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<p>This study investigated the regulatory role of CircCOG5 in the ferroptosis of ovarian cancer cells via the miR-532-3p/LPCAT3. The effects of CircCOG5 expression on proliferation, apoptosis, invasion, migration, oxidative stress, and ferroptosis of OVCAR-3 and SKOV3 cells were evaluated. CircCOG5 was lowly expressed in ovarian cancer tissues. Overexpression of CircCOG5 inhibited the proliferation, invasion, and migration of OVCAR-3 and SKOV3 cells, promoted cell oxidative stress, and aggravated apoptosis and ferroptosis. Dual luciferase assays confirmed the targeted regulation of CircCOG5 on miR-532-3p, with LPCAT3 identified as a direct target of miR-532-3p. Overexpression of CircCOG5 increased LPCAT3 expression by decreasing miR-532-3p expression in OVCAR-3 and SKOV3 cells, thereby promoting apoptosis, oxidative stress, and ferroptosis in OVCAR-3 and SKOV3 cells. Overexpression of miR-532-3p reversed the effect of overexpression of CircCOG5 on the proliferation, apoptosis, oxidative stress and ferroptosis of OVCAR-3 and SKOV3 cells. LPCAT3 overexpression antagonized the effects of miR-532-3p overexpression on the proliferation, apoptosis, oxidative stress, and ferroptosis of OVCAR-3 and SKOV3 cells. These findings suggested that CircCOG5 could modulate the ferroptosis of OVCAR-3 and SKOV3 cells through targeting regulation of miR-532-3p/LPCAT3. </p>

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The Role and Mechanism of CircCOG5 in Regulating Ferroptosis in Ovarian Cancer Cells by Targeting miR-532-3p/LPCAT3

  • 期刊论文

  • 发表日期：

    2025年7月10日

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  • Yongfeng Guo,
  • Min Wei,
  • Jingjing Fan,
  • Yulan Wang,
  • Jing Shi,
  • Jie Wang,
  • Na Lu,
  • Yuping Suo

摘要

This study investigated the regulatory role of CircCOG5 in the ferroptosis of ovarian cancer cells via the miR-532-3p/LPCAT3. The effects of CircCOG5 expression on proliferation, apoptosis, invasion, migration, oxidative stress, and ferroptosis of OVCAR-3 and SKOV3 cells were evaluated. CircCOG5 was lowly expressed in ovarian cancer tissues. Overexpression of CircCOG5 inhibited the proliferation, invasion, and migration of OVCAR-3 and SKOV3 cells, promoted cell oxidative stress, and aggravated apoptosis and ferroptosis. Dual luciferase assays confirmed the targeted regulation of CircCOG5 on miR-532-3p, with LPCAT3 identified as a direct target of miR-532-3p. Overexpression of CircCOG5 increased LPCAT3 expression by decreasing miR-532-3p expression in OVCAR-3 and SKOV3 cells, thereby promoting apoptosis, oxidative stress, and ferroptosis in OVCAR-3 and SKOV3 cells. Overexpression of miR-532-3p reversed the effect of overexpression of CircCOG5 on the proliferation, apoptosis, oxidative stress and ferroptosis of OVCAR-3 and SKOV3 cells. LPCAT3 overexpression antagonized the effects of miR-532-3p overexpression on the proliferation, apoptosis, oxidative stress, and ferroptosis of OVCAR-3 and SKOV3 cells. These findings suggested that CircCOG5 could modulate the ferroptosis of OVCAR-3 and SKOV3 cells through targeting regulation of miR-532-3p/LPCAT3.