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Original Research

Open Access

Knockdown of GDF15 inhibits endometrial cancer cell proliferation and EMT

  • Litao Yu1,*,
  • Jing Shi2
  • Kedan Cao1

1Department of Obstetrics and Gynecology, Changzhou Maternal and Child Health Care Hospital, 213000 Changzhou, Jiangsu, China

2Department of Gastroenterology, Changzhou Tumor Hospital, 213000 Changzhou, Jiangsu, China

DOI: 10.22514/ejgo.2024.053 Vol.45,Issue 3,June 2024 pp.95-101

Submitted: 12 February 2024 Accepted: 09 April 2024

Published: 15 June 2024

*Corresponding Author(s): Litao Yu E-mail: tli_yu0311@163.com

Abstract

Endometrial cancer (EC) is a malignant tumor affecting the uterine upper layer. Despite recent advancements, identifying new therapeutic targets remains important for improving patient prognosis. Growth differentiation factor 15 (GDF15) belongs to the Transforming Growth Factor (TGF)-β superfamily and is often upregulated in pathological conditions, including injury and cancers. However, its involvement in EC remains poorly understood. This study aims to elucidate the significance of GDF15 in EC and its potential underlying mechanism. Our results indicate increased GDF15 expression levels in EC tissues, and the knockdown of GDF15 was found to suppress EC cell growth and epithelial-mesenchymal transition (EMT). Moreover, GDF15 depletion inhibited the TGF-β pathway activation. In summary, GDF15 can promote EC cell growth and EMT by modulating the TGF-β/Smad2/Smad3 axis.


Keywords

Endometrial cancer (EC); Growth differentiation factor 15 (GDF15); Growth; EMT; TGF-β/Smad2/Smad3 axis


Cite and Share

Litao Yu,Jing Shi,Kedan Cao. Knockdown of GDF15 inhibits endometrial cancer cell proliferation and EMT. European Journal of Gynaecological Oncology. 2024. 45(3);95-101.

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