2. Academic Validation
  3. Luteolin combined with low-dose paclitaxel synergistically inhibits epithelial-mesenchymal transition and induces cell apoptosis on esophageal carcinoma in vitro and in vivo

Luteolin combined with low-dose paclitaxel synergistically inhibits epithelial-mesenchymal transition and induces cell apoptosis on esophageal carcinoma in vitro and in vivo

  • Phytother Res. 2021 Nov;35(11):6228-6240. doi: 10.1002/ptr.7267.
Tiantian Qin 1 2 3,  Jinzhu Zhao 1 2 3,  Xiaojie Liu 1 2 3,  Leilei Li 1 2 3,  Xueyan Zhang 1 2 3,  Xiaoli Shi 4,  Yu Ke 1 2 3,  Weihua Liu 1 2 3,  Junfeng Huo 1 2 3,  Yalong Dong 1 2 3,  Yiwei Shen 1,  Yanyu Li 1,  Mingjing He 1,  Shuhua Han 1,  Linlin Li 1,  Chengxue Pan 1 2 3,  Cong Wang 1 2 3
Affiliations

Affiliations

  • 1 School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, China.
  • 2 State Key Laboratory of Esophageal Cancer Prevention and treatment, Zhengzhou, China.
  • 3 Key Laboratory of Advanced Drug Preparation Technologies, Ministry of Education of China, Zhengzhou, China.
  • 4 Department of Pharmacy, The Affiliated Hospital of Qingdao University, Qingdao, China.
PMID: 34494324 DOI: 10.1002/ptr.7267
Abstract

Although paclitaxel is a promising frontline chemotherapy agent for various malignancies, the clinical applications have been restricted by side effects, drug resistance, and Cancer metastasis. The combination of paclitaxel and other agents could be the promising strategies against malignant tumor, which enhances the antitumor effect through synergistic effects, reduces required drug concentrations, and also suppresses tumorigenesis in multiple ways. In this study, we found that luteolin, a natural flavonoid compound, combined with low-dose paclitaxel synergistically regulated the proliferation, migration, epithelial-mesenchymal transition (EMT), and Apoptosis of esophageal Cancer cells in vitro, as well as synergistically inhibited tumor growth without obvious toxicity in vivo. The molecular mechanism of inhibiting cell migration and EMT processes may be related to the inhibition of SIRT1, and the mechanism of Apoptosis induction is associated with the Reactive Oxygen Species (ROS)/c-Jun N-terminal kinase (JNK) pathway-mediated activation of mitochondrial apoptotic pathway.

Keywords

EMT; apoptosis; esophageal carcinoma; luteolin; paclitaxel.

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