Canonical TGFβ Signaling and Its Contribution to Endometrial Cancer Development and Progression-Underestimated Target of Anticancer Strategies.
Smad proteins
TGFβ co-receptors
TGFβ isoforms
TGFβR1
TGFβR2
betaglycan
endoglin
endometrial cancer
Journal
Journal of clinical medicine
ISSN: 2077-0383
Titre abrégé: J Clin Med
Pays: Switzerland
ID NLM: 101606588
Informations de publication
Date de publication:
30 Aug 2021
30 Aug 2021
Historique:
received:
12
08
2021
revised:
24
08
2021
accepted:
26
08
2021
entrez:
10
9
2021
pubmed:
11
9
2021
medline:
11
9
2021
Statut:
epublish
Résumé
Endometrial cancer is one of the leading gynecological cancers diagnosed among women in their menopausal and postmenopausal age. Despite the progress in molecular biology and medicine, no efficient and powerful diagnostic and prognostic marker is dedicated to endometrial carcinogenesis. The canonical TGFβ pathway is a pleiotropic signaling cascade orchestrating a variety of cellular and molecular processes, whose alterations are responsible for carcinogenesis that originates from different tissue types. This review covers the current knowledge concerning the canonical TGFβ pathway (Smad-dependent) induced by prototypical TGFβ isoforms and the involvement of pathway alterations in the development and progression of endometrial neoplastic lesions. Since Smad-dependent signalization governs opposed cellular processes, such as growth arrest, apoptosis, tumor cells growth and differentiation, as well as angiogenesis and metastasis, TGFβ cascade may act both as a tumor suppressor or tumor promoter. However, the final effect of TGFβ signaling on endometrial cancer cells depends on the cancer disease stage. The multifunctional role of the TGFβ pathway indicates the possible utilization of alterations in the TGFβ cascade as a potential target of novel anticancer strategies.
Identifiants
pubmed: 34501347
pii: jcm10173900
doi: 10.3390/jcm10173900
pmc: PMC8432036
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
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