Qualitative and Quantitative Analysis of ROS-Mediated Oridonin-Induced Oesophageal Cancer KYSE-150 Cell Apoptosis by Atomic Force Microscopy

Pi, Jiang; Cai, Huaihong; Jin, Hua; Yang, Fen; Jiang, Jie; Wu, An-Guo; Zhu, Haiyan; Liu, Jianxin; Su, Xiaohui; Yang, Peihui; Cai, Jun

doi:10.1371/journal.pone.0140935

Cited by 28 publications

(23 citation statements)

References 44 publications

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“…It has been reported that oridonin could inhibit in vitro or in vivo growth of several human malignancies, such as oral cancer, gallbladder cancer, glioma, pancreatic cancer, cervical cancer . Our previous work also proved that oridonin could induce ROS‐mediated esophageal cancer KYSE‐150 cell apoptosis, but the exact mechanism and the underlying signaling pathway of oridonin on human esophageal cancer remained poorly characterized. In the current study, we aimed to explore the anticancer effects of oridonin and its underlying molecular mechanism in esophageal cancer.…”

Section: Introductionmentioning

confidence: 99%

Oridonin‐induced mitochondria‐dependent apoptosis in esophageal cancer cells by inhibiting PI3K/AKT/mTOR and Ras/Raf pathways

Jiang

Jin

et al. 2018

J of Cellular Biochemistry

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Oridonin, an active diterpenoid isolated from Rabdosia rubescens, has been reported for its antitumor activity on several cancers. However, its effect on human esophageal cancer remains unclear. In this study, we demonstrated that oridonin could inhibit the growth of human esophageal cancer cells both in vitro and in vivo. Oridonin not only suppressed the proliferation, but also induced cell cycle arrest and mitochondrial-mediated apoptosis in KYSE-30, KYSE-150, and EC9706 cells with dose-dependent manner. Further mechanism studies revealed that oridonin led cell cycle arrest in esophageal cancer cells via downregulating cell cycle-related proteins, such as cyclin B1 and CDK2, while upregulating p53 and p21. Oridonin also increased proapoptotic protein Bax and reduced antiapoptotic protein Bcl-2, as well as the increased expression of cleaved caspase-3, -8, and -9. In addition, oridonin treatment could significantly inhibit the PI3K/Akt/mTOR and Ras/Raf signaling pathway. In vivo results further demonstrated that oridonin treatment markedly inhibited tumor growth in the esophageal cancer xenograft mice model. Taken together, these results suggest that oridonin may be a potential anticancer agent for the treatment of esophageal cancer.

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Section: Introductionmentioning

confidence: 99%

Oridonin‐induced mitochondria‐dependent apoptosis in esophageal cancer cells by inhibiting PI3K/AKT/mTOR and Ras/Raf pathways

Jiang

Jin

et al. 2018

J of Cellular Biochemistry

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“…ROS, mainly produced from the mitochondrial electron transport of aerobic respiration, have a role in regulating cell signaling pathways, including the activation of cell signaling cascades, gene expression, and apoptosis [18–19]. A recent investigation found that ROS are implicated in cellular activity to a variety of inflammatory responses [20].…”

Section: Introductionmentioning

confidence: 99%

Fusobacterium nucleatum-Induced Impairment of Autophagic Flux Enhances the Expression of Proinflammatory Cytokines via ROS in Caco-2 Cells

et al. 2016

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Fusobacterium nucleatum (F. nucleatum) plays a critical role in gastrointestinal inflammation. However, the exact mechanism by which F. nucleatum contributes to inflammation is unclear. In the present study, it was revealed that F. nucleatum could induce the production of proinflammatory cytokines (IL-8, IL-1β and TNF-α) and reactive oxygen species (ROS) in Caco-2 colorectal) adenocarcinoma cells. Furthermore, ROS scavengers (NAC or Tiron) could decrease the production of proinflammatory cytokines during F. nucleatum infection. In addition, we observed that autophagy is impaired in Caco-2 cells after F. nucleatum infection. The production of proinflammatory cytokines and ROS induced by F. nucleatum was enhanced with either autophagy pharmacologic inhibitors (3-methyladenine, bafilomycin A1) or RNA interference in essential autophagy genes (ATG5 or ATG12) in Caco-2 cells. Taken together, these results indicate that F. nucleatum-induced impairment of autophagic flux enhances the expression of proinflammatory cytokines via ROS in Caco-2 Cells.

