2017
DOI: 10.1016/j.canlet.2017.06.014
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Bruceine D inhibits hepatocellular carcinoma growth by targeting β-catenin/jagged1 pathways

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Cited by 38 publications
(42 citation statements)
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“…In addition, p38-MAPK pathway activation and NF-kappaB inhibition were crucial for BD-mediated pancreatic cell death 9 . Furthermore, BD suppressed hepatocellular carcinoma growth in vivo and in vitro by diminishing Wnt translation activity 10 . Although the antitumor activity of BD has been reported in many studies, the exact mechanisms have not yet been demonstrated, particularly the mechanisms involved in BD-induced lung cancer cell proliferation inhibition.…”
Section: Introductionmentioning
confidence: 99%
“…In addition, p38-MAPK pathway activation and NF-kappaB inhibition were crucial for BD-mediated pancreatic cell death 9 . Furthermore, BD suppressed hepatocellular carcinoma growth in vivo and in vitro by diminishing Wnt translation activity 10 . Although the antitumor activity of BD has been reported in many studies, the exact mechanisms have not yet been demonstrated, particularly the mechanisms involved in BD-induced lung cancer cell proliferation inhibition.…”
Section: Introductionmentioning
confidence: 99%
“…Several studies have shown that BD exhibits numerous pharmacological traits including anti‐inflammatory, anti‐parasitic, and hypoglycemic activities . Furthermore, BD exhibits significant anti‐tumor activity in pancreatic cancer, human chronic myeloid leukemia, and hepatocellular carcinoma . However, the underlying mechanism of action of BD on osteosarcoma remains unclear.…”
Section: Introductionmentioning
confidence: 99%
“…17 Furthermore, BD exhibits significant anti-tumor activity in pancreatic cancer, 18 human chronic myeloid leukemia, 19 and hepatocellular carcinoma. 20 However, the underlying mechanism of action of BD on osteosarcoma remains unclear. Therefore, this study was designed to explore the role of BD on osteosarcoma in vitro and in vivo, to evaluate the underlying mechanism, and demonstrate its potential as a therapeutic candidate for osteosarcoma treatment.…”
mentioning
confidence: 99%
“…It is known that dysregulation of cell cycle leading to uncontrolled cell proliferation and apoptosis evasion are hallmarks of all cancer cell types [29,[38][39][40][41]. Indeed, through various cell proliferation assays like Sulforhodamine B assay, MTT assay, and Cell Counting Kit 8 assay, BD has been established to exhibit anti-proliferative properties against pancreatic cancer cells (PANC-1, SW1990, CAPAN-1) [29,37], lung cancer cells [A549, NCI-H292, non-small cell lung cancer (NSCLC) H460] [28,42,43], chronic myeloid leukemia (K562) [44], breast cancer cells (MDA-MB-231) [30], hepatocellular carcinoma cells (Bel7404, HepG2, Hep3B, Huh7, PLC) [45,46], and osteosarcoma cells (MNNG/HOS, U-2OS, MG-63, Saos-2) [47]. In all of the investigated cancer cell lines, there was increased activation of pro-apoptotic proteins like B-cell lymphoma 2 (Bcl-2) associated protein (Bax) and Bak and downregulation of anti-apoptotic proteins like Bcl-2 and myeloid cell leukemia 1 (Mcl-1) [48], all of which are tightly linked to cellular proliferation and apoptotic pathways like phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of Rapamycin (mTOR), c-Jun N-terminal kinase (JNK), mitogen-activated protein kinases (MAPK), and canonical Wnt signaling pathways ( Figure 1) [49][50][51][52].…”
Section: Anti-proliferative and Pro-apoptotic Effects Of Bdmentioning
confidence: 99%