Suppression of growth, migration and invasion of highly-metastatic human breast cancer cells by berbamine and its molecular mechanisms of action

Wang, Shan Shan; Liu, Qian; Zhang, Yingying; Liu, Ke-Xiang; Yu, Pengfei; Liu, Kun; Luan, Jinling; Duan, Huiying; Lu, Zhaoqiao; Wang, Fengfei; Wu, Erxi; Yagasaki, Kazumi; Zhang, Guoying

doi:10.1186/1476-4598-8-81

Cited by 116 publications

(107 citation statements)

References 45 publications

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“…Activation of p-Akt and the NF-jB/Bcl-2 pathway leads to inhibition of chemotherapy-induced apoptosis, which results in treatment resistance (Wang et al 1996). Our previous results confirmed that suppression of Akt and the NF-jB/Bcl-2 pathway by anticancer agents inhibited growth and induced apoptosis and cell cycle arrest in A549 cells and breast cancer MDA-MB-231 cells (Wang et al 2009;Yu et al 2009). In the present study, we indicated that bufalin and the inhibitor of PI3 K/Akt (LY294002) and of NF-jB (Bay) inhibited the A549 cell proliferation and the PI3 K/Akt and NF-jB pathway by suppressing the phosphorylation and expressions of Akt and NF-jB and activating the apoptotic pathway of Bcl-2/Bax-mitochondrial-caspase-3 in A549 cells.…”

Section: Bufalin Reduces the Receptor Phosphorylation And/or Protein supporting

confidence: 75%

“…Flow cytometry for cell cycle analysis and apoptosis These were done according to our published methods (Wang et al 2009;Yu et al 2009;Zhang et al 2000). In brief, A549 cells were treated for 48 h with bufalin at concentrations of 0, 2.5, 5, and 10 lM.…”

Section: Cell Culture and In Vitro Proliferation Assaymentioning

confidence: 99%

“…This was performed according to our published methods with some modifications (Wang et al 2009;Yu et al 2009;Zhang et al 2009). In brief, A549 cells were treated with bufalin (0, 2.5, 5 and 10 lM), or Ly294002 (LY, 50 lM), Bay (10 lM), PD98059 (PD, 7 lM), and SB203580 (SB, 50 lM).…”

Section: Western Blot Analysismentioning

confidence: 99%

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Effects of bufalin on the proliferation of human lung cancer cells and its molecular mechanisms of action

et al. 2010

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Bufalin, a naturally occurring small-molecule compound from Traditional Chinese Medicine (TCM) Chansu showed inhibitory effects against human prostate, hepatocellular, endometrial and ovarian cancer cells, and leukemia cells. However, whether or not bufalin has inhibitory activity against the proliferation of human non-small cell lung cancer (NSCLC) cells is unclear. The aim of this study is to study the effects of bufalin on the proliferation of NSCLC and its molecular mechanisms of action. The cancer cell proliferation was measured by MTT assay. The apoptosis and cell cycle distribution were analyzed by flow cytometry. The protein expressions and phosphorylation in the cancer cells were detected by Western blot analysis. In the present study, we have demonstrated that bufalin suppressed the proliferation of human NSCLC A549 cell line in time-and dosedependent manners. Bufalin induced the apoptosis and cell cycle arrest by affecting the protein expressions of Bcl-2/Bax, cytochrome c, caspase-3, PARP, p53, p21WAF1, cyclinD1, and COX-2 in A549 cells. In addition, bufalin reduced the protein levels of receptor expressions and/or phosphorylation of VEGFR1, VEGFR2, EGFR and/or c-Met in A549 cells. Furthermore, bufalin inhibited the protein expressions and phosphorylation of Akt, NF-jB, p44/42 MAPK (ERK1/2) and p38 MAPK in A549 cells. Our results suggest that bufalin inhibits the human lung cancer cell proliferation via VEGFR1/VEGFR2/EGFR/cMet-Akt/p44/42/p38-NF-jB signaling pathways; bufalin may have a wide therapeutic and/or adjuvant therapeutic application in the treatment of human NSCLC.

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Section: Bufalin Reduces the Receptor Phosphorylation And/or Protein supporting

confidence: 75%

Section: Cell Culture and In Vitro Proliferation Assaymentioning

confidence: 99%

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Effects of bufalin on the proliferation of human lung cancer cells and its molecular mechanisms of action

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“…Flow cytometry for cell cycle analysis and apoptosis These were done according to our published methods (Wang et al 2009;Yu et al 2009;Zhang et al 2000Zhang et al , 2012a. In brief, LLC cells were treated for 48 h with sodium valproate (VPA, 0.5 mM), coumarin-3-carboxylic acid (HCCA, 0.064 mM), or in combination of VPA (0.5 mM) and HCCA (0.064 mM).…”

