Molecular mechanisms of viral oncogenesis in humans

Krump, Nathan A.; You, Jianxin

doi:10.1038/s41579-018-0064-6

Cited by 212 publications

(229 citation statements)

References 152 publications

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“…miRNAs are a class of short (18–25 nucleotides) non-coding small RNAs, which are widely found in eukaryotes. The discovery of miRNAs ranks first among the world’s top 10 technological breakthroughs in Science in 2002. miRNAs are involved in the regulation of various biological processes including autophagy ( Hargarten and Williamson, 2018 ), tumors ( Krump and You, 2018 ), allergic diseases ( Tost, 2018 ), and T-cell immunity ( Giri et al, 2019 ) for mediating gene silencing. Numerous investigations have shown that miRNAs play a vital role in PNI and peripheral nerve repair; for instance, the expression of miRNAs in dorsal root ganglia (DRG) tissues after sciatic nerve injury in rats was significantly changed ( Li et al, 2012 ).…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture Promoted Nerve Repair After Peripheral Nerve Injury by Regulating miR-1b and Its Target Brain-Derived Neurotrophic Factor

et al. 2020

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Growing evidence indicates that electroacupuncture (EA) has a definite effect on the treatment of peripheral nerve injury (PNI), but its mechanism is not completely clear. MicroRNAs (miRNAs) are involved in the regulation of a variety of biological processes, and EA may enhance PNI repair by regulating miRNAs. In this study, the rat sciatic nerve injury model was treated with EA for 4 weeks. Acupoints Huantiao (GB30) and Zusanli (ST36) were stimulated by EA 20 min once a day, 6 days a week for 4 weeks. We found that EA treatment downregulated the expression of miR-1b in the local injured nerve. In vitro experiments showed that overexpression of miR-1b inhibited the expression of brain-derived neurotrophic factor (BDNF) in rat Schwann cell (SC) line, while BDNF knockdown inhibited the proliferation, migration, and promoted apoptosis of SCs. Subsequently, the rat model of sciatic nerve injury was treated by EA treatment and injection of agomir-1b or antagomir-1b. The nerve conduction velocity ratio (NCV), sciatic functional index (SFI), and S100 immunofluorescence staining were examined and showed that compared with the model group, NCV, SFI, proliferation of SC, and expression of BDNF in the injured nerves of rats treated with EA or EA + anti-miR-1b were elevated, while EA + miR-1b was reduced, indicating that EA promoted sciatic nerve function recovery and SC proliferation through downregulating miR-1b. To summarize, EA may promote the proliferation, migration of SC, and nerve repair after PNI by regulating miR-1b, which targets BDNF.

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Section: Discussionmentioning

confidence: 99%

Electroacupuncture Promoted Nerve Repair After Peripheral Nerve Injury by Regulating miR-1b and Its Target Brain-Derived Neurotrophic Factor

et al. 2020

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“…Although oncogenic viruses converge in common features from a broad perspective, divergent genomes, oncogenic factors, cellular tropism, and disease prevalence distinguish each of those infectious agents ( 12 , 13 ). Nonetheless, polyploidy appears to be a crossroad and a biological equivalency trait shared among oncoviruses, where the latter could be regarded as an initiating engine that fuels phenotypic diversity.…”

Section: Introductionmentioning

confidence: 99%

Polyploid Giant Cancer Cells, a Hallmark of Oncoviruses and a New Therapeutic Challenge

Herbein

Nehme

2020

Front. Oncol.

