Phthalate-treated endometrial cancer cell lines show increased AKR1C1 expression
Phthalate treatment of endometrial cancer cells increased aldo-keto reductase expression, stimulated prostaglandin production, and may contribute to progesterone resistance.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
This paper assessed gene expression changes in the endometrial cancer cell line ECC-1 after treatment with phthalate, a compound previously linked to gynecologic disorders, focusing on aldo-keto reductases involved in prostaglandin and progesterone metabolism. The authors report that phthalate increased expression of aldo-keto reductases in these endometrial cells and stimulated prostaglandin production, with the implication that this pathway could contribute to progesterone resistance. A key caveat is that the work uses an endometrial cancer cell model rather than patient tissues or in vivo exposure systems, limiting direct generalization. Relevance to endometriosis: the introduction explicitly frames endometriosis as involving inflammatory and prostaglandin changes and progesterone resistance, and the study’s mechanism is positioned as potentially contributing to these endometriosis-associated processes, though the experiments themselves are in endometrial cancer cells.
Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works
Full text
6,601 characters
· extracted from
oa-doi-fallback
· 2 sections
· click to expand
Abstract
References
Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.
My notes (saved in your browser only)
Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works
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 (35)
- Deficient 17β-Hydroxysteroid Dehydrogenase Type 2 Expression in Endometriosis: Failure to Metabolize 17β-Estradiol<sup>1</sup> via openalex
- Enzymes of the AKR1B and AKR1C Subfamilies and Uterine Diseases via openalex
- Estrogen metabolizing enzymes in endometrium and endometriosis via openalex
- High plasma concentrations of di-(2-ethylhexyl)-phthalate in women with endometriosis via openalex
- PGE2 and PGF2α release by human peritoneal macrophages in endometriosis via openalex
- Progestin effects on expression of AKR1C1–AKR1C3, SRD5A1 and PGR in the Z-12 endometriotic epithelial cell line via openalex
- W1980615604 via openalex
- W1984253132 via openalex
- W1984703484 via openalex
- W2032301907 via openalex
- W2032985381 via openalex
- W2036093969 via openalex
- W2053311013 via openalex
- W2056618157 via openalex
- W2056906238 via openalex
- W2058759573 via openalex
- W2060679474 via openalex
- W2078882789 via openalex
- W2079617901 via openalex
- W2088426128 via openalex
- W2092420554 via openalex
- W2116022066 via openalex
- W2141569270 via openalex
- W2143927632 via openalex
- W2151441217 via openalex
- W2171869152 via openalex
- W2320812424 via openalex
- W4211081176 via openalex
- W4235221123 via openalex
- W4249970982 via openalex
- W1968571183 via openalex
- W1973461890 via openalex
- W1974233507 via openalex
- W1980307905 via openalex
- W1980555326 via openalex
Cited by (1)
Source provenance
- openalex
- last seen: 2026-06-04T00:00:01.174412+00:00
- unpaywall
- last seen: 2026-06-17T06:32:23.968882+00:00