Hox B4 as potential marker of non-differentiated cells in human cervical cancer cells

Rosa, Ana Paulina Barba de la; Briones-Cerecero, Erika; Lugo-Melchor, Ofelia; León‐Rodríguez, Antonio De; Santos, Leticia; Castelo-Ruelas, Julio; Valdivia, Alejandra; Piña, Patricia; Chagolla-López, Alicia; Hernández-Cueto, Daniel Dimitri; Mantilla, Alejandra; Lazos-Ochoa, Minerva; González-Yebra, Beatriz; Salcedo, Mauricio

doi:10.1007/s00432-011-1081-2

Cited by 9 publications

(10 citation statements)

References 42 publications

(40 reference statements)

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“…Differential HOXC5 expression was also observed in a study where HOX gene expression in normal keratinocytes was compared to the HPV16 positive SiHa cervical carcinoma line. This study also provided evidence for increased expression of HOXC8 in SiHa cells [27], and another study provided additional evidence for HOXB4 overexpression in cervical carcinomas [28]. Collectively, however, these results are difficult to interpret and may simply reflect the differences in differentiation states of the normal keratinocytes and the cervical carcinoma lines that were analyzed.…”

Section: Dysregulation Of Homeobox Gene Expression In Cervical Canmentioning

confidence: 77%

Biochemical and Functional Interactions of Human Papillomavirus Proteins with Polycomb Group Proteins

McLaughlin-Drubin

Münger

2013

Viruses

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The role of enzymes involved in polycomb repression of gene transcription has been studied extensively in human cancer. Polycomb repressive complexes mediate oncogene-induced senescence, a principal innate cell-intrinsic tumor suppressor pathway that thwarts expansion of cells that have suffered oncogenic hits. Infections with human cancer viruses including human papillomaviruses (HPVs) and Epstein-Barr virus can trigger oncogene-induced senescence, and the viruses have evolved strategies to abrogate this response in order to establish an infection and reprogram their host cells to establish a long-term persistent infection. As a consequence of inhibiting polycomb repression and evading oncogene induced-senescence, HPV infected cells have an altered epigenetic program as evidenced by aberrant homeobox gene expression. Similar alterations are frequently observed in non-virus associated human cancers and may be harnessed for diagnosis and therapy.

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Section: Dysregulation Of Homeobox Gene Expression In Cervical Canmentioning

confidence: 77%

Biochemical and Functional Interactions of Human Papillomavirus Proteins with Polycomb Group Proteins

McLaughlin-Drubin

Münger

2013

Viruses

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“…HOXB4 has been reported to contribute to tumorigenesis in many cancers (48-51). Moreover, HOXB4 methylation could be a potential marker in human cervical cancer (52) and in extrahepatic cholangiocarcinoma (49). Hyper-methylation of the CDKL2 promoter has been suggested to play an important role in hepatocarcinogenesis and to be a potentially valuable biomarker for HCC (53,54).…”

Section: To Screen Genes With Different Levels Of Methylation Betweenmentioning

confidence: 99%

A novel DNA methylation-based model that effectively predicts prognosis in hepatocellular carcinoma

Hao

Shi

et al. 2021

Bioscience Reports

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Purpose: To build a novel predictive model for hepatocellular carcinoma (HCC) patients based on DNA methylation data.Methods: Four independent DNA methylation datasets for HCC were used to screen for common differentially methylated genes (CDMGs). Gene Ontology (GO) enrichment, and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis were used to explore the biological roles of CDMGs in HCC. Univariate Cox analysis and LASSO Cox analysis were performed to identify survival-related CDMGs (SR-CDMGs) and to build a predictive model. The importance of this model was assessed using Cox regression analysis, propensity score-matched (PSM) analysis and stratification analysis. A validation group from the Cancer Genome Atlas was constructed to further validate the model. Results: Four SR-CDMGs were identified and used to build the predictive model. The risk score of this model was calculated as follows: risk score = (0.01489826 × methylation level of WDR69) + (0.15868618 × methylation level of HOXB4) + (0.16674959 × methylation level of CDKL2) + (0.16689301 × methylation level of HOXA10). Kaplan-Meier analysis demonstrated that patients in the low-risk group had a significantly longer overall survival (log-rank P-value = 0.00071). The Cox model multivariate analysis and PSM analysis identified the risk score as an independent prognostic factor (P < 0.05). Stratified analysis results further confirmed this model performed well. By analyzing the validation group, the results of receiver operating characteristic curve analysis and survival analysis further validated this model. Conclusion: Our DNA-methylation-based prognosis predictive model is effective and reliable in predicting prognosis for patients with HCC.

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“…Indeed, HPV16 E7 associates with, as well as potentially modifies, activities of E2F6-containing PRCs and causes a reduction in the number of nuclear E2F6-containing polycomb bodies [ 76 ]. Moreover, PcG proteins are likely best known for their role in maintaining stable transcriptional repression of Homeobox ( HOX ) genes during development [ 100 , 101 ], and HOX family members are frequently dysregulated during carcinogenesis, including cervical carcinogenesis and in HPV16 E7-expressing cells [ 75 , 102 , 103 , 104 , 105 ].…”

Section: Regulation Of Histone Modificationsmentioning

confidence: 99%

Epigenetic Alterations in Human Papillomavirus-Associated Cancers

Soto

Song

McLaughlin-Drubin

2017

Viruses

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Approximately 15–20% of human cancers are caused by viruses, including human papillomaviruses (HPVs). Viruses are obligatory intracellular parasites and encode proteins that reprogram the regulatory networks governing host cellular signaling pathways that control recognition by the immune system, proliferation, differentiation, genomic integrity, and cell death. Given that key proteins in these regulatory networks are also subject to mutation in non-virally associated diseases and cancers, the study of oncogenic viruses has also been instrumental to the discovery and analysis of many fundamental cellular processes, including messenger RNA (mRNA) splicing, transcriptional enhancers, oncogenes and tumor suppressors, signal transduction, immune regulation, and cell cycle control. More recently, tumor viruses, in particular HPV, have proven themselves invaluable in the study of the cancer epigenome. Epigenetic silencing or de-silencing of genes can have cellular consequences that are akin to genetic mutations, i.e., the loss and gain of expression of genes that are not usually expressed in a certain cell type and/or genes that have tumor suppressive or oncogenic activities, respectively. Unlike genetic mutations, the reversible nature of epigenetic modifications affords an opportunity of epigenetic therapy for cancer. This review summarizes the current knowledge on epigenetic regulation in HPV-infected cells with a focus on those elements with relevance to carcinogenesis.

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Hox B4 as potential marker of non-differentiated cells in human cervical cancer cells

Abstract: Hox B4 protein is present in the precursor lesions as CC cells, suggesting that Hox B4 could be a protein related to the neoplastic state (non-differentiated cells) of human cervical epithelium.

Cited by 9 publications

References 42 publications

Biochemical and Functional Interactions of Human Papillomavirus Proteins with Polycomb Group Proteins

Biochemical and Functional Interactions of Human Papillomavirus Proteins with Polycomb Group Proteins

A novel DNA methylation-based model that effectively predicts prognosis in hepatocellular carcinoma

Epigenetic Alterations in Human Papillomavirus-Associated Cancers

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