Parasite-microbe-host interactions and cancer risk

Dheilly, Nolwenn M.; Ewald, Paul W.; Brindley, Paul J.; Fichorova, Raina N.; Thomas, Fréderic

doi:10.1371/journal.ppat.1007912

Cited by 21 publications

(21 citation statements)

References 81 publications

(75 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…We consider direct protective effects of microbiota well as the interplay between protective microbiota and parasites that contribute directly or indirectly to oncogenesis. This analysis complements recent papers that have considered the joint contributions of parasitic organisms to oncogenesis (Dheilly, Ewald, Brindley, Fichorova, & Thomas, 2019; Ewald & Swain Ewald, 2014) and protection against oncogenesis that arises from immune responses to pathogens that are not oncogenic (Cramer & Finn, 2011; Iheagwara et al, 2014; Jacqueline & Finn, 2020; Oh et al, 2019).…”

Section: Introduction: the Barrier Theory Of Cancer And The Symbiosissupporting

confidence: 71%

“…In the last few years, cancer research has increasingly recognized the need to understand the joint contribution of parasites to oncogenesis. Knowledge in this area has been integrated with the barrier theory with many illustrative examples (Ewald and Swain Ewald, 2014, Dheilly et al, 2019). A major challenge will be to broaden this understanding to determine the ways in which mutualists interact with parasites to inhibit oncogenesis.…”

Section: Interactions Among Parasites and Mutualistsmentioning

confidence: 99%

See 1 more Smart Citation

Integrating the microbiome into the barrier theory of cancer

Ewald

2020

Evolutionary Applications

Self Cite

View full text Add to dashboard Cite

The barrier theory of cancer integrates environmental, genetic, and infectious contributions to oncogenesis into a single framework. The full spectrum of symbiotic influences on oncogenesis, however, still needs to be brought into this framework, particularly for symbionts that are classified as commensals or mutualists. This paper contributes to this goal by presenting evidence that these symbionts may improve the effectiveness of immunological defenses against cancer and by drawing attention to the interactions between parasitic and mutualistic microbes in relation to oncogenesis. Although integration of protective symbionts with the barrier theory encompasses a variety of interactions, we highlight one particular aspect: effects of symbionts on the host’s ability to attack tumor cells through the relaxation of immune checkpoints.

show abstract

Section: Introduction: the Barrier Theory Of Cancer And The Symbiosissupporting

confidence: 71%

Section: Interactions Among Parasites and Mutualistsmentioning

confidence: 99%

Integrating the microbiome into the barrier theory of cancer

Ewald

2020

Evolutionary Applications

Self Cite

View full text Add to dashboard Cite

show abstract

“…2 Occurrence of oral cancer is associated with multiple risk factors, such as tobacco smoking, alcohol consumption and human papillomavirus (HPV) infections. [3][4][5][6] Increased understanding of the molecular mechanisms of oral cancer has provided novel insights into the treatment of this disease, while molecular pathways involved in this disease remain elusive. 7 The development and progression of oral cancer involve the regulations of multiple molecular pathways.…”

Section: Introductionmentioning

confidence: 99%

<p>LncRNA LUADT1 Promotes Oral Squamous Cell Carcinoma Cell Proliferation by Regulating miR-34a/GAS1 Axis</p>

Gao

Wang²,

Meng³

et al. 2020

CMAR

View full text Add to dashboard Cite

Introduction: The oncogenic role of lncRNA LUADT1 has been investigated only in lung cancer. This study aimed to investigate the role of LUADT1 in oral squamous cell carcinoma (OSCC). Patients and Methods: The expression levels of LUADT1 in paired OSCC and non-tumor tissues from OSCC patients were determined by RT-qPCR. A 5-year follow-up study was performed to analyze the prognostic value of LUADT1 for OSCC. Dual-luciferase assay and overexpression experiments were performed to assess the interactions among LUADT1, miR-34a and GASL1. Cell proliferation was analyzed by cell proliferation assay. Results: In this study, we found that LUADT1 was upregulated in OSCC and predicted poor survival. LUADT1 was predicted to interact with miR-34a, which was confirmed by dualluciferase activity assay. However, overexpression experiments showed that they did not affect the expression of each other. Interestingly, overexpression of LUADT1 resulted in upregulation of GAS1, a target of miR-34a. Cell proliferation assay revealed that overexpression of LUADT1 and GAS1 resulted in promoted cell proliferation. MiR-34a played an opposite role and reversed the effects of LUADT1 overexpression. Conclusion: LUADT1 may promote OSCC proliferation by regulating miR-34a/GAS1 axis.

show abstract

“…As the pathogens can be passed from one individual to other, these cancers present fascinating topics to study for both evolutionary biologists, disease epidemiologists, and oncologists. Undoubtedly one of the major innovative direction of this field to emerge recently is understanding the reciprocal interactions between parasites, host microbiota, and cancer dynamics (Dheilly et al., 2019). Ewald & Ewald (in press, This volume) discussed the idea that symbionts may improve the effectiveness of immunological defenses against cancer, through a diversity of interactions between parasitic and mutualistic microbes.…”

mentioning

confidence: 99%

“…A large proportion of cancers (app. 15%–20% across the globe) is initiated and caused by infectious agents, such as viruses, bacteria, and parasites (Dheilly, Ewald, Brindley, Fichorova, & Thomas, 2019; Plummer et al., 2016). These pathogens can disrupt signaling pathways that control cell proliferation, weaken the immune system, and/or cause chronic inflammation that can increase the risk of developing cancer (Ewald & Swain Ewald, 2014).…”

mentioning

confidence: 99%