Down-Regulation of Human Epidermal Growth Factor Receptor 2/neu Oncogene by Corosolic Acid Induces Cell Cycle Arrest and Apoptosis in NCI-N87 Human Gastric Cancer Cells

Lee, Myung Sun; Young, Eun; Thương, Phương Thiện; Kim, Ji Yeon; Ahn, Moonsang; Sul, Ji Young

doi:10.1248/bpb.33.931

Cited by 33 publications

(34 citation statements)

References 34 publications

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“…Namely, ATSCs promote and suppress the growth/invasion and the apoptosis of the cancer cells, respectively, enabling them to activate MAPK (pERK-1/2). Notably, ATSCs cause the cancer cells to inhibit the expression of HER2, which is a key molecule for the molecular-targeted therapy of advanced gastric cancer (Lee et al 2010). In turn, gastric cancer cell types induce the cancer-associated myofibroblast phenotype in ATSCs.…”

Section: Discussionmentioning

confidence: 99%

Interaction between adipose tissue stromal cells and gastric cancer cells in vitro

et al. 2011

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Adipose tissue exists in the gastric submucosa and subserosa. Thus, adipose tissue stromal cells (ATSCs), which include mesenchymal stem cells (MSCs), seem critical for the progression of gastric cancer but their interaction with the cancer cells is unknown. We demonstrated an interaction between these cells, using immunohistochemistry, Western blot and the collagen gel invasion assay system, in which the adenocarcinoma cells (well and poorly differentiated types, MKN28 and MKN45, respectively) were cultured on a ATSC-embedded or ATSC-non-embedded gel. ATSCs promoted the expression of the growth marker, proliferation cell nuclear antigen but inhibited that of the apoptosis marker, single-stranded DNA, in the cancer cell types. ATSCs accelerated the invasion of only MKN28 into the gel and promoted the expression of mitogen-activated protein kinase (MAPK, pERK-1/2) but decreased that of the molecularly targeted protein, HER2, in the cancer cells. ATSCs did not affect the expression of the prostaglandin biosynthetic enzyme cyclooxgenase-2 (COX-2) in the cancer cells. The COX-2 inhibitor celecoxib did not affect the morphology or invasion of the cancer cells. The cancer cell types in turn promoted the display of the myofibroblast marker, α-smooth muscle actin, whereas they decreased that of some MSC markers, e.g., CD44 and CD105, in ATSCs. The data suggest that (1) ATSCs influence the progression of gastric cancer by increasing their growth/invasion and decreasing their apoptosis through MAPK activation in a COX-2-independent way; (2) ATSCs adversely affect HER2-targeted therapy; (3) the cancer cells induce the cancer-associated myofibroblast phenotype in ATSCs.

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Section: Discussionmentioning

confidence: 99%

Interaction between adipose tissue stromal cells and gastric cancer cells in vitro

et al. 2011

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“…UA acts through multiple pathways, such as induction of apoptosis (Choi et al, 2000); activation of c-Jun N-terminal kinase (JNK) (Zhang et al, 2010); induction of Ca 2+ release (Baek et al, 1997); and attenuation of the activities of nuclear factor-jB (NF-jB) (Shishodia et al, 2003), and signal transducer and activator of transcription-3 (STAT-3) (Pathak et al, 2007). CA also modulates a wide array of signal transduction pathways, including STAT-3, protein kinase C (PKC), and the epidermal growth factor receptor (HER-2) (Fujiwara et al, 2011;Lee et al, 2010;Ahn et al, 1998). In the present study, we identified UA and its natural derivative CA as antagonists of the Wnt/b-catenin pathway.…”

Section: Introductionmentioning

confidence: 99%

Ursolic acid and its natural derivative corosolic acid suppress the proliferation of APC-mutated colon cancer cells through promotion of β-catenin degradation

Kim

Song

et al. 2014

Food and Chemical Toxicology

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“…These major triterpenes show anti-proliferative activities against gastric cancer cells (NCI-N87), colorectal cancer (HCT15), cervical cancer (HeLa), glioblastoma (U291, U373 and T98G) and colon cancer (HT29) cell lines [18–23]. As part of the ongoing study, our current screening of medicinal plants found promising antiproliferative effects of a methanol extract from E. japonica leaves on several human cancer cell lines.…”

Section: Introductionmentioning

confidence: 99%

Anti-Proliferative Activities and Apoptosis Induction by Triterpenes Derived from Eriobotrya japonica in Human Leukemia Cell Lines

Uto

Sakamoto

Tung

et al. 2013

IJMS

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Eriobotrya japonica leaf is a traditional herbal medicine that contains numerous triterpenes, which have various pharmacological properties. In this study, we investigated the anti-proliferative activity of four triterpenes derived from E. japonica, including corosolic acid (CA), ursolic acid (UA), maslinic acid (MA) and oleanolic acid (OA), in human leukemia cell lines. CA showed the strongest anti-proliferative activity in all of the leukemia cell lines tested, but not in normal human skin fibroblast cell lines. To determine the mechanism underlying the anti-proliferative effect of CA, we examined the effect of CA on molecular events known as apoptosis induction. CA induced chromatin condensation, DNA fragmentation, sub-G1 phase DNA, activation of caspase-3, -8 and -9 and the cleavage of PARP in HL-60. CA also activated Bid and Bax, leading to the loss of mitochondrial membrane potential (Δψm) and cytochrome c release into the cytosol, whereas Bcl-2 and Bcl-xL were unaffected by CA. These results suggest that CA has an anti-proliferative effect on leukemia cells via the induction of apoptosis mediated by mitochondrial dysfunction and caspase activation. CA may be a potential chemotherapeutic agent for the treatment of human leukemia.

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Down-Regulation of Human Epidermal Growth Factor Receptor 2/neu Oncogene by Corosolic Acid Induces Cell Cycle Arrest and Apoptosis in NCI-N87 Human Gastric Cancer Cells

Cited by 33 publications

References 34 publications

Interaction between adipose tissue stromal cells and gastric cancer cells in vitro

Interaction between adipose tissue stromal cells and gastric cancer cells in vitro

Ursolic acid and its natural derivative corosolic acid suppress the proliferation of APC-mutated colon cancer cells through promotion of β-catenin degradation

Anti-Proliferative Activities and Apoptosis Induction by Triterpenes Derived from Eriobotrya japonica in Human Leukemia Cell Lines

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