Human endogenous retroviruses role in cancer cell stemness

Matteucci, Claudia; Balestrieri, Emanuela; Argaw-Denboba, Ayele; Vallebona, P Sinibaldi

doi:10.1016/j.semcancer.2018.10.001

Cited by 63 publications

(74 citation statements)

References 231 publications

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“…Very recently, Matteucci et al (173) described and reviewed the pivotal role of human endogenous retrovirus (HERVs) activation in the promotion and maintenance of pluripotency and stem-like properties in melanoma CSCs. The authors also highlight the correlation between HERVs activation and aggressiveness features across several types of cancer.…”

Section: Interferon Type IImentioning

confidence: 99%

The Interactions Between Cancer Stem Cells and the Innate Interferon Signaling Pathway

Martín-Hijano

Sáinz

2020

Front. Immunol.

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Section: Interferon Type IImentioning

confidence: 99%

The Interactions Between Cancer Stem Cells and the Innate Interferon Signaling Pathway

Martín-Hijano

Sáinz

2020

Front. Immunol.

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“…The aberrant expression of HERV has been found in a number of human diseases, such as cancers [41], autoimmune diseases [42], and neurological diseases [43], possibly suggesting their role in pathogenesis. Current literature suggests that HERV can be activated by a plethora of microenvironmental stimuli such as hormones, cytokines, epigenetic modifications or exogenous microorganisms [44]. Interestingly, recent studies suggest that several viral infections, such as retroviruses (HIV, HTLV-1), herpesviruses (EBV, herpes simplex virus type 1 (HSV-1), KSHV), HBV, and influenza virus, can transactivate HERV [45].…”

Section: Herv Activation and The Paradigm Of Herv In Cancersmentioning

confidence: 99%

Contribution of Human Retroviruses to Disease Development—A Focus on the HIV– and HERV–Cancer Relationships and Treatment Strategies

Grandi

Palanivelu

Lin

2020

Viruses

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Animal retroviruses are known for their transforming potential, and this is also true for the ones hosted by humans, which have gathered expanding attention as one of the potent causative agents in various disease, including specific cancer types. For instance, Human T Lymphotropic virus (HTLV) is a well-studied class of oncoviruses causing T cell leukemia, while human immunodeficiency virus (HIV) leads to acquired immunodeficiency syndrome (AIDS), which is linked to a series of defining cancers including Kaposi sarcoma, certain types of non-Hodgkin lymphoma, and cervical cancer. Of note, in addition to these “modern” exogenous retroviruses, our genome harbors a staggering number of human endogenous retroviruses (HERVs). HERVs are the genetic remnants of ancient retroviral germline infection of human ancestors and are typically silenced in normal tissues due to inactivating mutations and sequence loss. While some HERV elements have been appropriated and contribute to human physiological functions, others can be reactivated through epigenetic dysregulations to express retroviral elements and promote carcinogenesis. Conversely, HERV replication intermediates or protein products can also serve as intrinsic pathogen-associated molecular patterns that cause the immune system to interpret it as an exogenous infection, thereby stimulating immune responses against tumors. As such, HERVs have also been targeted as a potential internal strategy to sensitize tumor cells for promising immunotherapies. In this review, we discuss the dynamic role of human retroviruses in cancer development, focusing on HIV and HERVs contribution. We also describe potential treatment strategies, including immunotherapeutic targeting of HERVs, inhibiting DNA methylation to expose HERV signatures, and the use of antiretroviral drugs against HIV and HERVs, which can be employed as prospective anti-cancer modalities.

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“…CSCs are thought to cause tumour relapse, metastasis, and chemo-resistance. 2,3 In 1994, Lapidot et al first isolated human acute myeloid leukaemia stem cells (LSCs) using specific cell surface markers. Their research revealed that only LSCs possessed the high self-renewal capacity necessary to maintain the malignant phenotype, strongly supporting the objective existence of CSCs.…”

Section: Introductionmentioning

confidence: 99%

<p>Self-Renewal Signalling Pathway Inhibitors: Perspectives on Therapeutic Approaches for Cancer Stem Cells</p>

Zhu¹,

Shen²,

Chen³

et al. 2020

OTT

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The poor survival and prognosis of individuals with cancer are often attributed to tumour relapse and metastasis, which may be due to the presence of cancer stem cells (CSCs). CSCs have the characteristics of self-renewal, differentiation potential, high carcinogenicity, and drug resistance. In addition, CSCs exhibit many characteristics similar to those of embryonic or tissue stem cells while displaying persistent abnormal activation of self-renewal pathways associated with development and tissue homeostasis, including the Wnt, Notch, Hedgehog (Hh), TGF-β, JAK/STAT3, and NF-κB pathways. Therefore, we can eliminate CSCs by targeting these self-renewal pathways to constrain stem cell replication, survival and differentiation. At the same time, we cannot neglect the ping-pong effect of the tumour microenvironment, which releases cytokines and promotes self-renewal pathways in CSCs. Recently, meaningful progress has been made in the study of inhibitors of self-renewal pathways in tumours. This review primarily summarizes several representative and novel agents targeting these self-renewal signalling pathways and the tumour microenvironment and that represent a promising strategy for treating refractory and recurrent cancer.

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Human endogenous retroviruses role in cancer cell stemness

Cited by 63 publications

References 231 publications

The Interactions Between Cancer Stem Cells and the Innate Interferon Signaling Pathway

The Interactions Between Cancer Stem Cells and the Innate Interferon Signaling Pathway

Contribution of Human Retroviruses to Disease Development—A Focus on the HIV– and HERV–Cancer Relationships and Treatment Strategies

<p>Self-Renewal Signalling Pathway Inhibitors: Perspectives on Therapeutic Approaches for Cancer Stem Cells</p>

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