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Curcumin inhibits cell proliferation and migration in NSCLC through a synergistic effect on the TLR4/MyD88 and EGFR pathways.
Oncol Rep 2019OR

Abstract

Despite the increasing number of available therapeutic methods, the prognosis of non‑small cell lung cancer (NSCLC) remains poor. Furthermore, side effects are an important limiting factor in the treatment of NSCLC. Therefore, developing an efficacious, safe, affordable and easily accessible chemotherapeutic agent is necessary for NSCLC treatment. As a natural chemical produced by Zingiberaceae plants, curcumin exerts distinct antitumor effects on several tumor types. In the present study, curcumin was observed to inhibit not only cell proliferation and cell cycle transition, but also cell migration in NSCLC, as determined by a series of experiments (such as MTS assay, colony formation assay, flow cytometric analysis, Transwell migration assay and western blotting). Mechanistically, curcumin induced G2/M phase arrest by controlling cell cycle‑ and epithelial‑mesenchymal transition (EMT)‑related checkpoints. Furthermore, curcumin significantly inhibited the expression of Toll‑like receptor 4 (TLR4)/MyD88 and EGFR in a dose‑ and time‑dependent manner. Conversely, EGF reversed the inhibitory action of curcumin on TLR4/MyD88. In clinical specimens, TLR4 and MyD88 were highly expressed in NSCLC tissues, and a significant positive association was observed between TLR4 and MyD88 expression. These data suggested that curcumin may control the EGFR and TLR4/MyD88 pathways to synergistically downregulate downstream cell cycle‑ and EMT‑related regulators, in order to block cell proliferation and metastasis in NSCLC. These findings provide evidence for the clinical application of curcumin.

Authors+Show Affiliations

Cancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510315, P.R. China.Cancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510315, P.R. China.Department of Cancer Biotherapy Center, The Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province), Kunming, Yunnan 510118, P.R. China.Department of Cancer Biotherapy Center, The Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province), Kunming, Yunnan 510118, P.R. China.Department of Cancer Biotherapy Center, The Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province), Kunming, Yunnan 510118, P.R. China.Department of Cancer Biotherapy Center, The Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province), Kunming, Yunnan 510118, P.R. China.Department of Medical Oncology, The Central Hospital of Hengyang, Hengyang, Hunan 421000, P.R. China.Department of Cancer Biotherapy Center, The Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province), Kunming, Yunnan 510118, P.R. China.Department of Cancer Biotherapy Center, The Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province), Kunming, Yunnan 510118, P.R. China.Department of Cancer Biotherapy Center, The Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province), Kunming, Yunnan 510118, P.R. China.Department of Pathology, The Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province), Kunming, Yunnan 510118, P.R. China.Department of Cancer Biotherapy Center, The Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province), Kunming, Yunnan 510118, P.R. China.Central Laboratory of Yan'an Hospital Affiliated to Kunming Medical University, Kunming, Yunnan 650051, P.R. China.Department of Cancer Biotherapy Center, The Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province), Kunming, Yunnan 510118, P.R. China.Cancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510315, P.R. China.Cancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510315, P.R. China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31432177

Citation

Zhang, Lanfeng, et al. "Curcumin Inhibits Cell Proliferation and Migration in NSCLC Through a Synergistic Effect On the TLR4/MyD88 and EGFR Pathways." Oncology Reports, 2019.
Zhang L, Tao X, Fu Q, et al. Curcumin inhibits cell proliferation and migration in NSCLC through a synergistic effect on the TLR4/MyD88 and EGFR pathways. Oncol Rep. 2019.
Zhang, L., Tao, X., Fu, Q., Ge, C., Li, R., Li, Z., ... Song, X. (2019). Curcumin inhibits cell proliferation and migration in NSCLC through a synergistic effect on the TLR4/MyD88 and EGFR pathways. Oncology Reports, doi:10.3892/or.2019.7278.
Zhang L, et al. Curcumin Inhibits Cell Proliferation and Migration in NSCLC Through a Synergistic Effect On the TLR4/MyD88 and EGFR Pathways. Oncol Rep. 2019 Aug 14; PubMed PMID: 31432177.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Curcumin inhibits cell proliferation and migration in NSCLC through a synergistic effect on the TLR4/MyD88 and EGFR pathways. AU - Zhang,Lanfeng, AU - Tao,Xingyu, AU - Fu,Qiaofen, AU - Ge,Chunlei, AU - Li,Ruilei, AU - Li,Zhen, AU - Zhu,Ye, AU - Tian,Hui, AU - Li,Qiaolin, AU - Liu,Min, AU - Hu,Hongyan, AU - Zeng,Baozhen, AU - Lin,Zhuyin, AU - Li,Chunyan, AU - Luo,Rongcheng, AU - Song,Xin, Y1 - 2019/08/14/ PY - 2018/09/28/received PY - 2019/05/31/accepted PY - 2019/8/22/entrez JF - Oncology reports JO - Oncol. Rep. N2 - Despite the increasing number of available therapeutic methods, the prognosis of non‑small cell lung cancer (NSCLC) remains poor. Furthermore, side effects are an important limiting factor in the treatment of NSCLC. Therefore, developing an efficacious, safe, affordable and easily accessible chemotherapeutic agent is necessary for NSCLC treatment. As a natural chemical produced by Zingiberaceae plants, curcumin exerts distinct antitumor effects on several tumor types. In the present study, curcumin was observed to inhibit not only cell proliferation and cell cycle transition, but also cell migration in NSCLC, as determined by a series of experiments (such as MTS assay, colony formation assay, flow cytometric analysis, Transwell migration assay and western blotting). Mechanistically, curcumin induced G2/M phase arrest by controlling cell cycle‑ and epithelial‑mesenchymal transition (EMT)‑related checkpoints. Furthermore, curcumin significantly inhibited the expression of Toll‑like receptor 4 (TLR4)/MyD88 and EGFR in a dose‑ and time‑dependent manner. Conversely, EGF reversed the inhibitory action of curcumin on TLR4/MyD88. In clinical specimens, TLR4 and MyD88 were highly expressed in NSCLC tissues, and a significant positive association was observed between TLR4 and MyD88 expression. These data suggested that curcumin may control the EGFR and TLR4/MyD88 pathways to synergistically downregulate downstream cell cycle‑ and EMT‑related regulators, in order to block cell proliferation and metastasis in NSCLC. These findings provide evidence for the clinical application of curcumin. SN - 1791-2431 UR - https://www.unboundmedicine.com/medline/citation/31432177/Curcumin_inhibits_cell_proliferation_and_migration_in_NSCLC_through_a_synergistic_effect_on_the_TLR4/MyD88_and_EGFR_pathways L2 - http://www.spandidos-publications.com/10.3892/or.2019.7278 DB - PRIME DP - Unbound Medicine ER -