EUVIMEDOpdag EUVIMED
CrossrefInfokort

CEACAM1 participation in breast cancer progression

Mykola Lyndin, Irina Kube‐Golovin, Anatolii Romaniuk, Gunther Wennemuth

Molecular Oncology · 2026-11 · 20 (11) · 2805-2819

DOI: 10.1002/1878-0261.70306 ↗
AbstractBibliografiske oplysninger

Abstract

Carcinoembryonic antigen‐related cell adhesion molecule 1 (CEACAM1) is widely expressed in human cells and undergoes marked alterations during tumorigenesis. However, its functional significance in invasive breast cancer (BC) remains insufficiently understood. In this study, CEACAM1 expression patterns in invasive BC tissues were analyzed and correlated with the proliferative index (PI) of the tumor cells. To assess isoform‐specific functional effects and identify CEACAM1‐responsive genes involved in key proliferation‐associated pathways, MCF‐7 cells were transfected with either CEACAM1 short cytoplasmic domain isoform (CEACAM1‐4S) or CEACAM1 long cytoplasmic domain isoform (CEACAM1‐4L). BC tissues exhibited substantial heterogeneity in CEACAM1 expression, which correlated with the PI of the tumor cells. Functional in vitro studies demonstrated that the CEACAM1‐4L isoform exclusively suppresses cell proliferation. Transcriptome and protein‐level analyses revealed that CEACAM1‐4L regulates the expression of key mediators involved in cell cycle control, apoptosis, extracellular matrix organization, and growth factor‐dependent signaling pathways. These findings highlight the biological significance of CEACAM1‐4L isoform in BC, its potential diagnostic relevance for patient stratification, as well as its possible consideration in future therapeutic approaches.

Viden, der passer til dit arbejde.

Fra en gratis start over personlig litteratursøgning til den komplette Research Suite.

Se priser →

Er alle forlagsfuldtekster inkluderet?

Nej. Bibliografiske referencer, abstracts og fuldtekster er forskellige typer indhold. Om en fuldtekst er tilgængelig, afhænger af kilden, Open Access og dine eksisterende licenser. Et EUVIMED-abonnement erstatter ikke yderligere forlagsrettigheder.

Se priser →