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Tumors are renowned as intricate systems that harbor heterogeneous cancer cells with distinctly diverse molecular signatures, sizes and genomic contents. Among those various genomic clonal populations within the complex tumoral architecture are the polyploid giant cancer cells (PGCC). Although described for over a century, PGCC are increasingly being recognized for their prominent role in tumorigenesis, metastasis, therapy resistance and tumor repopulation after therapy. A shared characteristic among all tumors triggered by oncoviruses is the presence of polyploidy. Those include Human Papillomaviruses (HPV), Epstein Barr Virus (EBV), Hepatitis B and C viruses (HBV and HCV, respectively), Human T-cell lymphotropic virus-1 (HTLV-1), Kaposi's sarcoma herpesvirus (KSHV) and Merkel polyomavirus (MCPyV). Distinct viral proteins, for instance Tax for HTLV-1 or HBx for HBV have demonstrated their etiologic role in favoring the appearance of PGCC. Different intriguing biological mechanisms employed by oncogenic viruses, in addition to viruses with high oncogenic potential such as human cytomegalovirus, could support the generation of PGCC, including induction of endoreplication, inactivation of tumor suppressors, development of hypoxia, activation of cellular senescence and others. Interestingly, chemoresistance and radioresistance have been reported in the context of oncovirus-induced cancers, for example KSHV and EBV-associated lymphomas and high-risk HPV-related cervical cancer. This points toward a potential linkage between the previously mentioned players and highlights PGCC as keystone cancer cells in virally-induced tumors. Subsequently, although new therapeutic approaches are actively needed to fight PGCC, attention should also be drawn to reveal the relationship between PGCC and oncoviruses, with the ultimate goal of establishing effective therapeutic platforms for treatment of virus-associated cancers. This review discusses the presence of PGCCs in tumors induced by oncoviruses, biological mechanisms potentially favoring their appearance, as well as their consequent implication at the clinical and therapeutic level.

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“…The classification of gastric carcinomas of diffuse type as adenocarcinomas, despite no glandular growth pattern, is partly based upon periodic acid-Schiff (PAS) positivity regarded as a marker of mucin. However, when applying much more sensitive and specific methods like immunohistochemistry and in situ hybridization, we could not find any mucin in the PAS positive cancer cells [35,38]. Thus, the ECL cell, a well differentiated cell, can divide, and it is possible to follow the tumorigenic process via hyperplasia to rather benign NETs, highly malignant NECs, and further to some carcinomas hitherto classified as adenocarcinomas.…”

Section: Gastric Cancermentioning

confidence: 83%

Correct Identification of Cell of Origin May Explain Many Aspects of Cancer: The Role of Neuroendocrine Cells as Exemplified from the Stomach

Mjønes

2020

IJMS

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Cancers are believed to originate from stem cells. Previously, the hypothesis was that tumors developed due to dedifferentiation of mature cells. We studied the regulation of gastric acid secretion and showed that gastrin through the gastrin receptor stimulates enterochromaffin-like (ECL) cell histamine release and proliferation. In animal and human studies, we and others showed that long-term hypergastrinemia results in ECL cell-derived tumor through a sequence of hyperplasia, dysplasia, neuroendocrine tumors (NETs), and possibly neuroendocrine carcinomas (NECs) and adenocarcinomas of diffuse type. Perhaps, other cancers may also have their origin in differentiated cells. Knowledge of the growth regulation of the cell of origin is important in cancer prophylaxis and treatment. Physiology plays a central role in carcinogenesis through hormones and other growth factors. Every cell division implies a small risk of mutation; thus mitogens are also mutagens. Moreover, metastasis of slow proliferating cells may also explain so-called tumor dormancy and late recurrence.

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Molecular mechanisms of viral oncogenesis in humans

Cited by 212 publications

References 152 publications

Electroacupuncture Promoted Nerve Repair After Peripheral Nerve Injury by Regulating miR-1b and Its Target Brain-Derived Neurotrophic Factor

Electroacupuncture Promoted Nerve Repair After Peripheral Nerve Injury by Regulating miR-1b and Its Target Brain-Derived Neurotrophic Factor

Polyploid Giant Cancer Cells, a Hallmark of Oncoviruses and a New Therapeutic Challenge

Correct Identification of Cell of Origin May Explain Many Aspects of Cancer: The Role of Neuroendocrine Cells as Exemplified from the Stomach

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