The epithelial–mesenchymal transition (EMT) is regulated by oncoviruses in cancer

Xue, Chen; Bode, Ann M.; Dong, Zigang; Cao, Yang

doi:10.1096/fj.201600388r

Cited by 56 publications

(44 citation statements)

References 121 publications

(154 reference statements)

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“…While HPV infections are eradicated by the immune system, persistent chronic infections associated with high expression levels of E6/E7 (viral oncogenes) as well as accretion of cellular mutations may cause alterations in TP53 and RB expressions, which are known as tumor suppressor genes [6]. Additionally, it has been reported that high-risk HPVs (E5 and E6/E7) oncoproteins, can enhance cancer progression of human carcinomas via the initiation of the epithelial-mesenchymal transition (EMT) which is a hallmark of cancer metastasis [7][8][9]. On the other hand, it is important to note that HPVs transmissions may be enhanced by the presence of rough or macerated epithelial surfaces [10].…”

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confidence: 99%

“…LMP-1 variants are divided into 7 core groups including B95-8, Alaskan, China 1, China 2, Med+ , Med− , and NC [18,23,24]. LMP1 can stimulate several signaling pathways especially those involved in the induction of EMT such as NF-κB, PI3K/Akt, and MAPK [7]. The other EBV onco-protein, LMP2A [25] regulates the invasive/migratory ability and stimulates changes in EMT-like cellular biomarkers [26] by targeting the rapamycin (mTOR) pathway [22].…”

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confidence: 99%

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Co-prevalence of human Papillomaviruses (HPV) and Epstein–Barr virus (EBV) in healthy blood donors from diverse nationalities in Qatar

et al. 2020

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Background: Infections by both human oncoviruses, human Papillomaviruses (HPV) and Epstein-Barr virus (EBV) are very common in the adult human population and are associated with various malignancies. While HPV is generally transmitted sexually or via skin-to-skin contact, EBV is frequently transmitted by oral secretions, blood transfusions and organ transplants. This study aims to determine the prevalence and circulating genotypes of HPV and EBV in healthy blood donors in Qatar. Methods: We explored the co-prevalence of high-risk HPVs and EBV in 378 males and only 7 females blood donors of different nationalities (mainly from Qatar, Egypt, Syria, Jordan, Pakistan, and India) residing in Qatar, using polymerase chain reaction (PCR). DNA was extracted from the buffy coat and genotyping was performed using PCR and nested-PCR targeting E6 and E7 as well as LMP-1 of HPV and EBV, respectively. Results: We found that from the total number of 385 cases of healthy blood donors studied, 54.8% and 61% of the samples are HPVs and EBV positive, respectively. Additionally, our data revealed that the co-presence of both high-risk HPVs and EBV is 40.4% of the total samples. More significantly, this study pointed out for the first time that the most frequent high-risk HPV types in Qatar are 59 (54.8%), 31 (53.7%), 52 (49.1%), 51 (48.6%), 58 (47%) and 35 (45.5%), while the most commonly expressed low-risk HPV types are 53 (50.6%), 11 (45.5), 73 (41.7%) and 6 (41.3%), with all the cases showing multiple HPVs infection. Conclusion: In this study, we demonstrated for the first time that HPV and EBV are commonly co-present in healthy blood donors in Qatar. On the other hand, it is important to highlight that these oncoviruses can also be co-present in several types of human cancers where they can cooperate in the initiation and/or progression of these cancers. Therefore, more studies regarding the co-presence of these oncoviruses and their interaction are necessary to understand their cooperative role in human diseases.

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confidence: 99%

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confidence: 99%

Co-prevalence of human Papillomaviruses (HPV) and Epstein–Barr virus (EBV) in healthy blood donors from diverse nationalities in Qatar

et al. 2020

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“…Microbial pathogens that induce chronic inflammation can promote EMT (14). Bacteria such as Helicobacter pylori, Escherichia coli, and Klebsiella pneumoniae and viruses such as Epstein-Barr virus (EBV) and hepatitis C virus (HCV) are known to induce EMT (15,16). We hypothesized that persistent TGEV infection would have the same effect on cells and that after EMT, cells would be more susceptible to bacterial pathogens.…”

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confidence: 99%

Persistent Transmissible Gastroenteritis Virus Infection Enhances Enterotoxigenic Escherichia coli K88 Adhesion by Promoting Epithelial-Mesenchymal Transition in Intestinal Epithelial Cells

