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<p>Palmitic acid (PA), a long-chain saturated fatty acid abundantly present in dietary lipids and endogenous metabolic pathways, has traditionally been associated with metabolic dysregulation. However, emerging experimental evidence has revealed a contrasting role for PA in cancer biology. This review critically summarizes recent <i>in vitro</i> and <i>in vivo</i> studies investigating the anticancer potential of PA across multiple malignancies, including gastric, breast, colorectal, prostate, and endometrial cancers. Accumulating data demonstrate that PA suppresses tumor cell proliferation, induces apoptosis and autophagy, and inhibits invasion and metastasis through modulation of key molecular pathways such as STAT3, PI3K/Akt, ER stress signaling, and cell cycle regulators. In addition, PA-based delivery systems and combination strategies have shown enhanced antitumor efficacy by promoting macrophage repolarization and improving chemotherapeutic outcomes. Despite these findings, the anticancer effects of PA appear to be highly context-dependent, influenced by concentration, exposure duration, and tumor type. Collectively, this review highlights the mechanistic basis and therapeutic relevance of PA in cancer models while emphasizing the need for careful interpretation and further validation before clinical translation.</p> Graphical abstract <p></p>

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Palmitic acid in cancer research: mechanistic insights from in vitro and in vivo studies

  • 期刊论文

  • 发表日期：

    2026年6月19日

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  • Muhammad Muzammil Nazir,
  • Sehrish Muzaffar,
  • Saima Muzammil,
  • Asma Ashraf

摘要

Palmitic acid (PA), a long-chain saturated fatty acid abundantly present in dietary lipids and endogenous metabolic pathways, has traditionally been associated with metabolic dysregulation. However, emerging experimental evidence has revealed a contrasting role for PA in cancer biology. This review critically summarizes recent in vitro and in vivo studies investigating the anticancer potential of PA across multiple malignancies, including gastric, breast, colorectal, prostate, and endometrial cancers. Accumulating data demonstrate that PA suppresses tumor cell proliferation, induces apoptosis and autophagy, and inhibits invasion and metastasis through modulation of key molecular pathways such as STAT3, PI3K/Akt, ER stress signaling, and cell cycle regulators. In addition, PA-based delivery systems and combination strategies have shown enhanced antitumor efficacy by promoting macrophage repolarization and improving chemotherapeutic outcomes. Despite these findings, the anticancer effects of PA appear to be highly context-dependent, influenced by concentration, exposure duration, and tumor type. Collectively, this review highlights the mechanistic basis and therapeutic relevance of PA in cancer models while emphasizing the need for careful interpretation and further validation before clinical translation.

Graphical abstract