Peer Review #2 of "TET1 may contribute to hypoxia-induced epithelial to mesenchymal transition of endometrial epithelial cells in endometriosis (v0.2)"

2020 · doi:10.7287/peerj.9950v0.2/reviews/2 · W4254566937
peer-review OA: gold CC0
🔓 Open OA copy View on OpenAlex View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-09 ⓘ

TET1, a demethylation enzyme, was elevated in endometriosis lesions and promoted epithelial-mesenchymal transition via hypoxia-induced expression regulated by HIF-2α.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

Background.Endometriosis (EMs) is a non-malignant gynecological disease, whose pathogenesis remains to be clarified.Recent studies have found that hypoxia induces epithelial-mesenchymal transition (EMT) as well as epigenetic modification in EMs.However, the relationship between EMT and demethylation modification under hypoxia status in EMs remains unknown.Methods.The expression of N-cadherin, E-cadherin and TET1 in normal endometria, eutopic endometria and ovarian endometriomas was assessed by immunohistochemistry and immunofluorescence double staining.5-hmC was detected by fluorescence-based ELISA kit using a specific 5-hmC antibody.Overexpression and inhibition of TET1 or hypoxia-inducible factor 2α (HIF-2α) were performed by plasmid and siRNA transfection.The expression of HIF-2α, TET1 and EMT markers in Ishikawa (ISK) cells (widely used as endometrial epithelial cells) was evaluated by western blotting.The interaction of HIF-2α and TET1 was analyzed by chromatin immunoprecipitation.Results.Demethylation enzyme TET1 (ten-eleven translocation1) was elevated in glandular epithelium of ovarian endometrioma, along with the activation of EMT (increased expression of N-cadherin, and decreased expression of E-cadherin) and global increase of epigenetic modification marker 5-hmC(5hydroxymethylcytosine).Besides, endometriosis lesions had more TET1 and N-cadherin co-localized cells.Further study showed that ISK cells exhibited enhanced EMT, and increased expression of TET1 and HIF-2α under hypoxic condition.Hypoxia-induced EMT was partly regulated by TET1 and HIF-2α.HIF-2α inhibition mitigated TET1 expression changes provoked by hypoxia.Conclusions.Hypoxia induces the expression of TET1 regulated by HIF-2α, thus may promote EMT in endometriosis.

My notes (saved in your browser only)

Condition tags

endometriosisendometrioma

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (51)

Source provenance

openalex
last seen: 2026-06-04T00:00:01.174412+00:00
License: CC0 · commercial use OK