Dai

et al. 2017

J Virol

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Transmissible gastroenteritis virus (TGEV) is a coronavirus characterized by diarrhea and high morbidity rates, and the mortality rate is 100% in piglets less than 2 weeks old. Pigs infected with TGEV often suffer secondary infection by other pathogens, which aggravates the severity of diarrhea, but the mechanisms remain unknown. Here, we hypothesized that persistent TGEV infection stimulates the epithelial-mesenchymal transition (EMT), and thus enterotoxigenic (ETEC) can more easily adhere to generating cells. Intestinal epithelial cells are the primary targets of TGEV and ETEC infections. We found that TGEV can persistently infect porcine intestinal columnar epithelial cells (IPEC-J2) and cause EMT, consistent with multiple changes in key cell characteristics. Infected cells display fibroblast-like shapes; exhibit increases in levels of mesenchymal markers with a corresponding loss of epithelial markers; have enhanced expression levels of interleukin-1β (IL-1β), IL-6, IL-8, transforming growth factor β (TGF-β), and tumor necrosis factor alpha (TNF-α) mRNAs; and demonstrate increases in migratory and invasive behaviors. Additional experiments showed that the activation of the phosphatidylinositol 3-kinase (PI3K)/Akt and extracellular signal-regulated kinase (ERK) signaling pathways via TGF-β is critical for the TGEV-mediated EMT process. Cellular uptake is also modified in cells that have undergone EMT. TGEV-infected cells have higher levels of integrin α5 and fibronectin and exhibit enhanced ETEC K88 adhesion. Reversal of EMT reduces ETEC K88 adhesion and inhibits the expression of integrin α5 and fibronectin. Overall, these results suggest that TGEV infection induces EMT in IPEC-J2 cells, increasing the adhesion of ETEC K88 in the intestine and facilitating dual infection. Transmissible gastroenteritis virus (TGEV) causes pig diarrhea and is often followed by secondary infection by other pathogens. In this study, we showed that persistent TGEV infection induces an EMT in porcine intestinal columnar epithelial cells (IPEC-J2) and enhances the adhesion of the secondary pathogen ETEC K88. Additional experiments suggest that integrin α5 and fibronectin play an important role in TGEV-enhanced ETEC K88 adhesion. Reversal of EMT reduces the expression of integrin α5 and fibronectin and also reduces ETEC K88 adhesion. We conclude that TGEV infection triggers EMT and facilitates dual infection. Our results provide new insights into secondary infection and suggest that targeted anti-EMT therapy may have implications for the prevention and treatment of secondary infection.

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“…1Y3 Recent investigations suggested that HPV pushes cancer progression through EMT event. 24,25 To test if HPVoncoproteins affect the YB-1YSnail-EMTaxis, we knocked down HPV18 E6 from Hela cells to observe the change of mRNA and protein levels of YB-1 and Snail. The results showed that E6 knockdown decreased YB-1 and Snail expressions, which indicated that E6 could control the YB-1YSnail-EMTaxis.…”

Section: Discussionmentioning

confidence: 99%

Y Box-Binding Protein 1 Promotes Epithelial-Mesenchymal Transition, Invasion, and Metastasis of Cervical Cancer via Enhancing the Expressions of Snail

Pang¹,

Zhang

et al. 2017

International Journal of Gynecological Cancer

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The results firstly reported that YB-1 whose mRNA expression is regulated by HPV18 E6 promotes epithelial-mesenchymal transition and progression of cervical cancer via enhancing the expressions of Snail, which indicated that YB-1/Snail/epithelial-mesenchymal transition axis could have a potential use in the diagnosis and therapy of cervical cancer metastasis as a cancer marker and molecular target.

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The epithelial–mesenchymal transition (EMT) is regulated by oncoviruses in cancer

Cited by 56 publications

References 121 publications

Co-prevalence of human Papillomaviruses (HPV) and Epstein–Barr virus (EBV) in healthy blood donors from diverse nationalities in Qatar

Co-prevalence of human Papillomaviruses (HPV) and Epstein–Barr virus (EBV) in healthy blood donors from diverse nationalities in Qatar

Persistent Transmissible Gastroenteritis Virus Infection Enhances Enterotoxigenic Escherichia coli K88 Adhesion by Promoting Epithelial-Mesenchymal Transition in Intestinal Epithelial Cells

Y Box-Binding Protein 1 Promotes Epithelial-Mesenchymal Transition, Invasion, and Metastasis of Cervical Cancer via Enhancing the Expressions of Snail

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