Analysis of KAP1 expression patterns and human endogenous retrovirus Env proteins in ovarian cancer

Jeon, Kyung-Yoon; Ko, Eun‐Ji; Oh, Young Lim; Kim, Hongbae; Eo, Wan Kyu; Kim, Ari; Sun, Han Gyu; Ock, Mee Sun; Kim, Ki Hyung; Cha, Hee‐Jae

doi:10.1007/s13258-020-00979-9

Cited by 7 publications

(6 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This was accompanied by the recruitment of the histone-lysine N-methyltransferase SETDB1, deposition of the repressive H3K9me3 histone mark, and consequent silencing of transcription ( 58 ). However, this mechanism may not ubiquitously regulate HERV-K members as no association was observed between KAP1 and HML-2 expression in ovarian cancer tissues ( 59 ). In a follow up paper the same group showed enrichment of the active H3K27ac chromatin mark accompanied by KLF4 and OCT4 binding at LTR5Hs elements.…”

Section: Transcriptional Post-transcriptional and Epigenetic Regulation Of Hml-2mentioning

confidence: 99%

Ancient Adversary – HERV-K (HML-2) in Cancer

et al. 2021

View full text Add to dashboard Cite

Human endogenous retroviruses (HERV), ancient integrations of exogenous viruses, make up 8% of our genome. Long thought of as mere vestigial genetic elements, evidence is now accumulating to suggest a potential functional role in numerous pathologies including neurodegenerative diseases, autoimmune disorders, and multiple cancers. The youngest member of this group of transposable elements is HERV-K (HML-2). Like the majority of HERV sequences, significant post-insertional mutations have disarmed HERV-K (HML-2), preventing it from producing infectious viral particles. However, some insertions have retained limited coding capacity, and complete open reading frames for all its constituent proteins can be found throughout the genome. For this reason HERV-K (HML-2) has garnered more attention than its peers. The tight epigenetic control thought to suppress expression in healthy tissue is lost during carcinogenesis. Upregulation of HERV-K (HML-2) derived mRNA and protein has been reported in a variety of solid and liquid tumour types, and while causality has yet to be established, progressively more data are emerging to suggest this phenomenon may contribute to tumour growth and metastatic capacity. Herein we discuss its potential utility as a diagnostic tool and therapeutic target in light of the current in vitro, in vivo and clinical evidence linking HERV-K (HML-2) to tumour progression.

show abstract

Section: Transcriptional Post-transcriptional and Epigenetic Regulation Of Hml-2mentioning

confidence: 99%

Ancient Adversary – HERV-K (HML-2) in Cancer

et al. 2021

View full text Add to dashboard Cite

show abstract

“…It is reported, HERV-K env protein in normal tissues was low but higher in bronchus submucosal gland, salivary gland acini, pancreas acini, testis seminiferous tubule, uterine cervix epithelium, ovary stroma, skin epidermis, and heart [ 24 ]. HERV-R env and KAP1 proteins were lower in normal tissues than ovarian cancerous ones, but HERV-K env did not illustrate a meaningful change in cancerous tissues [ 25 ]. Patients suffering from advanced-stage ovarian clear cell carcinoma, decrease in HERV-K, HERV-E, and LINE-1 were observed [P = 0.0179, P = 0.0021, and P = 0.0307, respectively], and the more methylated [hypomethylated] HERV-K existed, the less chance of survival [P = 0.006] can be seen [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

