Progressive loss of E-cadherin immunoexpression during cervical carcinogenesis

Cavalcante, José Roosevelt; Sampaio, João P.A.; Filho, João Tarcísio Alves Maia; Vieira, Renato Braga; Eleutério, José; Lima, Roberto César Pereira; Ribeiro, Ronaldo A.; Almeida, Paulo Roberto Carvalho de

doi:10.1590/s0102-8650201400160007

Cited by 11 publications

(6 citation statements)

References 34 publications

(27 reference statements)

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“…However, human KCs transfected with HPV8 E7 protein exhibited decreased CCL20 expression by preventing binding of C/EBP to the CCL20 promoter [67] , suggesting a possible mechanism for HPV oncoprotein interference with KC-derived CCL20, which attracts LCs. Similarly, lower E-cadherin expression on HPV-infected KCs is correlated with cervical lesion severity [59] , [68] , [69] and reduced numbers of LCs in HPV-infected epidermis [60] , [70] . In vitro , inhibition of HPV16 E6 and E7 oncoproteins restored E-cadherin expression and LC adhesion to KCs [69] , [70] .…”

Section: Impact Of Hpv Infection On Antigen Presentation To the Adaptmentioning

confidence: 93%

Modulation of antigen presenting cell functions during chronic HPV infection

Bashaw

Leggatt

Chandra

et al. 2017

Papillomavirus Research

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High-risk human papillomaviruses (HR-HPV) infect basal keratinocytes, where in some individuals they evade host immune responses and persist. Persistent HR-HPV infection of the cervix causes precancerous neoplasia that can eventuate in cervical cancer. Dendritic cells (DCs) are efficient in priming/cross-priming antigen-specific T cells and generating antiviral and antitumor cytotoxic CD8+ T cells. However, HR-HPV have adopted various immunosuppressive strategies, with modulation of DC function crucial to escape from the host adaptive immune response. HPV E6 and E7 oncoproteins alter recruitment and localization of epidermal DCs, while soluble regulatory factors derived from HPV-induced hyperplastic epithelium change DC development and influence initiation of specific cellular immune responses. This review focuses on current evidence for HR-HPV manipulation of antigen presentation in dendritic cells and escape from host immunity.

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Section: Impact Of Hpv Infection On Antigen Presentation To the Adaptmentioning

confidence: 93%

Modulation of antigen presenting cell functions during chronic HPV infection

Bashaw

Leggatt

Chandra

et al. 2017

Papillomavirus Research

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“…Abnormal DNA methylation patterns related to persistent infection of human papilloma virus (HPV) represent an early and frequent alteration in cervical carcinogenesis . Indeed, several genes, such as those for p16, death‐associated protein kinase, tissue inhibitor of metalloproteinases‐3 , E‐cadherin , cell adhesion molecule 1 and T‐cell differentiation protein , are down‐regulated through DNA methylation, contributing to the development, progression and/or metastasis of cervical cancer. Identification of new gene targets of epigenetic regulation might be useful to shed light on the biological processes and the molecular basis of the development of cervical cancer.…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, several genes, such as those Abbreviations 5-Aza, 5-aza-2 0 -deoxycytidine; CBS, cystathionine b-synthase; ChIP, chromatin immunoprecipitation; Cytb, cytochrome b; dC 2 0 -deoxycytidine; GSH, reduced glutathione; GSSG, oxidized glutathione; HPV, human papilloma virus; mdC, 5-methyl-2 0 -deoxycytidine; MeCP2, methyl CpG binding protein 2; mtDNA, mitochondrial DNA; ROS, reactive oxygen species; SAMC, S-adenosylmethionine carrier; SAM, S-adenosylmethionine. for p16, death-associated protein kinase, tissue inhibitor of metalloproteinases-3 [3], E-cadherin [4,5], cell adhesion molecule 1 and T-cell differentiation protein [6,7], are down-regulated through DNA methylation, contributing to the development, progression and/or metastasis of cervical cancer. Identification of new gene targets of epigenetic regulation might be useful to shed light on the biological processes and the molecular basis of the development of cervical cancer.…”

