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已发表论文
番茄红素通过抑制 PI3K/Akt 信号通路并逆转上皮-间质转化增强口腔鳞状细胞癌对顺铂的敏感性
Authors Wang R, Lu X, Yu R, Shan Z
Received 21 August 2025
Accepted for publication 19 January 2026
Published 13 February 2026 Volume 2026:20 557101
DOI https://doi.org/10.2147/DDDT.S557101
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Leonidas D. Panos
Ran Wang,1,2,* Xinxing Lu,3,* Riyue Yu,2 Zhaochen Shan1
1Outpatient Department of Oral and Maxillofacial Surgery, School of Stomatology, Capital Medical University, Beijing, People’s Republic of China; 2Department of Stomatology, Beijing Shijitan Hospital, Capital Medical University, Beijing, People’s Republic of China; 3Gastrointestinal Cancer Center, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute, Beijing, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Zhaochen Shan, Outpatient Department of Oral and Maxillofacial Surgery, School of Stomatology, Capital Medical University, Beijing, 100071, People’s Republic of China, Email shanzhch629@163.com
Background: Cisplatin-based chemotherapy for oral squamous cell carcinoma (OSCC) is limited by intrinsic inefficacy and toxicity. Lycopene, a natural carotenoid, may enhance cisplatin’s therapeutic potential.
Objective: To explore lycopene’s chemo-sensitizing effects on cisplatin and its mechanisms in OSCC.
Methods: In vitro, CAL-27/SCC-9 cells were treated with lycopene and/or cisplatin; cell viability, colony formation, migration, invasion, and apoptosis were detected, and protein expression of MRP-1, PI3K/Akt/mTOR pathway components, and EMT markers was analyzed by Western blot. In vivo, a nude mouse xenograft model was used to verify the combination’s effect on tumor growth.
Results: Compared with cisplatin alone, the lycopene-cisplatin combination significantly inhibited OSCC cell proliferation, colony formation, migration, and invasion, while promoting apoptosis. Mechanistically, lycopene reversed cisplatin-induced upregulation of MRP-1 and activation of the PI3K/Akt/mTOR pathway, and restored cisplatin-suppressed E-cadherin while reducing N-cadherin and EpCAM. In vivo, the combination reduced tumor growth vs cisplatin alone without increasing toxicity.
Conclusion: This is the first report that lycopene enhances cisplatin sensitivity in OSCC by coupling inhibition of MRP-1-mediated drug efflux with suppression of PI3K/Akt/mTOR and EMT/stemness—filling the gap of lycopene’s synergistic mechanism with cisplatin, offering a strategy to improve therapeutic efficacy without exacerbating toxicity.
Keywords: oral squamous cell carcinoma, lycopene, cisplatin, chemoresistance, PI3K/Akt pathway
1Outpatient Department of Oral and Maxillofacial Surgery, School of Stomatology, Capital Medical University, Beijing, People’s Republic of China; 2Department of Stomatology, Beijing Shijitan Hospital, Capital Medical University, Beijing, People’s Republic of China; 3Gastrointestinal Cancer Center, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute, Beijing, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Zhaochen Shan, Outpatient Department of Oral and Maxillofacial Surgery, School of Stomatology, Capital Medical University, Beijing, 100071, People’s Republic of China, Email shanzhch629@163.com
Background: Cisplatin-based chemotherapy for oral squamous cell carcinoma (OSCC) is limited by intrinsic inefficacy and toxicity. Lycopene, a natural carotenoid, may enhance cisplatin’s therapeutic potential.
Objective: To explore lycopene’s chemo-sensitizing effects on cisplatin and its mechanisms in OSCC.
Methods: In vitro, CAL-27/SCC-9 cells were treated with lycopene and/or cisplatin; cell viability, colony formation, migration, invasion, and apoptosis were detected, and protein expression of MRP-1, PI3K/Akt/mTOR pathway components, and EMT markers was analyzed by Western blot. In vivo, a nude mouse xenograft model was used to verify the combination’s effect on tumor growth.
Results: Compared with cisplatin alone, the lycopene-cisplatin combination significantly inhibited OSCC cell proliferation, colony formation, migration, and invasion, while promoting apoptosis. Mechanistically, lycopene reversed cisplatin-induced upregulation of MRP-1 and activation of the PI3K/Akt/mTOR pathway, and restored cisplatin-suppressed E-cadherin while reducing N-cadherin and EpCAM. In vivo, the combination reduced tumor growth vs cisplatin alone without increasing toxicity.
Conclusion: This is the first report that lycopene enhances cisplatin sensitivity in OSCC by coupling inhibition of MRP-1-mediated drug efflux with suppression of PI3K/Akt/mTOR and EMT/stemness—filling the gap of lycopene’s synergistic mechanism with cisplatin, offering a strategy to improve therapeutic efficacy without exacerbating toxicity.
Keywords: oral squamous cell carcinoma, lycopene, cisplatin, chemoresistance, PI3K/Akt pathway