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Updated: Feb 13, 2026

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
09:40

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer

Published on: August 2, 2024

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Epitranscriptomic Regulation of Platinum Resistance via the METTL3-ADAM23 Axis in Ovarian Cancer

Ujin Kim1, Junzui Li1, Daniela Matei1,2,3

  • 1Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.

Cells
|February 12, 2026
PubMed

Insights

N6-methyladenosine (m6A) regulates gene control, and its role in chemotherapy resistance is emerging. This study reveals METTL3-ADAM23 interactions impacting platinum resistance in ovarian cancer, suggesting METTL3 as a therapeutic target.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • N6-methyladenosine (m6A) is a key regulator of gene expression.
  • Its role in chemotherapy resistance, particularly in ovarian cancer, is not fully understood.
  • Platinum-based chemotherapy is a cornerstone treatment for ovarian cancer, but resistance remains a challenge.

Purpose of the Study:

  • To investigate the role of the m6A epitranscriptomic regulator METTL3 in platinum resistance in ovarian cancer.
  • To identify novel m6A-associated regulatory pathways involved in chemoresistance.
  • To evaluate METTL3 as a potential therapeutic target for overcoming platinum resistance.

Main Methods:

  • Analysis of m6A levels and METTL3 expression following cisplatin treatment in ovarian cancer cells.
  • Functional studies involving METTL3 knockdown, overexpression, and pharmacologic inhibition (STM2457).
  • Transcriptomic profiling to identify m6A-modified targets, including ADAM23.
  • In vitro and in vivo assessment of drug sensitivity and tumor response.

Main Results:

  • Cisplatin treatment increased global m6A levels and METTL3 expression in ovarian cancer cells.
  • METTL3 overexpression conferred cisplatin resistance, while METTL3 inhibition sensitized cells to platinum treatment.
  • ADAM23 was identified as a METTL3-dependent transcript, with its expression inversely correlated with METTL3 levels and platinum treatment.
  • METTL3 inhibition improved platinum response in vivo.

Conclusions:

  • METTL3-mediated m6A modification plays a significant role in platinum resistance in ovarian cancer.
  • The METTL3-ADAM23 axis is a key epitranscriptomic regulatory mechanism contributing to chemoresistance.
  • Targeting METTL3 presents a promising therapeutic strategy to enhance platinum efficacy in ovarian cancer.
Keywords:
ADAM23METTL3RNA methylationepitranscriptomicovarian cancerplatinum resistance

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