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“…1), is a diterpenoid compound (10). Previous studies have shown that oridonin has antitumor activities in vivo and in vitro (11)(12)(13), and oridonin inhibited proliferation of cancer cells by inducing autophagic pathways (14)(15)(16)(17)(18), arresting the cell cycle on G 0 /G 1 phase (19) or G 2 /M phase (20)(21)(22)(23)(24), inducing apoptosis of human laryngeal cancer cells (25), esophageal cancer (26), colorectal carcinoma (27), pancreatic cancer (28), hepato cellular carcinoma (29,30). However, few reports exist on oridonin-induced apoptosis on gastric cancer.…”

Section: Introductionmentioning

confidence: 99%

Oridonin induces apoptosis through the mitochondrial pathway in human gastric cancer SGC-7901 cells

Gao

Tan

Zhu

et al. 2016

International Journal of Oncology

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Abstract.Oridonin is one of the most important antitumor active ingredients of Rabdosia rubescens. Recently published studies from our laboratory have demonstrated that oridonin was able to arrest human gastric cancer SGC-7901 cells at G 2 /M phase. However, little is known about inducing apoptosis in gastric cancer. The aim of this study was to investigate the effect of oridonin on antineoplastic capability of SGC-7901 cells and the detailed molecular mechanism of oridoninmediated intrinsic pathway of apoptosis. Cell proliferation was assessed by MTT assay while apoptosis induced by oridonin was determined by Hoechst 33342 staining assay and Annexin V/PI double staining assay. Early apoptotic rate was stained by Annexin V/PI and detected by flow cytometry. Apoptosis pathway was analyzed by western blot analysis of Bcl-2, Bax, cytochrome c and caspase-3 expression. The results showed that oridonin was able to inhibit the SGC-7901 cell proliferation, the 50% growth inhibition (IC 50 ) was 22.74 µM. Oridonin could induce cell apoptosis of SGC-7901 cells and the early apoptotic rates induced by 0, 20, 40, 80 µmol/l oridonin were 1.53±0.67, 3.33±0.29, 84.80±0.82 and 96.43±0.51%, respectively. Western blot analysis revealed that oridonin downregulated Bcl-2 protein (the anti-apoptotic factor) and upregulated Bax protein (pro-apoptotic factor), eventually leading to a reduction in the ratio of Bcl-2/Bax proteins. Furthermore, oridonin induced the release of cytochrome c from the mitochondria to the cytosol and the activation of caspase-3. Taken together, the current study suggested that oridonin induced apoptosis in SGC-7901 cells via the mitochondrial signal pathway, which may represent one of the major mechanisms of oridonin-mediated apoptosis in SGC-7901 cells.

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Qualitative and Quantitative Analysis of ROS-Mediated Oridonin-Induced Oesophageal Cancer KYSE-150 Cell Apoptosis by Atomic Force Microscopy

Cited by 28 publications

References 44 publications

Oridonin‐induced mitochondria‐dependent apoptosis in esophageal cancer cells by inhibiting PI3K/AKT/mTOR and Ras/Raf pathways

Oridonin‐induced mitochondria‐dependent apoptosis in esophageal cancer cells by inhibiting PI3K/AKT/mTOR and Ras/Raf pathways

Fusobacterium nucleatum-Induced Impairment of Autophagic Flux Enhances the Expression of Proinflammatory Cytokines via ROS in Caco-2 Cells

Oridonin induces apoptosis through the mitochondrial pathway in human gastric cancer SGC-7901 cells

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