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Updated: Jul 17, 2025

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel
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Knockdown of PROM2 Enhances Paclitaxel Sensitivity in Endometrial Cancer Cells by Regulating the AKT/FOXO1 Pathway

Jun Jiang1, Chen Zhang1, Jianfen Wang1

  • 1Department of Gynecology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, 310006, China.

Anti-Cancer Agents in Medicinal Chemistry
|September 6, 2023
PubMed
Abstract

Insights

Reducing PROM2 levels improves paclitaxel chemotherapy effectiveness in endometrial cancer by targeting the AKT/FOXO1 pathway. This suggests PROM2 is a potential therapeutic target for enhancing endometrial cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Endometrial cancer is a prevalent and lethal malignancy in women.
  • Paclitaxel (PTX) is a standard chemotherapy drug for endometrial cancer.
  • PROM2's role in cancer progression is known, but its function in PTX-treated endometrial cancer is unclear.

Purpose of the Study:

  • To investigate the role of PROM2 in paclitaxel (PTX) resistance in endometrial cancer.
  • To explore PROM2 as a potential therapeutic target for improving PTX efficacy.

Main Methods:

  • Bioinformatic analysis to assess PROM2 expression in endometrial cancer.
  • Cell viability (CCK8 assay), gene/protein expression (RT-qPCR, western blot), proliferation (colony formation, EdU assays), and apoptosis (flow cytometry) were evaluated.
  • PTX-resistant cell lines (HEC-1A/PTX, KLE/PTX) were established and treated with PTX.
  • PROM2 was suppressed (knockdown) and its effect on PTX sensitivity and the AKT/FOXO1 pathway was analyzed.
  • Rescue assays with an AKT activator (SC79) were performed.

Main Results:

  • PROM2 expression is upregulated in endometrial cancer, correlating with poorer patient survival.
  • PROM2 suppression enhanced PTX sensitivity, reducing viability and proliferation in PTX-resistant cells.
  • Knockdown of PROM2 promoted apoptosis in HEC-1A/PTX and KLE/PTX cells.
  • Silencing PROM2 was found to retard the AKT/FOXO1 signaling pathway.
  • AKT activation reversed the enhanced PTX sensitivity observed after PROM2 inhibition.

Conclusions:

  • PROM2 knockdown enhances paclitaxel sensitivity in endometrial cancer by modulating the AKT/FOXO1 pathway.
  • PROM2 represents a potential therapeutic target for overcoming paclitaxel resistance in endometrial cancer treatment.
Keywords:
AKT/FOXO1 pathwayPROM2SC79 treatment.UCEC patientsendometrial cancerpaclitaxel sensitivity

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