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Peer-reviewedCC BYArchives of pharmacal research

Targeting oral cancer with curcumin and its structural analogs: molecular mechanisms, pharmacokinetic optimization, and clinical translation.

  • Shih-Chi Su1,2
  • Chun-Wen Su3,4
  • Chia-Yi Lee3
  • Chiao-Wen Lin5,6
  • Shun-Fa Yang7,8
8 affiliations
  1. 1Whole-Genome Research Core Laboratory of Human Diseases, Chang Gung Memorial Hospital, Keelung, Taiwan.
  2. 2Department of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
  3. 3Institute of Medicine, Chung Shan Medical University, Taichung, 402, Taiwan.
  4. 4Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
  5. 5Institute of Oral Sciences, Chung Shan Medical University, Taichung, Taiwan. [email protected].
  6. 6Department of Dentistry, Chung Shan Medical University Hospital, Taichung, Taiwan. [email protected].
  7. 7Institute of Medicine, Chung Shan Medical University, Taichung, 402, Taiwan. [email protected].
  8. 8Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan. [email protected].
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Abstract

Curcumin is a naturally occurring polyphenol extracted from turmeric (Curcuma longa) and is known for its diverse biological functions, such as antioxidant, anti-inflammatory, anti-migratory, and anticancer activities. However, its use in clinical cancer treatment remains constrained due to challenges like limited absorption, rapid metabolic breakdown, a short half-life, and generally low bioavailability. To overcome these limitations, various curcumin analogs and formulation strategies have been developed to enhance its therapeutic efficacy. In oral cancer, a malignancy characterized by high recurrence rates, therapeutic resistance, and substantial treatment-related morbidity, novel multi-targeted and low-toxicity strategies remain urgently needed. Yet, the intersection between curcumin's pharmacological constraints and the specific therapeutic vulnerabilities of oral cancer has not been critically synthesized. This review addresses this gap by integrating pharmacokinetic limitations, molecular mechanisms of action, and disease-specific signaling dependencies in oral cancer. We systematically examine evidence demonstrating that curcumin and its derivatives suppress proliferation, invasion, metastasis, angiogenesis, and inflammatory signaling through modulation of pathways such as nuclear factor-κB (NF-κB), phosphoinositide 3-kinase (PI3K)/Akt, mitogen-activated protein kinase (MAPK), and apoptosis-related cascades. Importantly, we critically evaluate next-generation curcumin analogs and advanced delivery systems that are designed to overcome bioavailability barriers and enhance tumor-specific efficacy. Collectively, the available evidence positions curcumin as an investigational multi-target scaffold, with its clinical translation in oral cancer dependent on rational formulation strategies and rigorous validation. Bridging mechanistic insights with pharmacokinetic optimization and well-designed clinical trials will be essential to define the therapeutic value of optimized curcumin-based adjunctive approaches.

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Cite

BibTeXRIS
BibTeX
@article{su2026targeting,
  title = {{Targeting oral cancer with curcumin and its structural analogs: molecular mechanisms, pharmacokinetic optimization, and clinical translation.}},
  author = {Shih-Chi Su and Chun-Wen Su and Chia-Yi Lee and Chiao-Wen Lin and Shun-Fa Yang},
  journal = {Archives of pharmacal research},
  year = {2026},
  month = oct,
  doi = {10.1007/s12272-026-01635-8},
  url = {https://europepmc.org/article/MED/42836892},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Targeting oral cancer with curcumin and its structural analogs: molecular mechanisms, pharmacokinetic optimization, and clinical translation.
AU  - Shih-Chi Su
AU  - Chun-Wen Su
AU  - Chia-Yi Lee
AU  - Chiao-Wen Lin
AU  - Shun-Fa Yang
PY  - 2026
DA  - 2026/10/06
JO  - Archives of pharmacal research
DO  - 10.1007/s12272-026-01635-8
UR  - https://europepmc.org/article/MED/42836892
AB  - Curcumin is a naturally occurring polyphenol extracted from turmeric (Curcuma longa) and is known for its diverse biological functions, such as antioxidant, anti-inflammatory, anti-migratory, and anticancer activities. However, its use in clinical cancer treatment remains constrained due to challenges like limited absorption, rapid metabolic breakdown, a short half-life, and generally low bioavailability. To overcome these limitations, various curcumin analogs and formulation strategies have been developed to enhance its therapeutic efficacy. In oral cancer, a malignancy characterized by high recurrence rates, therapeutic resistance, and substantial treatment-related morbidity, novel multi-targeted and low-toxicity strategies remain urgently needed. Yet, the intersection between curcumin's pharmacological constraints and the specific therapeutic vulnerabilities of oral cancer has not been critically synthesized. This review addresses this gap by integrating pharmacokinetic limitations, molecular mechanisms of action, and disease-specific signaling dependencies in oral cancer. We systematically examine evidence demonstrating that curcumin and its derivatives suppress proliferation, invasion, metastasis, angiogenesis, and inflammatory signaling through modulation of pathways such as nuclear factor-κB (NF-κB), phosphoinositide 3-kinase (PI3K)/Akt, mitogen-activated protein kinase (MAPK), and apoptosis-related cascades. Importantly, we critically evaluate next-generation curcumin analogs and advanced delivery systems that are designed to overcome bioavailability barriers and enhance tumor-specific efficacy. Collectively, the available evidence positions curcumin as an investigational multi-target scaffold, with its clinical translation in oral cancer dependent on rational formulation strategies and rigorous validation. Bridging mechanistic insights with pharmacokinetic optimization and well-designed clinical trials will be essential to define the therapeutic value of optimized curcumin-based adjunctive approaches.
SN  - 0253-6269
SN  - 1976-3786
ER  -