The possible role furin and furin inhibitors in endometrial adenocarcinoma: A narrative review.

endometrial adenocarcinoma furin inflammatory signaling invasion metastasis proliferation

Journal

Cancer reports (Hoboken, N.J.)
ISSN: 2573-8348
Titre abrégé: Cancer Rep (Hoboken)
Pays: United States
ID NLM: 101747728

Informations de publication

Date de publication:
28 Nov 2023
Historique:
revised: 29 09 2023
received: 02 08 2023
accepted: 09 10 2023
medline: 29 11 2023
pubmed: 29 11 2023
entrez: 29 11 2023
Statut: aheadofprint

Résumé

Endometrial adenocarcinoma (EAC) is a malignant tumor of the endometrium. EAC is the most common female malignancy following the menopause period. About 40% of patients with EAC are linked with obesity and interrelated with hypertension, diabetes mellitus, and high circulating estrogen levels. Proprotein convertase (PC) furin was involved in the progression of EAC. Furin is a protease enzyme belonging to the subtilisin PC family called PC subtilisin/kexin type 3 that converts precursor proteins to biologically active forms and products. Aberrant activation of furin promotes abnormal cell proliferation and the development of cancer. Furin promotes angiogenesis, malignant cell proliferation, and tissue invasion by malignant cells through its pro-metastatic and oncogenic activities. Furin activity is correlated with the malignant proliferation of EAC. Higher expression of furin may increase the development of EAC through overexpression of pro-renin receptors and disintegrin and metalloprotease 17 (ADAM17). As well, inflammatory signaling in EAC promotes the expression of furin with further propagation of malignant transformation. Furin is associated with the development and progression of EAC through the induction of proliferation, invasion, and metastasis of malignant cells of EAC. Furin induces ontogenesis in EAC through activation expression of ADAM17, pro-renin receptor, CD109, and TGF-β. As well, EAC-mediated inflammation promotes the expression of furin with further propagation of neoplastic growth and invasion.

Sections du résumé

BACKGROUND BACKGROUND
Endometrial adenocarcinoma (EAC) is a malignant tumor of the endometrium. EAC is the most common female malignancy following the menopause period. About 40% of patients with EAC are linked with obesity and interrelated with hypertension, diabetes mellitus, and high circulating estrogen levels. Proprotein convertase (PC) furin was involved in the progression of EAC.
RECENT FINDINGS RESULTS
Furin is a protease enzyme belonging to the subtilisin PC family called PC subtilisin/kexin type 3 that converts precursor proteins to biologically active forms and products. Aberrant activation of furin promotes abnormal cell proliferation and the development of cancer. Furin promotes angiogenesis, malignant cell proliferation, and tissue invasion by malignant cells through its pro-metastatic and oncogenic activities. Furin activity is correlated with the malignant proliferation of EAC. Higher expression of furin may increase the development of EAC through overexpression of pro-renin receptors and disintegrin and metalloprotease 17 (ADAM17). As well, inflammatory signaling in EAC promotes the expression of furin with further propagation of malignant transformation.
CONCLUSION CONCLUSIONS
Furin is associated with the development and progression of EAC through the induction of proliferation, invasion, and metastasis of malignant cells of EAC. Furin induces ontogenesis in EAC through activation expression of ADAM17, pro-renin receptor, CD109, and TGF-β. As well, EAC-mediated inflammation promotes the expression of furin with further propagation of neoplastic growth and invasion.

Identifiants

pubmed: 38018319
doi: 10.1002/cnr2.1920
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1920

Subventions

Organisme : University of Witten-Herdecke Germany

Informations de copyright

© 2023 The Authors. Cancer Reports published by Wiley Periodicals LLC.

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Auteurs

Hayder M Al-Kuraishy (HM)

Department of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.

Thabat J Al-Maiahy (TJ)

Department of Gynecology and Obstetrics, College of Medicine, Mustansiriyah University, Baghdad, Iraq.

Ali I Al-Gareeb (AI)

Department of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.

Athanasios Alexiou (A)

University Centre for Research & Development, Chandigarh University, Chandigarh-Ludhiana Highway, Mohali, Punjab, India.
Department of Research & Development, Funogen, Athens, Greece.
Department of Research & Development, AFNP Med, Wien, Austria.
Department of Science and Engineering, Novel Global Community Educational Foundation, Hebersham, New South Wales, Australia.

Marios Papadakis (M)

Department of Surgery II, University Hospital Witten-Herdecke, University of Witten-Herdecke, Wuppertal, Germany.

Hebatallah M Saad (HM)

Department of Pathology, Faculty of Veterinary Medicine, Matrouh University, Matrouh, Egypt.

Gaber El-Saber Batiha (GE)

Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, AlBeheira, Egypt.

Classifications MeSH