Honokiol induces apoptosis through p53-independent pathway in human colorectal cell line RKO

Wang, Tao; Chen, Fei; Chen, Zhe; Wu, Yifeng; Xu, Xiu; Hu, Xun

doi:10.3748/wjg.v10.i15.2205

Cited by 108 publications

(91 citation statements)

References 21 publications

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“…Growth inhibition was observed in all breast cancer cell lines tested, regardless of their HR, HER2 or p53 status, but it was not observed for glioblastoma multiforme cells. Similar to other tumors (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20), our studies revealed LC50 at a range of 29-50 μM for breast cancer cell lines. Of interest, the lowest LC50 values were observed for the HR-negative, p53-mutated MDA-MB-231 and SK-BR-3 cell lines.…”

Section: Discussionsupporting

confidence: 56%

“…HNK stimulated cleavage of PARP and upregulation of expression of BAX, but did not affect levels of BAD or Bcl-2. Upregulation of BAX was also observed in B-CLL following HNK treatment, while upregulation of Bad was observed in colon and lung cancers (10,11,14,15). Thus, HNK may be involved in the activation of different members of the Bcl-2 family in different tumors.…”

Section: Discussionmentioning

confidence: 86%

“…In the promyelocytic cell line HL-60, HNK induces differentiation, and shows cytostatic activity (7)(8)(9), and in B-cell chronic lymphocytic leukemia (B-CLL) and multiple myeloma, it induces caspase-dependent and -independent apoptosis, enhances cell kill and overcomes resistance to cytotoxic chemotherapy (10)(11)(12). HNK was also shown to have potent cytotoxic activities against colon and lung cancers, hepatoma and skin tumors (13)(14)(15)(16)(17). Interestingly, HNK has also been shown recently to overcome the multidrug resistance (MDR) of the breast cancer cell line MCF-7/ ADR (18).…”

Section: Introductionmentioning

confidence: 99%

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Honokiol, a natural biphenyl, inhibits in vitro and in vivo growth of breast cancer through induction of apoptosis and cell cycle arrest

Wolf¹,

O’Kelly

Wakimoto

et al. 2007

Int J Oncol

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Abstract. Honokiol (HNK), a naturally occurring biphenyl, possesses potent antineoplastic and antiangiogenic properties. We investigated the in vitro and in vivo activity of HNK against breast cancer. HNK exhibited potent anti-proliferative activity against breast cancer cell lines and enhanced the activity of other drugs used for the treatment of breast cancer. In vivo, HNK was highly effective against breast cancer in nude mice. We identified two different effects of HNK on breast cancer cells: cell cycle inhibition, observed at lower doses of HNK, and induction of apoptosis, observed at higher doses of the compound. Our data suggest that HNK is a systemically available, non-toxic inhibitor of breast cancer growth and should be examined for clinical applications.

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Section: Discussionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 86%

Section: Introductionmentioning

confidence: 99%

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Honokiol, a natural biphenyl, inhibits in vitro and in vivo growth of breast cancer through induction of apoptosis and cell cycle arrest

Wolf¹,

O’Kelly

Wakimoto

et al. 2007

Int J Oncol

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“…This is consistent with other studies showing that M. officinalis extract treatment induces cell growth inhibition in several cell lines (24,25,35). The inhibition was due to cell cycle arrest in G1 phase.…”

Section: Discussionsupporting

confidence: 82%

Aqueous extract of Magnolia officinalis mediates proliferative capacity, p21WAF1 expression and TNF-α-induced NF-κB activity in human urinary bladder cancer 5637 cells; involvement of p38 MAP kinase

