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Targeting RAD51 enhances chemosensitivity of adult T‑cell leukemia‑lymphoma cells by reducing DNA double‑strand break

Meng Yang1, Xiaoxue Tian1, Zhuoyi Fan1

  • 1Department of Hematology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, P.R China.

Oncology Reports
|October 23, 2019
PubMed

Insights

Targeting RAD51, a key DNA repair protein, can sensitize adult T-cell leukemia-lymphoma cells to chemotherapy. Suppressing RAD51 enhances cancer cell death and may improve patient survival.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • RAD51 is a crucial homologous recombination protein involved in DNA repair, gene stability, and diversity.
  • Overexpression of RAD51 is linked to chemotherapy resistance in tumor cells.
  • Enhanced DNA damage repair (DDR) activity contributes to chemotherapy resistance in adult T-cell leukemia-lymphoma (ATL).

Purpose of the Study:

  • To investigate the potential of targeting RAD51 to sensitize ATL cells to chemotherapy.
  • To explore the role of RAD51 in DNA damage repair and its impact on ATL cell survival.
  • To evaluate the efficacy of RAD51 downregulation in combination with etoposide treatment.

Main Methods:

  • Utilized short hairpin RNA (shRNA) to downregulate RAD51 expression.
  • Administered imatinib to inhibit RAD51 activity.
  • Treated Jurkat cells (a model for ATL) with etoposide.
  • Assessed homologous recombination (HR) activity, cell proliferation, and apoptosis.

Main Results:

  • Downregulation of RAD51 by shRNA and imatinib sensitized Jurkat cells to etoposide by reducing HR activity.
  • Suppression of RAD51 inhibited tumor cell proliferation and increased apoptosis after etoposide treatment.
  • Imatinib-mediated RAD51 downregulation significantly enhanced etoposide-induced apoptosis in Jurkat cells.

Conclusions:

  • RAD51 is a promising therapeutic target for adult T-cell leukemia-lymphoma (ATL).
  • Targeting RAD51 can enhance the efficacy of chemotherapy by inducing DNA damage and promoting cancer cell death.
  • Inhibition of RAD51 may improve clinical outcomes and survival rates for leukemia patients.

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