Quercetin enhances the effects of 5-fluorouracil-mediated growth inhibition and apoptosis of esophageal cancer cells by inhibiting NF-κB

被引:40
作者
Lu Chuang-Xin [1 ]
Wang Wen-Yu [1 ]
Cui Yao [1 ]
Li Xiao-Yan [1 ]
Zhou Yun [1 ]
机构
[1] Zhengzhou Univ, Henan Peoples Hosp, Dept Oncol, Zhengzhou 450003, Henan, Peoples R China
关键词
quercetin; 5-fluorouracil; esophageal cancer; NF-kappa B; CHEMOSENSITIVITY; CHEMOTHERAPY; INDUCTION; SENSITIVITY; SUPPRESSION; EXPRESSION; FLAVONOIDS; THERAPY;
D O I
10.3892/ol.2012.829
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Despite its limited success, 5-fluorouracil (5-FU) remains the primary chemotherapy agent for the treatment of esophageal cancer. Quercetin has been demonstrated to inhibit the growth of transformed cells. The present study was conducted to examine whether quercetin combined with conventional chemotherapeutic agents would improve the therapeutic strategy for esophageal cancer. In this study, an MTT assay was used to determine the effects of quercetin on the proliferation of EC9706 and Eca109 cells. Annexin V-FITC/propidium iodide (PI)-stained fluorescence-activated cell sorter (FACS) analysis was used to detect the apoptotic fraction of treated cells, and western blot analysis was used to examine the protein levels. The results of our study demonstrated that quercetin in combination with 5-FU significantly inhibited growth (P<0.05) and stimulated apoptosis (P<0.005) in EC9706 and Eca109 esophageal cancer cells compared with quercetin or 5-FU alone. These changes were associated with the decreased expression of a phosphorylated inhibitory molecule of NF-kappa B (pI kappa B alpha), which was activated by exposure to 5-FU alone. We suggest that inclusion of quercetin to the conventional chemotherapeutic agent 5-FU may be an effective therapeutic strategy for esophageal cancer.
引用
收藏
页码:775 / 778
页数:4
相关论文
共 27 条
[1]   Constitutively active NFκB is required for the survival of S-type neuroblastoma [J].
Bian, X ;
Opipari, AW ;
Ratanaproeksa, AB ;
Boitano, AE ;
Lucas, PC ;
Castle, VP .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (44) :42144-42150
[2]   Effects of structurally related flavonoids on cell cycle progression of human melanoma cells: regulation of cyclin-dependent kinases CDK2 and CDK1 [J].
Casagrande, F ;
Darbon, JM .
BIOCHEMICAL PHARMACOLOGY, 2001, 61 (10) :1205-1215
[3]   Tumor promoting or tumor suppressing of NF-κB, a matter of cell context dependency [J].
Chen, Fei ;
Beezhold, Kevin ;
Castranova, Vince .
INTERNATIONAL REVIEWS OF IMMUNOLOGY, 2008, 27 (04) :183-204
[4]   Molecular mechanisms in the antiproliferative action of quercetin [J].
Csokay, B ;
Prajda, N ;
Weber, G ;
Olah, E .
LIFE SCIENCES, 1997, 60 (24) :2157-2163
[5]  
Cusack JC, 2001, CANCER RES, V61, P3535
[6]   APOPTOSIS IN CANCER-THERAPY - CROSSING THE THRESHOLD [J].
FISHER, DE .
CELL, 1994, 78 (04) :539-542
[7]   Involvement of the CD95 (APO-1/Fas) receptor/ligand system in drug-induced apoptosis in leukemia cells [J].
Friesen, C ;
Herr, I ;
Krammer, PH ;
Debatin, KM .
NATURE MEDICINE, 1996, 2 (05) :574-577
[8]  
Fulda S, 1998, CANCER RES, V58, P4453
[9]   Cancer statistics, 2000 [J].
Greenlee, RT ;
Murray, T ;
Bolden, S ;
Wingo, PA .
CA-A CANCER JOURNAL FOR CLINICIANS, 2000, 50 (01) :7-33
[10]   The hallmarks of cancer [J].
Hanahan, D ;
Weinberg, RA .
CELL, 2000, 100 (01) :57-70