Scholarlink

<p>Ovarian cancer is classified as a female malignancy commonly known as a silent killer with no early detection symptoms. Extracellular matrix protein 1 (ECM1) is associated with the Epithelial-mesenchymal transition (EMT) and metastasis process in different cancers. However, the function of ECM1 in mitochondrial dynamics in ovarian cancer is yet to be determined. Myricetin (MYR) is a flavonoid with medicinal impact on cell proliferation, inflammation, and metastasis. The role of MYR in influencing ECM1 levels to counter ovarian cancer remains unexplored. Chinese hamster ovary (CHO) cells are known to produce protein-based biotherapeutics for various diseases; here, CHO cell-derived extracellular vesicles (CE) can serve as a delivery vehicle of MYR in translational medicine. The current research focused on developing a Myricetin-loaded CHO cell-derived extracellular vesicles (CE + MYR) formulation to facilitate efficient delivery of MYR to target OVCAR3 tumor cells, thereby affecting the ECM1 signaling mechanism. An investigation was carried out to assess the cytotoxic effects of CE + MYR on ovarian cells using an MTT assay to compare the viability of normal CHO cells and the tumor OVCAR3 cells. A decrease in the viability of OVCAR3 cells was observed at IC50 42&#xa0;µM with MYR treatment and at 30&#xa0;µM with CE + MYR treatment, indicating the efficiency of CE in delivering MYR; nonetheless, CHO cells remained unaffected at these concentrations. There was an alteration in cell morphology, nuclear fragmentation, decreased migration, and lower mitochondrial membrane potential in the OVCAR3 cells, whereas the CHO cells remained unaffected. There were more apoptotic cells in tumor-treated cells. CE + MYR reduces the expression of ECM1, NF-κB, and TGFβ, whereas the expression of PTEN, p53, and caspases was enhanced. Myricetin inhibited mitochondrial fission (DRP1 and FIS1) and favored mitochondrial fusion (MFN1 and MFN2). Encapsulating myricetin in CE enhanced antitumor efficacy against ovarian cancer by suppressing proliferation and mitochondrial fission, thereby promoting mitochondrial fusion and apoptosis.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Extracellular vesicle delivery of Myricetin suppresses ovarian cancer through mitochondrial dynamics by downregulating the ECM1/NF-κB/TGFβ signaling pathway

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月16日

查看全文
  • Kaumudi Pande,
  • Sridevi Annapurna Singh,
  • Anbarasu Kannan

摘要

Ovarian cancer is classified as a female malignancy commonly known as a silent killer with no early detection symptoms. Extracellular matrix protein 1 (ECM1) is associated with the Epithelial-mesenchymal transition (EMT) and metastasis process in different cancers. However, the function of ECM1 in mitochondrial dynamics in ovarian cancer is yet to be determined. Myricetin (MYR) is a flavonoid with medicinal impact on cell proliferation, inflammation, and metastasis. The role of MYR in influencing ECM1 levels to counter ovarian cancer remains unexplored. Chinese hamster ovary (CHO) cells are known to produce protein-based biotherapeutics for various diseases; here, CHO cell-derived extracellular vesicles (CE) can serve as a delivery vehicle of MYR in translational medicine. The current research focused on developing a Myricetin-loaded CHO cell-derived extracellular vesicles (CE + MYR) formulation to facilitate efficient delivery of MYR to target OVCAR3 tumor cells, thereby affecting the ECM1 signaling mechanism. An investigation was carried out to assess the cytotoxic effects of CE + MYR on ovarian cells using an MTT assay to compare the viability of normal CHO cells and the tumor OVCAR3 cells. A decrease in the viability of OVCAR3 cells was observed at IC50 42 µM with MYR treatment and at 30 µM with CE + MYR treatment, indicating the efficiency of CE in delivering MYR; nonetheless, CHO cells remained unaffected at these concentrations. There was an alteration in cell morphology, nuclear fragmentation, decreased migration, and lower mitochondrial membrane potential in the OVCAR3 cells, whereas the CHO cells remained unaffected. There were more apoptotic cells in tumor-treated cells. CE + MYR reduces the expression of ECM1, NF-κB, and TGFβ, whereas the expression of PTEN, p53, and caspases was enhanced. Myricetin inhibited mitochondrial fission (DRP1 and FIS1) and favored mitochondrial fusion (MFN1 and MFN2). Encapsulating myricetin in CE enhanced antitumor efficacy against ovarian cancer by suppressing proliferation and mitochondrial fission, thereby promoting mitochondrial fusion and apoptosis.