HV) is their ability to establish stable non-productive infections of peripheral neurons termed latency. This specialized gene expression program is the foundation of an evolutionarily successful strategy to ensure lifelong persistence in the host. Various physiological stresses can induce reactivation in a subset of latently-infected neurons allowing a new cycle of viral productive cycle gene expression and synthesis of infectious virus. Recurring reactivation events ensure transmission of the virus to new hosts and contributes to pathogenesis. Efforts to define the molecular basis of α-HV latency and reactivation have been notoriously difficult because the neurons harboring latent virus in humans and in experimentally infected live-animal models, are rare and largely inaccessible to study. Increasingly, researchers are turning to cultured neuron infection models as simpler experimental platforms from which to explore latency and reactivation at the molecular level. In this review, I reflect on the strengths and weaknesses of existing neuronal models and briefly summarize the important mechanistic insights these models have provided. I also discuss areas where prioritization will help to ensure continued progress and integration.
Topics: Animals; Herpesviridae; Herpesvirus 1, Human; Neurons; Oncogenic Viruses; Virus Activation; Virus Latency
PubMed: 35746680
DOI: 10.3390/v14061209 -
Viruses Dec 2021During initial infection, human papillomaviruses (HPV) take an unusual trafficking pathway through their host cell. It begins with a long period on the cell surface,... (Review)
Review
During initial infection, human papillomaviruses (HPV) take an unusual trafficking pathway through their host cell. It begins with a long period on the cell surface, during which the capsid is primed and a virus entry platform is formed. A specific type of clathrin-independent endocytosis and subsequent retrograde trafficking to the trans-Golgi network follow this. Cellular reorganization processes, which take place during mitosis, enable further virus transport and the establishment of infection while evading intrinsic cellular immune defenses. First, the fragmentation of the Golgi allows the release of membrane-encased virions, which are partially protected from cytoplasmic restriction factors. Second, the nuclear envelope breakdown opens the gate for these virus-vesicles to the cell nucleus. Third, the dis- and re-assembly of the PML nuclear bodies leads to the formation of modified virus-associated PML subnuclear structures, enabling viral transcription and replication. While remnants of the major capsid protein L1 and the viral DNA remain in a transport vesicle, the viral capsid protein L2 plays a crucial role during virus entry, as it adopts a membrane-spanning conformation for interaction with various cellular proteins to establish a successful infection. In this review, we follow the oncogenic HPV type 16 during its long journey into the nucleus, and contrast pro- and antiviral processes.
Topics: Animals; Capsid Proteins; Endocytosis; Epithelial Cells; Human papillomavirus 16; Humans; Papillomavirus Infections; Virus Internalization; trans-Golgi Network
PubMed: 34960729
DOI: 10.3390/v13122460