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Related Experiment Video

Updated: May 20, 2025

Visualizing DNA Damage Repair Proteins in Patient-Derived Ovarian Cancer Organoids via Immunofluorescence Assays
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HELQ upregulates PARP1 to drive platinum resistance and predict therapeutic response in ovarian cancer.

Shuran Tan1, Fang Zhu1, Yi Li1

  • 1Department of Gynecology, Xiangya Hospital, Central South University, Changsha, Hunan, , 410008, PR China; Gynecological Oncology Research and Engineering Center of Hunan Province, XiangyaHospital, Changsha, Hunan, , 410008, PR China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Changsha, Hunan, 410008, PR China.

Translational Oncology
|May 17, 2025
PubMed
Summary

POLQ-like helicase (HELQ) promotes platinum resistance in ovarian cancer by upregulating PARP1. Lower HELQ levels enhance sensitivity to chemotherapy and PARP inhibitors, suggesting HELQ as a potential biomarker.

Keywords:
DNA helicaseHELQOvarian carcinomaPARP inhibitorsPlatinum resistance

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Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Ovarian cancer (OC) often develops platinum resistance, a major clinical challenge.
  • POLQ-like helicase (HELQ) is overexpressed in platinum-resistant OC, correlating with poor prognosis.
  • The precise role of HELQ in chemoresistance remains largely unknown.

Purpose of the Study:

  • To elucidate the mechanisms by which HELQ contributes to platinum resistance in ovarian cancer.
  • To investigate the potential of HELQ as a predictive biomarker for chemotherapy and PARP inhibitor (PARPi) response.

Main Methods:

  • In vitro and in vivo OC models were utilized.
  • Immunofluorescence and western blot assays assessed DNA damage repair markers (γH2AX, RPA1, 53BP1).
  • PARP1 expression and its regulation by HELQ were analyzed, alongside patient tumor tissue analysis (immunohistochemistry).

Main Results:

  • Elevated HELQ expression increased chemoresistance, while reduced HELQ enhanced sensitivity to platinum agents.
  • HELQ promotes platinum-induced DNA damage repair and upregulates poly (ADP-ribose) polymerase 1 (PARP1) expression, mediating platinum resistance.
  • HELQ overexpression sensitized OC cells to PARPi, and diminished HELQ in patient tumors correlated with disease progression during PARPi therapy.

Conclusions:

  • HELQ promotes platinum resistance in ovarian cancer by upregulating PARP1.
  • HELQ acts as a key regulator of DNA damage repair in response to platinum chemotherapy.
  • HELQ is a potential predictive biomarker for therapeutic response to chemotherapy and PARPi in ovarian cancer.