Lee¹,

Kim²,

Cho³

et al. 2007

Oncol Rep

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Abstract. Magnolia officinalis is a commonly used herb in East Asian countries and has multiple pharmacological effects. Although Magnolia officinalis has a variety of pharmacological effects on certain cancer cell types, the molecular mechanisms on urinary bladder cancer are unclear. An aqueous extract of M. officinalis inhibited cell proliferation in cultured human urinary bladder cancer 5637 cells. Inhibition of proliferation was associated with G1 cell cycle arrest. Treatment with M. officinalis extract blocked the cell cycle in the G1 phase, down-regulated the expression of cyclins and CDKs and up-regulated the expressions of p21WAF1 and p27 Kip1, which are CDK inhibitors. In addition, M. officinalis extract induced a marked activation of p38 MAP kinase and JNK. SB203580, a p38 MAP kinase specific inhibitor, blocked the expression of M. officinalis extract-dependent p38 MAP kinase and p21WAF1. Blockage of the p38 MAPK kinase function reversed M. officinalis extract-induced cell proliferation. These data demonstrate that M. officinalis extractinduced cell growth inhibition appears to be linked to the activation of p38 MAP kinase through p21WAF1 expression. Moreover, treatment of 5637 cells with M. officinalis extract suppressed constitutive and TNF-α-induced-nuclear factor-κ B (NF-κB) activation. Furthermore, the transactivation of TNF-α-stimulated NF-κB was inhibited by SB203580 treatment. Collectively, these results suggest that the p38 MAP kinase pathway contributes, at least partially, to the anti-cancer activity of M. officinalis extract in human urinary bladder tumor 5637 cells. IntroductionThe p38 MAP kinase is one of at least three mammalian MAPKs [the other two being extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase/stress activated protein kinase (JNK/SAPK)] that are activated by three homologous but distinct signaling pathways (1,2). The activation is effected by dual Ser/Thr and tyrosine phosphorylation that is catalyzed by a specific upstream MAPK kinase. Proliferative potential can be regulated by various signals, blocking growth or inducing apoptosis (3). JNK and p38 MAP kinase are known examples of such stress-activated protein kinases, because they are strongly activated in response to stressful stimuli. The p38 MAP kinase has been linked to apoptosis, proliferation and differentiation (2-5).The molecular and genetic alterations that precede morphologic changes and are responsible for tumorigenesis and progression of bladder cancer also include alterations in cell cycle regulators causing uncontrolled cancer growth. Cell proliferation depends on an ordered and tightly regulated process known as the cell cycle, involving multiple checkpoints assessing extracellular growth signals, cell size and DNA integrity (6). In general, the progression of the cell cycle in eukaryotes is a complex process including resting G0 phase and cell growth involving G1, S and G2/M phases ONCOLOGY REPORTS 18: 729-736, 2007 Abbreviations: p38 MAP kinase, p38 mitogen activated protein kinase...

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“…Previous reports have demonstrated that honokiol induces cell apoptosis in several cell lines, such as leukemia cell lines HL-60, colon cancer cell lines RKO, lung cancer cell lines A549 and CH27. [9][10][11][12][13][14] It also has remarkable in vivo antitumor activities in tumor mouse models. 15 Honokiol has demonstrated potent antiangiogenic and antitumor properties against aggressive angiosarcoma by blocking of VEGF-induced VEGF receptor 2 autophosphorylation.…”

mentioning

confidence: 99%

Liposomal honokiol inhibits VEGF‐D‐induced lymphangiogenesis and metastasis in xenograft tumor model

Wen

Chen

et al. 2009

Intl Journal of Cancer

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Lymph nodes metastasis of tumor could be a crucial early step in the metastatic process. Induction of tumor lymphangiogenesis by vascular endothelial growth factor-D may play an important role in promoting tumor metastasis to regional lymph nodes and these processes can be inhibited by inactivation of the VEGFR-3 signaling pathway. Honokiol has been reported to possess potent antiangiogenesis and antitumor properties in several cell lines and xenograft tumor models. However, its role in tumor-associated lymphangiogenesis and lymphatic metastasis remains unclear. Here, we established lymph node metastasis models by injecting overexpressing VEGF-D Lewis lung carcinoma cells into C57BL/6 mice to explore the effect of honokiol on tumor-associated lymphangiogenesis and related lymph node metastasis. The underlying mechanisms were systematically investigated in vitro and in vivo. In in vivo study, liposomal honokiol significantly inhibited the tumor-associated lymphangiogenesis and metastasis in Lewis lung carcinoma model. A remarkable delay of tumor growth and prolonged life span were also observed. In in vitro study, honokiol inhibited VEGF-D-induced survival, proliferation and tube-formation of both human umbilical vein endothelial cells (HUVECs) and lymphatic vascular endothelial cells (HLECs). Western blotting analysis showed that liposomal honokiol-inhibited Akt and MAPK phosphorylation in 2 endothelial cells, and downregulated expressions of VEGFR-2 of human vascular endothelial cells and VEGFR-3 of lymphatic endothelial cells. Thus, we identified for the first time that honokiol provided therapeutic benefit not only by direct effects on tumor cells and antiangiogenesis but also by inhibiting lymphangiogenesis and metastasis via the VEGFR-3 pathway. The present findings may be of importance to investigate the molecular mechanisms underlying the spread of cancer via the lymphatics and explore the therapeutical strategy of honokiol on antilymphangiogenesis and antimetastasis.

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Honokiol induces apoptosis through p53-independent pathway in human colorectal cell line RKO

Abstract: Honokiol can induce RKO cells apoptosis through activating caspase cascade by p53-indepenent pathway.

Cited by 108 publications

References 21 publications

Honokiol, a natural biphenyl, inhibits in vitro and in vivo growth of breast cancer through induction of apoptosis and cell cycle arrest

Honokiol, a natural biphenyl, inhibits in vitro and in vivo growth of breast cancer through induction of apoptosis and cell cycle arrest

Aqueous extract of Magnolia officinalis mediates proliferative capacity, p21WAF1 expression and TNF-α-induced NF-κB activity in human urinary bladder cancer 5637 cells; involvement of p38 MAP kinase

Liposomal honokiol inhibits VEGF‐D‐induced lymphangiogenesis and metastasis in xenograft tumor model

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