Costunolide induces mitochondria-mediated apoptosis in human gastric adenocarcinoma BGC-823 cells

Yan, Zhanpeng; Xu, Tingting; An, Zhentao; Ying, Hanjie; Chen, Wanzhen; Ma, Jinxia; Shao, Chenhui; Zhu, Fang

doi:10.1186/s12906-019-2569-6

Cited by 29 publications

(16 citation statements)

References 23 publications

(38 reference statements)

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“…Costunolide is a sesquiterpene lactone (24), which has been reported to exert antiproliferative effects against a wide range of cancer cells, including gastric cancer (25), leukemia (26), colorectal cancer (27) and lung cancer (16). The results of the present study demonstrated that costunolide inhibited the proliferation of H1299 NSCLC cells, with an IC 50 value of 23.93±1.67 µM.…”

Section: Discussionsupporting

confidence: 48%

Costunolide induces apoptosis and inhibits migration and invasion in H1299 lung cancer cells

Wei

Qiu

et al. 2020

Oncol Rep

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Costunolide being a sesquiterpene lactone, is known to have anticancer properties. The present study investigated the anticancer effects of costunolide against the H1299 human non-small-cell lung cancer (NSCLC) cell line. Inhibition of cell viability by costunolide was assessed via a MTT assay. Furthermore, the apoptotic rate was detected using Annexin V/propidium iodide labeling. A colony forming cell assay was performed to investigate the antiproliferative effects of costunolide. Wound healing and Transwell assays were performed to determine the inhibitory effects of costunolide on migration and invasion, respectively. Western blot analysis was undertaken to determine protein expression, and reverse transcription-quantitative PCR was performed to assess mRNA expression levels. The results demonstrated that costunolide inhibited the viability of H1299 cells, with a half maximal inhibitory concentration value of 23.93±1.67 µM and induced cellular apoptosis in a dose-dependent manner. Furthermore, the colony formation, migrative and invasive abilities of the H1299 cells were inhibited in a dose-or time-dependent manner. The protein expression levels of E-cadherin increased and those of N-cadherin decreased following treatment with costunolide, which suggested that costunolide inhibited epithelial-to-mesenchymal transition. The mRNA levels of B-Raf, E-cadherin, N-cadherin, integrins α2 and β1, as well as matrix metalloproteinases 2 were also found to be regulated costunolide. These findings indicate the potential of costunolide in the treatment of NSCLC.

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Section: Discussionsupporting

confidence: 48%

Costunolide induces apoptosis and inhibits migration and invasion in H1299 lung cancer cells

Wei

Qiu

et al. 2020

Oncol Rep

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“…Costunolide, a sesquiterpene lactone exist in the genus Compositae and Magnoiaceae (Park et al, 2001), was also detected in MsHE. It has been reported to have many physiological activities, such as antioxidant, anti‐inflammation, anti‐allergic, antimicrobial and can induce apoptosis of gastric adenocarcinoma (Yan et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Ameliorative effects of Magnolia sieboldii buds hexane extract on experimental reflux esophagitis

Nam

Park

et al. 2020

Phytotherapy Research

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Gastroesophageal reflux disease (GERD) is a disease that stomach contents continually refluxing into esophagus causes symptoms and/or complications. The study was working to find natural plant extracts with good effects and small side effects to treat reflux esophagitis (RE). The anti‐inflammatory effects of hexane extract of Magnolia sieboldii (MsHE) were conducted on lipopolysaccharide (LPS)‐stimulated RAW 264.7 macrophage cells. The ameliorative effects of MsHE on esophageal damage in rats induced by gastric acid reflux was explored in vivo. The results showed that MsHE decreased the production of nitric oxide (NO) and expression levels of iNOS, COX‐2 and TNF‐α on LPS‐stimulated RAW 264.7 cells and MsHE treatment ameliorated the rats' esophageal tissue damage induced by gastric acid and inhibited the increase of inflammatory mediators and pro‐inflammatory cytokines by regulating NF‐κB signaling pathway. In addition, MsHE protected the function of barrier of epithelial cells against inflammatory conditions through increasing the expression of tight junctions. Furthermore, liquid chromatography‐mass spectrometry analysis was used for determine the active ingredients contained in MsHE. The results show that MsHE can alleviate experimental rat RE by regulating NF‐κB signaling pathway. In summary, MsHE may be used as a source material of drug candidate for the treatment of RE.

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“…Previous studies revealed that CTD suppressed cancer cell proliferation by altering cell cycle progression through the regulation of cyclins and cyclin-dependent kinases (CDK) [ 33 , 36 , 37 ]. Additional literature has also reported that CTD can induce apoptosis via activated p53 or mitochondrial damage through increased production of reactive oxygen species (ROS) in colon, gastric and lung cancers [ 21 , 37 , 38 , 39 ]. These observations suggest that CTD-induced ROS generation played a critical role in this process, which is consistent with our results.…”

Section: Discussionmentioning

confidence: 99%

Costunolide Induces Apoptosis via the Reactive Oxygen Species and Protein Kinase B Pathway in Oral Cancer Cells

Huang

Yi²,

Lim

et al. 2021

IJMS

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Oral cancer (OC) has been attracted research attention in recent years as result of its high morbidity and mortality. Costunolide (CTD) possesses potential anticancer and bioactive abilities that have been confirmed in several types of cancers. However, its effects on oral cancer remain unclear. This study investigated the potential anticancer ability and underlying mechanisms of CTD in OC in vivo and in vitro. Cell viability and anchorage-independent colony formation assays were performed to examine the antigrowth effects of CTD on OC cells; assessments for migration and invasion of OC cells were conducted by transwell; Cell cycle and apoptosis were investigated by flow cytometry and verified by immunoblotting. The results revealed that CTD suppressed the proliferation, migration and invasion of oral cancer cells effectively and induced cell cycle arrest and apoptosis; regarding the mechanism, CTD bound to AKT directly by binding assay and repressed AKT activities through kinase assay, which thereby downregulating the downstream of AKT. Furthermore, CTD remarkably promotes the generation of reactive oxygen species by flow cytometry assay, leading to cell apoptosis. Notably, CTD strongly suppresses cell-derived xenograft OC tumor growth in an in vivo mouse model. In conclusion, our results suggested that costunolide might prevent progression of OC and promise to be a novel AKT inhibitor.

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Costunolide induces mitochondria-mediated apoptosis in human gastric adenocarcinoma BGC-823 cells

Cited by 29 publications

References 23 publications

Costunolide induces apoptosis and inhibits migration and invasion in H1299 lung cancer cells

Costunolide induces apoptosis and inhibits migration and invasion in H1299 lung cancer cells

Ameliorative effects of Magnolia sieboldii buds hexane extract on experimental reflux esophagitis

Costunolide Induces Apoptosis via the Reactive Oxygen Species and Protein Kinase B Pathway in Oral Cancer Cells

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