Analysing the HERV-K env, np9, rec and gag expression in cervical tissues

Tavakolian

Goudarzi

Moridi

et al. 2021

New Microbes and New Infections

View full text Add to dashboard Cite

Cervical cancer is considered to be the fourth common cancer. It is assumed that numerous risk factors, especially infectious ones, can have a detrimental effect on cervical cancer. In this study, we evaluated the expression of Herv-K env, np9, rec and gag in cervical tissues. After RNA extraction and cDNA sensitizing of 12 cervical cancer tissues and CIN3, 51 CIN1,2 and 18 normal ones, Herv-K env, np9, rec and gag were assessed using quantitative real-time PCR analysis. There was a decrease in the level of HERV-K env expression in cervical cancer and CIN 1-3 in compression with normal tissues. Cervical cancer and CIN3 indicated the most increase in expression. Meanwhile, we observed an increase in gag and rec expression in CIN 1,2; although cervical cancer and CIN 3 had a decrease in rec and gag expression, we did not report any changes in np expression. In conclusion, given the relationship between HERV-associated genes and cervical cancer, our study suggests that these genes can be useful for cancer diagnosis. However, further investigations are needed to provide a better perspective about the effectiveness of these genes in the diagnostic strategies of gastrointestinal cancer. These results are just an observation that could open a wider investigation to test the correlation between the expression of these genes and cervical cancer.

show abstract

“…HERV-E Clear cell kidney cancer (Cherkasova et al, 2011), breast cancer (Frank et al, 2008) HERV-F Soft tissue sarcoma (Giebler et al, 2018), breast cancer (Frank et al, 2008) HERV-H Gastrointestinal and pancreatic neuroendocrine tumors (Yuan et al, 2021), colon cancer (Liang et al, 2009a(Liang et al, ,b, 2012Li et al, 2012), lung cancer (Zare et al, 2018), breast cancer (Rhyu et al, 2014) HERV-K Breast cancer (Wang-Johanning et al, 2003), soft tissue sarcoma (Giebler et al, 2018), melanoma (Singh et al, 2013(Singh et al, , 2020, germ cell tumor (Chan et al, 2019), leukemia (Chen et al, 2013), colon cancer (Dolci et al, 2020a,b), Hodgkin lymphoma (Barth et al, 2019), lung cancer (Zare et al, 2018) HERV-P Lung cancer (Zare et al, 2018), breast cancer (Tavakolian et al, 2019), primary cutaneous t-cell lymphomas (Bergallo et al, 2018) HERV-R Colon cancer (Dolci et al, 2020a), lung cancer (Zare et al, 2018), breast cancer (Rhyu et al, 2014), ovarian cancer (Jeon et al, 2020), primary cutaneous T-cell lymphomas (Bergallo et al, 2018) HERV-W Endometrial (Strissel et al, 2012), testicular cancer (Gimenez et al, 2010), germ cell tumors (Benesova et al, 2017), non-small cell lung cancer (NSCLC) , endometrial carcinoma (Liu et al, 2019) HERV-FRD Seminomas (Benesova et al, 2017), glioblastoma (Diaz-Carballo et al, 2017) HEMO breast cancer and ovarian cancer (Heidmann et al, 2017), endometrial cancer (Kasperek et ...…”

Section: Herv Family Cancer Typementioning

confidence: 99%

Transcriptional and reverse transcriptional regulation of host genes by human endogenous retroviruses in cancers

2022

View full text Add to dashboard Cite

Human endogenous retroviruses (HERVs) originated from ancient retroviral infections of germline cells millions of years ago and have evolved as part of the host genome. HERVs not only retain the capacity as retroelements but also regulate host genes. The expansion of HERVs involves transcription by RNA polymerase II, reverse transcription, and re-integration into the host genome. Fast progress in deep sequencing and functional analysis has revealed the importance of domesticated copies of HERVs, including their regulatory sequences, transcripts, and proteins in normal cells. However, evidence also suggests the involvement of HERVs in the development and progression of many types of cancer. Here we summarize the current state of knowledge about the expression of HERVs, transcriptional regulation of host genes by HERVs, and the functions of HERVs in reverse transcription and gene editing with their reverse transcriptase.

show abstract

Analysis of KAP1 expression patterns and human endogenous retrovirus Env proteins in ovarian cancer

Cited by 7 publications

References 27 publications

Ancient Adversary – HERV-K (HML-2) in Cancer

Ancient Adversary – HERV-K (HML-2) in Cancer

Analysing the HERV-K env, np9, rec and gag expression in cervical tissues

Transcriptional and reverse transcriptional regulation of host genes by human endogenous retroviruses in cancers

Contact Info

Product

Resources

About