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<p>Triple-negative breast cancer (TNBC) is a highly aggressive subtype with limited therapeutic options. An urgent need thus exists to develop novel therapeutic strategies to treat TNBC. We previously demonstrated that 1‑palmitoyl‑4‑piperidinopiperidine (PPI), a derivative of palmitic acid, exerts anticancer effects against human colon carcinoma cells and human pancreatic ductal adenocarcinoma cells by inhibiting signal transducer and activator of transcription 3 (STAT3) phosphorylation. To date, no studies have assessed PPI potency in murine TNBC EO771 cells. We examined cell viability after treatment with PPI for 48&#xa0;h, and evaluated the expression levels of apoptosis- and cell cycle-related proteins using immunocytochemistry and western blotting. PPI inhibited cell proliferation in a dose-dependent manner, with an IC<sub>50</sub> of 3.06&#xa0;µM. PPI treatment was found to induce apoptosis. We also observed G1 cell cycle arrest as indicated by cyclin D1 and Cdk2 downregulation. Phosphorylated STAT3 levels and those of downstream proteins including CXCR4, MMP2, MMP9, TWIST, VEGF, and Vimentin, decreased following PPI treatment. STAT3 knockdown modestly reduced the sensitivity of EO771 cells to PPI, supporting partial involvement of STAT3 signaling in the anticancer effects of PPI. These results suggest that PPI exerts anticancer effects on EO771 cells that are associated with suppression of STAT3 signaling.</p>

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1-Palmitoyl-4-piperidinopiperidine exhibits anticancer effects in murine triple-negative breast cancer EO771 cells associated with STAT3 signaling suppression

  • 期刊论文

  • 发表日期：

    2026年7月4日

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  • Hiroki Yoshioka,
  • Junya Hamanaka,
  • Ayane Horiuchi,
  • Hanane Horita,
  • Rion Uno,
  • Azumi Noguchi,
  • Yuki Matsushita,
  • Masumi Suzui

摘要

Triple-negative breast cancer (TNBC) is a highly aggressive subtype with limited therapeutic options. An urgent need thus exists to develop novel therapeutic strategies to treat TNBC. We previously demonstrated that 1‑palmitoyl‑4‑piperidinopiperidine (PPI), a derivative of palmitic acid, exerts anticancer effects against human colon carcinoma cells and human pancreatic ductal adenocarcinoma cells by inhibiting signal transducer and activator of transcription 3 (STAT3) phosphorylation. To date, no studies have assessed PPI potency in murine TNBC EO771 cells. We examined cell viability after treatment with PPI for 48 h, and evaluated the expression levels of apoptosis- and cell cycle-related proteins using immunocytochemistry and western blotting. PPI inhibited cell proliferation in a dose-dependent manner, with an IC50 of 3.06 µM. PPI treatment was found to induce apoptosis. We also observed G1 cell cycle arrest as indicated by cyclin D1 and Cdk2 downregulation. Phosphorylated STAT3 levels and those of downstream proteins including CXCR4, MMP2, MMP9, TWIST, VEGF, and Vimentin, decreased following PPI treatment. STAT3 knockdown modestly reduced the sensitivity of EO771 cells to PPI, supporting partial involvement of STAT3 signaling in the anticancer effects of PPI. These results suggest that PPI exerts anticancer effects on EO771 cells that are associated with suppression of STAT3 signaling.