Regulating cellular plasticity to persist: a way for tumor viruses to triumph

Yilmaz, Vural; Strati, Katerina

doi:10.1016/j.coviro.2019.06.007

Cited by 3 publications

(2 citation statements)

References 61 publications

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“…Infection of the basal layer stem cell helps establish a long-term infection as the viral DNA is maintained in these cells in low copy number and these infected cells escape immune surveillance by a variety of virus-driven mechanisms, including inhibition of antigen presentation and interference with dendritic cell function (Doorbar et al 2015;Yilmaz & Strati, 2019).…”

Section: Hpv Infection and Life Cyclementioning

confidence: 99%

Human papillomavirus-mediated carcinogenesis and tumor progression

Abboodi

Delva

Emmel

et al. 2021

GENOME INSTAB. DIS.

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High-risk human papillomaviruses (HPV) cause 5% of all human cancers and are primary etiologic agents of cervical, anal, and oropharyngeal cancer. HPV infection is necessary, but not sufficient per se to produce cancer: additional changes must occur that transform HPV-infected cells to malignancy. The HPV oncoproteins E6 and E7 immortalize human keratinocytes, cervical cells, and fibroblasts in culture. Each oncoprotein interacts with a variety of cellular binding partners; most important for transformation are E6 and E7's interactions with p53 and RB (respectively) which lead to degradation of p53 and RB through the ubiquitin pathway. Inactivation of p53 and RB leads to inactivation of pivotal cell cycle checkpoints, thereby stimulating cell proliferation and allowing cell division to occur independently of the presence of DNA damage, replicative stress, and other such insults, leading to genome instability. Continuous expression of E6/E7 drives the proliferation and progression of most HPV-mediated cancers of the cervix and a substantial fraction of those of the oropharynx. However, at both cancer sites, "HPV-inactive" tumors that contain HPV DNA, but do not express E6/E7 arise. We propose that these HPV-inactive cancers begin as HPV-driven lesions, but lose E6/E7 expression at some point during progression. We have recently shown that p53 deletion in HPV-immortalized, premalignant cells allows for the emergence of cell populations that no longer express E6/E7. These findings corroborate the notion of a pivotal role of p53 in the context of HPV-mediated transformation, both at the initiation and progression stages of cancer development.

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Section: Hpv Infection and Life Cyclementioning

confidence: 99%

Human papillomavirus-mediated carcinogenesis and tumor progression

Abboodi

Delva

Emmel

et al. 2021

GENOME INSTAB. DIS.

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“…Viral oncoproteins influence cell signaling pathways and escape from cellular defense mechanisms, such as inhibiting apoptosis, to promote abnormal cell growth. The subsequent inhibition of cellular metastasis suppressor proteins causes initial malignant cells to spread [ 34 , 35 ] …”

Section: Introductionmentioning

confidence: 99%

The role of oncolytic virotherapy and viral oncogenes in the cancer stem cells: a review of virus in cancer stem cells

Faghihkhorasani,

Dalvand,

Derafsh

et al. 2023

Cancer Cell Int

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Cancer Stem Cells (CSCs) are the main “seeds” for the initiation, growth, metastasis, and recurrence of tumors. According to many studies, several viral infections, including the human papillomaviruses, hepatitis B virus, Epstein–Barr virus, and hepatitis C virus, promote the aggressiveness of cancer by encouraging the development of CSC features. Therefore, a better method for the targeted elimination of CSCs and knowledge of their regulatory mechanisms in human carcinogenesis may lead to the development of a future tool for the management and treatment of cancer. Oncolytic viruses (OVs), which include the herpes virus, adenovirus, vaccinia, and reovirus, are also a new class of cancer therapeutics that have favorable properties such as selective replication in tumor cells, delivery of numerous eukaryotic transgene payloads, induction of immunogenic cell death and promotion of antitumor immunity, as well as a tolerable safety profile that essentially differs from that of other cancer therapeutics. The effects of viral infection on the development of CSCs and the suppression of CSCs by OV therapy were examined in this paper. The purpose of this review is to investigate the dual role of viruses in CSCs (oncolytic virotherapy and viral oncogenes). Graphical Abstract

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Persistent Human Papillomavirus Infection

Fera

Warburton

Coursey

et al. 2021

Viruses

108

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Persistent infection with oncogenic human papillomavirus (HPV) types is responsible for ~5% of human cancers. The HPV infectious cycle can sustain long-term infection in stratified epithelia because viral DNA is maintained as low copy number extrachromosomal plasmids in the dividing basal cells of a lesion, while progeny viral genomes are amplified to large numbers in differentiated superficial cells. The viral E1 and E2 proteins initiate viral DNA replication and maintain and partition viral genomes, in concert with the cellular replication machinery. Additionally, the E5, E6, and E7 proteins are required to evade host immune responses and to produce a cellular environment that supports viral DNA replication. An unfortunate consequence of the manipulation of cellular proliferation and differentiation is that cells become at high risk for carcinogenesis.

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Regulating cellular plasticity to persist: a way for tumor viruses to triumph

Abstract: This review comes from a themed issue on Viruses and cancer.

Cited by 3 publications

References 61 publications

Human papillomavirus-mediated carcinogenesis and tumor progression

Human papillomavirus-mediated carcinogenesis and tumor progression

The role of oncolytic virotherapy and viral oncogenes in the cancer stem cells: a review of virus in cancer stem cells

Persistent Human Papillomavirus Infection

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