Regulation of Proliferation and Invasion in Endometriosis

In: ISGE Series · 2019 · pp. 167–175 · doi:10.1007/978-3-030-14358-9_13 · W2954782991
book-chapter OA: closed CC0 ⤵ 1 in-corpus citation
Full text JSON View on OpenAlex View at publisher
AI-generated summary by claude@2026-06+body, 2026-06-08

This paper discusses endometriosis as a chronic disease affecting women, characterized by endometrial tissue outside the uterus, causing pain, reproductive issues, and infertility.

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

AI-generated deep summary by claude@2026-06, 2026-06-10 · read from full text

This chapter reviews how proliferation and invasion are regulated in endometriosis, describing evidence that endometriosis involves changes in apoptosis/proliferation, cell migration and invasion, and phenotypes associated with pluripotency and epithelial-to-mesenchymal transition. It focuses on mechanistic findings and molecular regulators discussed across studies, including microRNAs (e.g., miR-145, miR-200b, miR-142-3p) and pathways/targets affecting cytoskeletal elements, stemness factors, ZEB1/2, and related invasion-associated factors like syndecan-1 and IL-6 signaling, with some reference to animal or in vitro endometriosis models. The main limitation is that the text provided is a book chapter/overview rather than a single original experiment, so specific experimental conditions and effect sizes from each cited study are not fully specified here. This paper is centrally about endometriosis — specifically, it regulates proliferation and invasion through molecular and microRNA-mediated mechanisms described in the endometriosis literature.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Full text 6,450 characters · extracted from oa-doi-fallback · 2 sections · click to expand

Abstract

Endometriosis is a common disease in young women, which affects approximately 6–10% of the female German population. It is defined as endometrium-like glands and stroma cells outside the uterus and can cause severe and chronic pain (dysmenorrhea, dyspareunia, abdominal pain) as well as reproductive problems and infertility [1, 2]. Endometriosis triggers a decrease in the quality of life similar to other chronic diseases such as arthritis or heart conditions [3]. Access this chapter Tax calculation will be finalised at checkout Purchases are for personal use only Similar content being viewed by others

