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<p>This study investigated whether the microrchidia family CW-type zinc finger 2(MORC2) decreases cellular response to paclitaxel by modulating glycolysis in ovarian cancer.&#xa0;In resistant ovarian cancer cell sublines for paclitaxel, including A2780/Taxol and SKOV3/Taxol, and parental cell lines, including A2780 and SKOV3, the differential expression of MORC2 was confirmed via qRT-PCR at the mRNA level and through western blot analysis at the protein level. shRNA interference was used to downregulate MORC2 in paclitaxel-resistant cells, and the actions of MORC2 reduction on paclitaxel resistance, cell cycle distribution, the uptake of glucose, and lactate production were investigated.&#xa0;As shown in A2780/Taxol and SKOV3/Taxol cells, MORC2 was highly expressed, and MORC2 protein expression was related to the time and concentration of paclitaxel. MORC2 downregulation made paclitaxel-resistant ovarian cancer cells more sensitive to paclitaxel, which indicated that more cells were arrested at the G0/G1 phase, suppressed glucose metabolism-related indicators (GLUT4, LDHA, and HK2). MORC2 knockdown reduced tumor growth and glycolysis, and enhanced paclitaxel sensitivity in vivo.&#xa0;These findings suggest MORC2 is upregulated in paclitaxel-resistant ovarian cancer cells, and that downregulation of MORC2 may reduce glycolysis and improve sensitivity to paclitaxel should be further examined.</p>

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The impact of MORC2 on glycolysis and the responsiveness of paclitaxel-resistant ovarian cancer cells

  • 期刊论文

  • 发表日期：

    2025年11月8日

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  • Na Dong,
  • Peng Lei,
  • Huilan Cai,
  • Ling Shi,
  • Lu Huang

摘要

This study investigated whether the microrchidia family CW-type zinc finger 2(MORC2) decreases cellular response to paclitaxel by modulating glycolysis in ovarian cancer. In resistant ovarian cancer cell sublines for paclitaxel, including A2780/Taxol and SKOV3/Taxol, and parental cell lines, including A2780 and SKOV3, the differential expression of MORC2 was confirmed via qRT-PCR at the mRNA level and through western blot analysis at the protein level. shRNA interference was used to downregulate MORC2 in paclitaxel-resistant cells, and the actions of MORC2 reduction on paclitaxel resistance, cell cycle distribution, the uptake of glucose, and lactate production were investigated. As shown in A2780/Taxol and SKOV3/Taxol cells, MORC2 was highly expressed, and MORC2 protein expression was related to the time and concentration of paclitaxel. MORC2 downregulation made paclitaxel-resistant ovarian cancer cells more sensitive to paclitaxel, which indicated that more cells were arrested at the G0/G1 phase, suppressed glucose metabolism-related indicators (GLUT4, LDHA, and HK2). MORC2 knockdown reduced tumor growth and glycolysis, and enhanced paclitaxel sensitivity in vivo. These findings suggest MORC2 is upregulated in paclitaxel-resistant ovarian cancer cells, and that downregulation of MORC2 may reduce glycolysis and improve sensitivity to paclitaxel should be further examined.