Section: Introductionmentioning

confidence: 99%

SLC25A26 overexpression impairs cell function via mtDNA hypermethylation and rewiring of methyl metabolism

et al. 2017

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Cancer cells down-regulate different genes to give them a selective advantage in invasiveness and/or metastasis. The SLC25A26 gene encodes the mitochondrial carrier that catalyzes the import of S-adenosylmethionine (SAM) into the mitochondrial matrix, required for mitochondrial methylation processes, and is down-regulated in cervical cancer cells. In this study we show that SLC25A26 is down-regulated due to gene promoter hypermethylation, as a mechanism to promote cell survival and proliferation. Furthermore, overexpression of SLC25A26 in CaSki cells increases mitochondrial SAM availability and promotes hypermethylation of mitochondrial DNA, leading to decreased expression of key respiratory complex subunits, reduction of mitochondrial ATP and release of cytochrome c. In addition, increased SAM transport into mitochondria leads to impairment of the methionine cycle with accumulation of homocysteine at the expense of glutathione, which is strongly reduced. All these events concur to arrest the cell cycle in the S phase, induce apoptosis and enhance chemosensitivity of SAM carrier-overexpressing CaSki cells to cisplatin.

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“…It was estimated that there were 570,000 new cases and 311,000 deaths of cervical cancer worldwide in 2018 [1]. Cervical squamous cell carcinoma (CSCC) represents the most common histologic subtype of cervical cancer and accounts for 85-90% of cases [2]. Cervical carcinogenesis is a very complex multistep progression.…”

Section: Introductionmentioning

confidence: 99%

“…Normal cervix first progresses to low-grade squamous intraepithelial lesions (LSIL) and then to high-grade squamous intraepithelial lesions (HSIL), thus eventually shaping CSCC. Although persistent infection with high-risk human papillomavirus (HPV), such as HPV16 and HPV18, is well known as the cause of CSCC and CSSS related precancerous lesions, there exist more pathogenic factors in CSCC progression [2, 3].…”

Section: Introductionmentioning

confidence: 99%

Vasculogenic Mimicry Formation Is Associated with Erythropoietin Expression but Not with Erythropoietin Receptor Expression in Cervical Squamous Cell Carcinoma

Qing

Tao

et al. 2019

BioMed Research International

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Background. Vasculogenic mimicry (VM), as an endothelium-independent cancer microcirculation, has been observed in many malignancies including cervical cancer. Erythropoietin (EPO) and erythropoietin receptor (EPO-R) could produce an angiogenic effect to promote cervical squamous cell carcinoma (CSCC) progression. However, the association between VM formation and EPO/EPO-R expression in CSCC is poorly explored. Methods. Seventy-six paraffin-embedded CSCC samples, 25 high-grade squamous intraepithelial lesion (HSIL) samples, 20 low-grade squamous intraepithelial lesion (LSIL) samples, and 20 normal cervix samples were collected. Immunohistochemistry SP method was performed to detect EPO/EPO-R expression and CD31/periodic acid-Schiff (PAS) double staining was performed to detect VM formation. The associations of EPO/EPO-R and VM with clinicopathological parameters of CSCC were analyzed. The associations between VM formation and EPO/EPO-R expression were also analyzed. Results. The positive expression rates of EPO and EPO-R were gradually increasing along the progression of normal cervix-LSIL-HSIL-CSCC sequence (P<0.05). EPO and EPO-R expression were not significantly associated with clinicopathological parameters of CSCC patients (P>0.05). VM was significantly associated with FIGO stage, lymphovascular space involvement, and lymph node metastasis (P<0.05). VM was positively associated with EPO expression (r=0.284, P<0.05) but was not associated with EPO-R expression (P>0.05). Conclusion. These data suggest that increased EPO/EPO-R expression may play an important role in cervical carcinogenesis. EPO overexpression may promote VM formation in CSCC.

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Progressive loss of E-cadherin immunoexpression during cervical carcinogenesis

Cited by 11 publications

References 34 publications

Modulation of antigen presenting cell functions during chronic HPV infection

Modulation of antigen presenting cell functions during chronic HPV infection

SLC25A26 overexpression impairs cell function via mtDNA hypermethylation and rewiring of methyl metabolism

Vasculogenic Mimicry Formation Is Associated with Erythropoietin Expression but Not with Erythropoietin Receptor Expression in Cervical Squamous Cell Carcinoma

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