References

Adammek M, Greve B, Kässens N, et al. MicroRNA miR-145 inhibits proliferation, invasiveness, and stem cell phenotype of an in vitro endometriosis model by targeting multiple cytoskeletal elements and pluripotency factors. Fertil Steril. 2013;99(5):1346–1355.e5. Sampson JA. Metastatic or embolic endometriosis, due to the menstrual dissemination of endometrial tissue into the venous circulation. Am J Pathol. 1927;3(2):93–110.43. Simoens S, Dunselman G, Dirksen C, et al. The burden of endometriosis: costs and quality of life of women with endometriosis and treated in referral centres. Hum Reprod. 2012;27(5):1292–9. Nisolle MDJ. Peritoneal endometriosis, ovarian endometriosis, and adenomyotic nodules of the rectovaginal septum are three different entities. Fertil Steril. 1997;68(4):585–96. Strowitzki T, Germeyer A, Popovici R, von Wolff M. The human endometrium as a fertility-determining factor. Hum Reprod Update. 2006;12(5):617–30. https://doi.org/10.1093/humupd/dml033. Götte M, Wolf M, Staebler A, et al. Aberrant expression of the pluripotency marker SOX-2 in endometriosis. Fertil Steril. 2011;95(1):338–41. Schüring AN, Schulte N, Kelsch R, et al. Characterization of endometrial mesenchymal stem-like cells obtained by endometrial biopsy during routine diagnostics. Fertil Steril. 2011;95(1):423–6. Anaf V, Simon P, El Nakadi I, et al. Relationship between endometriotic foci and nerves in rectovaginal endometriotic nodules. Hum Reprod. 2000;15(8):1744–50. Donnez O, Orellana R, Van Kerk O, Dehoux JP, Donnez J, Dolmans MM. Invasion process of induced deep nodular endometriosis in an experimental baboon model. Fertil Steril. 2015;104(2):491–497.e2. Orellana R, García-Solares J, Donnez J, van Kerk O, Dolmans MM, Donnez O. Important role of collective cell migration and nerve fiber density in the development of deep nodular endometriosis. Fertil Steril. 2017;107(4):987–995.e5. Béliard A, Noël A, Foidart J-M. Reduction of apoptosis and proliferation in endometriosis. Fertil Steril. 2004;82(1):80–5. Saare M, Rekker K, Laisk-Podar T, et al. Challenges in endometriosis miRNA studies – from tissue heterogeneity to disease specific miRNAs. Biochim Biophys Acta. 2017;1863(9):2282–92. MacFarlane L-A, Murphy PR. MicroRNA. Curr Genomics. 2010;11(7):537–61. NCBI. SOX2 SRY-box 2 [Homo sapiens (human)]. 2018. https://www.ncbi.nlm.nih.gov/gene/6657. Zugriff am 28 Mar 2018. Go MJ, Takenaka C, Ohgushi H. Forced expression of Sox2 or Nanog in human bone marrow derived mesenchymal stem cells maintains their expansion and differentiation capabilities. Exp Cell Res. 2008;314(5):1147–54. NCBI. IL6ST interleukin 6 signal transducer [Homo sapiens (human)]. May 2014. https://www.ncbi.nlm.nih.gov/gene/3572. Zugriff am 29 Mar 2018. Kästingschäfer CS, Schäfer SD, Kiesel L, et al. miR-142-3p is a novel regulator of cell viability and proinflammatory signalling in endometrial stroma cells. Reprod Biomed Online. 2015;30(5):553–6. Yuan ZL, Guan YJ, Wang L, et al. Central role of the threonine residue within the p+1 loop of receptor tyrosine kinase in STAT3 constitutive phosphorylation in metastatic cancer cells. Mol Cell Biol. 2004;24(21):9390–400. Kaponis A, Iwabe T, Taniguchi F, et al. The role of NF-kappaB in endometriosis. Front Biosci (Schol Ed). 2012;4:1213–34. Bao H, Yao Q-P, Huang K, et al. Platelet-derived miR-142-3p induces apoptosis of endothelial cells in hypertension. Cell Mol Biol (Noisy-le-Grand). 2017;63(4):3–9. Carraro G, Shrestha A, Rostkovius J, et al. miR-142-3p balances proliferation and differentiation of mesenchymal cells during lung development. Development. 2014;141(6):1272–81. NCBI. STS steroid sulfatase [Homo sapiens (human)]. Mar 2016. Zugriff am 30 Mar 2018. Colette S, Defrere S, Lousse JC, et al. Inhibition of steroid sulfatase decreases endometriosis in an in vivo murine model. Hum Reprod. 2011;26(6):1362–70. Eggers JC, Martino V, Reinbold R, et al. microRNA miR-200b affects proliferation, invasiveness and stemness of endometriotic cells by targeting ZEB1, ZEB2 and KLF4. Reprod Biomed Online. 2016;32(4):434–45. Shields JM, Christy RJ, Yang VW. Identification and characterization of a gene encoding a gut-enriched Krüppel-like factor expressed during growth arrest. J Biol Chem. 1996;271(33):20009–17. NCBI. ZEB1 zinc finger E-box binding homeobox 1 [Homo sapiens (human)]. 2010. Zugriff am 30 Mar 2018. Yang Y-M, Yang W-X. Epithelial-to-mesenchymal transition in the development of endometriosis. Oncotarget. 2017;8(25):41679–89. Gumbiner BM. Regulation of cadherin-mediated adhesion in morphogenesis. Nat Rev Mol Cell Biol. 2005;6(8):622–34. Ibrahim SA, Yip GW, Stock C, et al. Targeting of syndecan-1 by microRNA miR-10b promotes breast cancer cell motility and invasiveness via a Rho-GTPase- and E-cadherin-dependent mechanism. Int J Cancer. 2012;131(6):E884–96. Schneider C, Kassens N, Greve B, et al. Targeting of syndecan-1 by micro-ribonucleic acid miR-10b modulates invasiveness of endometriotic cells via dysregulation of the proteolytic milieu and interleukin-6 secretion. Fertil Steril. 2013;99(3):871–881.e1. Author information Authors and Affiliations Corresponding author Editor information Editors and Affiliations Rights and permissions Copyright information © 2019 International Society of Gynecological Endocrinology About this chapter Cite this chapter Rohloff, N., Götte, M., Kiesel, L. (2019). Regulation of Proliferation and Invasion in Endometriosis. In: Berga, S., Genazzani, A., Naftolin, F., Petraglia, F. (eds) Menstrual Cycle Related Disorders. ISGE Series. Springer, Cham. https://doi.org/10.1007/978-3-030-14358-9_13 Download citation DOI: https://doi.org/10.1007/978-3-030-14358-9_13 Published: Publisher Name: Springer, Cham Print ISBN: 978-3-030-14357-2 Online ISBN: 978-3-030-14358-9 eBook Packages: MedicineMedicine (R0)

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)

Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback

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

Condition tags

endometriosis

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 (26)

Cited by (1)

Source provenance

openalex
last seen: 2026-06-04T00:00:01.174412+00:00
unpaywall
last seen: 2026-06-04T02:00:05.705006+00:00
License: CC0 · commercial use OK