Section: Cell Culture and In Vitro Proliferation Assaymentioning

confidence: 99%

Enhanced suppression of proliferation and migration in highly-metastatic lung cancer cells by combination of valproic acid and coumarin-3-carboxylic acid and its molecular mechanisms of action

et al. 2012

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Valproic acid (VPA) as a broad-spectrum inhibitor of histone deacetylase, has been used in cancer therapy. Recently, the combination of VPA with other anticancer agents has been considered as a useful and necessary strategy to inhibit tumor growth and progression. The coumarin derivates from natural plants have been shown to be the promising natural anticancer agents. However, no literature is available on the anticancer effects of the combination of VPA and coumarin-3-carboxylic acid (HCCA). Here we show that this combination significantly increases inhibitory effects against the proliferation and migration in highly-metastatic lung cancer cells by inducing apoptosis and cell cycle arrest as well as regulating related protein expressions. Our results indicate that this combination of VPA with HCCA not only enhances the protein levels of Bax, cytosolic cytochrome c, caspase-3 and PARP-1 but also reduces the protein expressions of Bcl-2, cyclin D1 and NF-jB as well as inhibits the phosphorylation and expressions of Akt, EGFR, VEGFR2 and c-Met in the cancer cells. Our results suggest that the combination of VPA with HCCA suppresses the proliferation and migration of lung cancer cells via EGFR/VEGFR2/c-Met-Akt-NFjB signaling pathways; this combination may have a wide therapeutic and/or adjuvant therapeutic application in the treatment of lung cancer.

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“…Two of the major biological characteristics of cancer cells are their unusual growth and metastasis, which combined is the major cause of morbidity and mortality in several patients with the disease [112]. Metastasis occurs in approximately half of the cases with apparently localized breast cancer, and death occurs in majority of the cases from the spreading of these cancer cells and their ultimate proliferation at secondary sites [113].…”

Section: Chapter 5 Novel Therapeutic Compound Suppresses Breast Tumomentioning

confidence: 99%

Inhibition of Breast Cancer Angiogenesis and Metastasis ay Targeting Hypoxia-Inducible Factor-1α

Madu¹

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DEDICATION"To (God) who is able to do immeasurably more than all we ask or imagine, according to his power that is at work within us"-Ephesians 3:20.And to my family-my wife, Pamela; and my children, Chinua and Elechi. For all you did to sustain my choice. Without you, this will not be.iv ACKNOWLEDGEMENTS I observe this dissertation today not as a completion of a search, but a celebration of success; symbolizing a temporary end as well as a beginning-signifying an achievement as well as triumph.This project culminating into this dissertation would not have been possible if it were not for the contributions and assistance I received from several people. In an attempt to express my appreciation, it will be very difficult to find words that have not already been used over again-a situation where statements will seem no longer sufficient and words inadequate. However I still wish to acknowledge the following persons who stood by me and contributed to make this long-nursed dream a reality.I would like thank my mentor, Dr Yi Lu, for the opportunity to work in his lab, and supervising this project. To my committee members, Dr Wei Li (for providing the compounds used in this project), Dr Leonard Lothstein (for his input, valuable discussions, and accessibility; for listening and reassuring), Dr Ram I Mahato (for his kind words of encouragement and permitting me to use his lab equipment), Dr Andrzej T Slominski (for his wise suggestions). Thank you for accepting to serve as members of this committee, your thoughtful criticism, and involvement during the course of this project. I would like to thank Dr liyuan Li for the lab training. I gratefully acknowledge Dr Pfeffer for his advice, and unending encouragement and support.My mother merits special thanks for her support and sacrifice through the years. So does my father-in-law, Obong Okon Mkpong, for his prayers and encouragement. Sufficient words fail me in expressing my gratitude to my wife, Eno-Obong Pamela, whose love, dedication, and relentless confidence in me was the driving force behind all of this. You are the bedrock upon which the past twelve years of my life have been built. My ambition was great, but your faith in me was greater. I love you dearly! To my children Chinua and Elechi, for their love, and understanding during the long years of my education, and sacrificially spending three summers with me in the lab-I promise, this is it! This project would never have been completed without the encouragement and devotion of all of you, and so many other family members and friends. In the words of President John F. Kennedy, "In your hands, more than mine, rest the final success of (my) course". Thank you! v ABSTRACTThe current clinical chemotherapy agents are not ideal for breast cancer as they are not curative, but only provide a modest extension of survival with sometimes a severely adverse effect on the patient's quality of life. There is, therefore, an urgent need to search for new and more effective anti-breast cancer drugs. However, the existing screening sy...

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Suppression of growth, migration and invasion of highly-metastatic human breast cancer cells by berbamine and its molecular mechanisms of action

Cited by 116 publications

References 45 publications

Effects of bufalin on the proliferation of human lung cancer cells and its molecular mechanisms of action

Effects of bufalin on the proliferation of human lung cancer cells and its molecular mechanisms of action

Enhanced suppression of proliferation and migration in highly-metastatic lung cancer cells by combination of valproic acid and coumarin-3-carboxylic acid and its molecular mechanisms of action

Inhibition of Breast Cancer Angiogenesis and Metastasis ay Targeting Hypoxia-Inducible Factor-1α

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