The effect of cuproptosis-relevant genes on the immune infiltration and metabolism of gynecological oncology by multiply analysis and experiments validation

© 2023. The Author(s)..

Gynecological cancers are a leading cause of mortality for women, including ovarian cancer (OC), cervical squamous cell carcinoma (CESC), and uterine corpus endometrial carcinoma (UCEC). Nevertheless, these gynecological cancer types have not elucidated the role of cuproptosis and the correlated tumor microenvironment (TME) infiltration features. CRGs had important potential molecular functions and prognostic significance in gynecological cancers, especially in UCEC. Hub CRG, FDX1, was correlated with the CD8+ T cell immune infiltration in UCEC and CESC. FDX1 OE could significantly repress the proliferation ability in UCEC cells by MTT, EdU, and clone formation. High levels of FDX1 could repress ATP and lactic acid but enhance ROS and glucose levels by metabolism assay. The xenograft tumor model indicated that FDX1 OE significantly inhibited the growth of UCEC and attenuated the PCNA, HK2, PKM2, and Ki-67 expression. These CRGs are significant roles that could be potential markers and treatment targets to optimize the TME immune cell infiltration features for gynecological cancer types. FDX1 is a hub CRGs in UCEC to promote immune infiltration and attenuate proliferation and metabolism.

Medienart:

E-Artikel

Erscheinungsjahr:

2023

Erschienen:

2023

Enthalten in:

Zur Gesamtaufnahme - volume:13

Enthalten in:

Scientific reports - 13(2023), 1 vom: 09. Nov., Seite 19474

Sprache:

Englisch

Beteiligte Personen:

Ran, Xiao-Min [VerfasserIn]
Xiao, Hui [VerfasserIn]
Tang, Yan-Xiang [VerfasserIn]
Jin, Xia [VerfasserIn]
Tang, Xing [VerfasserIn]
Zhang, Juan [VerfasserIn]
Li, Hui [VerfasserIn]
Li, Yu-Kun [VerfasserIn]
Tang, Zhen-Zi [VerfasserIn]

Links:

Volltext

Themen:

789U1901C5
Copper
Journal Article

Anmerkungen:

Date Completed 14.12.2023

Date Revised 14.12.2023

published: Electronic

Citation Status MEDLINE

doi:

10.1038/s41598-023-45076-5

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM364373202