Related Experiment Video

Updated: Feb 4, 2026

Analysis of Lymph Node Volume by Ultra-High-Frequency Ultrasound Imaging in the Braf/Pten Genetically Engineered Mouse Model of Melanoma
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Analysis of Lymph Node Volume by Ultra-High-Frequency Ultrasound Imaging in the Braf/Pten Genetically Engineered Mouse Model of Melanoma

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PTEN enhances the radiosensitivity of melanoma by inhibiting DNA-PKcs

Shengqian Zhu1, Haitao Xu1, Fu Shen2

  • 1Department of Plastic and Reconstructive Surgery, The First Affiliated Hospital of Ningbo University, Ningbo, China.

Frontiers in Cell and Developmental Biology
|February 2, 2026
PubMed
Abstract

Insights

Phosphatase and tensin homolog (PTEN) deficiency worsens melanoma progression and radiotherapy tolerance. Restoring PTEN expression enhances melanoma radiosensitivity by inhibiting DNA repair pathways, suggesting PTEN as a biomarker and therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Radiotherapy Research

Background:

  • Phosphatase and tensin homolog (PTEN) is a tumor suppressor gene implicated in melanoma progression.
  • PTEN deficiency is linked to reduced radiotherapy tolerance in melanoma patients.
  • The precise role of PTEN in regulating melanoma radiosensitivity remains unclear.

Purpose of the Study:

  • To investigate the role of PTEN in modulating melanoma radiosensitivity.
  • To elucidate the molecular mechanisms by which PTEN affects cellular response to radiation.
  • To evaluate PTEN as a potential biomarker and therapeutic target for melanoma radiotherapy.

Main Methods:

  • Validated PTEN expression using TCGA, tissue microarrays, and melanoma cell lines.
  • Constructed PTEN knockdown (PTEN-KD) and overexpression (PTEN-OE) cell lines.
  • Assessed radiosensitivity via CCK-8, colony formation, flow cytometry, comet assays, cell cycle analysis, Western blotting, and in vivo xenograft models.

Main Results:

  • PTEN expression was significantly lower in melanoma tissues and cell lines compared to normal controls.
  • PTEN overexpression inhibited proliferation, reduced survival, increased apoptosis, and weakened G2/M arrest post-irradiation.
  • PTEN inhibited DNA-PKcs signaling and NHEJ repair, while PTEN knockdown activated ATM/Chk2 signaling, confirmed in vivo tumor growth reduction.

Conclusions:

  • PTEN enhances melanoma radiosensitivity by suppressing DNA repair pathways and promoting cell cycle recovery.
  • PTEN serves as a predictive biomarker for radiotherapy response in melanoma.
  • Targeting PTEN offers a promising strategy for improving melanoma radiotherapy efficacy.
Keywords:
DNA damage repairPTENimmunotherapyirradiationmelanoma

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