JSI-124 inhibits glioblastoma multiforme cell proliferation through G2/M cell cycle arrest and apoptosis augmentation

Su, Yuhang; Li, Gang; Zhang, Xulong; Gu, Jinhai; Zhang, Cai; Tian, Zhigang; Zhang, Jian

doi:10.4161/cbt.7.8.6263

Cited by 79 publications

(68 citation statements)

References 28 publications

(52 reference statements)

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“…The IC 50 values of cucurbitacin I against U251 and T98MG cells were 170 and 245 nM, respectively. Treatment with cucurbitacin I resulted in growth inhibition of U251 and T98G cells in a dose-dependent manner, but their responses varied (Fig.…”

Section: Cucurbitacin I Inhibited the Growth Of Gbm Cells In Vitro Anmentioning

confidence: 97%

Cucurbitacin I Induces Protective Autophagy in Glioblastoma in Vitro and in Vivo

Yuan

Yan

Xue

et al. 2014

Journal of Biological Chemistry

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Background: Targeting disruption of STAT3 results in inhibition of tumor growth and survival in malignant glioma. Results: Cucurbitacin I triggers protective autophagy through the AMPK/mTOR/p70S6K pathway and down-regulates HIF-1␣. Conclusion: Autophagy blockade sensitizes glioblastoma to cucurbitacin I treatment. Significance: This study provides new insights into the biological and antiproliferative activities of cucurbitacin I against glioblastoma.

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Section: Cucurbitacin I Inhibited the Growth Of Gbm Cells In Vitro Anmentioning

confidence: 97%

Cucurbitacin I Induces Protective Autophagy in Glioblastoma in Vitro and in Vivo

Yuan

Yan

Xue

et al. 2014

Journal of Biological Chemistry

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“…Cucurbitacin I, also known as elatericin B, is a member of a family of natural occurring compounds with potent antitumor activity in many human cancers, including glioblastoma, adenocarcinoma of the lung and breast cancer cells (11)(12)(13). The cucurbitacin family comprises a group of triterpenoid compounds originally isolated from the plants of the Cucurbitaceae family.…”

Section: Introductionmentioning

confidence: 99%

“…Recently, these anticancer compounds have been observed in many plant families, including Cruciferae, Cucurbitaceae and Scrophulariaceae, and have been used as traditional or folk medicines for centuries in China, India, Brazil and Peru (13,14). Previous studies have demonstrated that cucurbitacin I inhibits the JAK/STAT3 pathway in a number of cancer cell lines and in vivo tumor models (11,15). Upon inhibition of STAT3-dependent gene transcription, cucurbitacin I elicits antiproliferative effects in glioma, lung and breast cancer cells with activated STAT3 (13,16).…”

Section: Introductionmentioning

confidence: 99%

Cucurbitacin I inhibits cell migration and invasion and enhances chemosensitivity in colon cancer

Song

Liu

et al. 2015

Oncology Reports

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Abstract. Colorectal cancers are the third most common types of cancers worldwide. Surgical resection is unable to eliminate tumors completely due to metastasis. A demand for new chemotherapeutic tools exists. In the present study, we examined the chemopreventive potential of cucurbitacin I, a natural component extracted from plants of the Cucurbitaceae family, in the colon cancer cell line COLO205. We hypothesized that cucurbitacin I would prevent colon cancer cell migration and invasion, and sensitize colon cancer cells to chemotherapy. Our data demonstrated that exposure of the COLO205 cells to cucurbitacin I significantly decreased cell viability. Furthermore our data demonstrated for the first time that in the COLO205 cells, cucurbitacin I could suppress the cell migration and invasion, and harbor chemosensitization activity against colon cancer. The anticancer activity of cucurbitacin I was accomplished by downregulating p-STAT3 and MMP-9 expression. Collectively, our results suggest that cucurbitacin I may be a potent adjuvant chemotherapeutic agent for colon cancer with anti-migration, anti-invasion and chemosensitizing activities.

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“…Glioblastoma multiforme (GBM) is the most common and most virulent primary brain tumor in adults and accounts for at least 80% of malignant gliomas (1,2). Over 12,000 patients die because of primary brain tumor in United States every year.…”

Section: Introductionmentioning

confidence: 99%

Alantolactone induces apoptosis in glioblastoma cells via GSH depletion, ROS generation, and mitochondrial dysfunction

et al. 2012

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Glioblastoma multiforme (GBM) is the most malignant and aggressive primary brain tumor in adults. Despite concerted efforts to improve current therapies, the prognosis of glioblastoma remains very poor. Alantolactone, a sesquiterpene lactone compound, has been reported to exhibit antifungal, antibacteria, antihelminthic, and anticancer properties. In this study, we found that alantolactone effectively inhibits growth and triggers apoptosis in glioblastoma cells in a time‐ and dose‐dependent manner. The alantolactone‐induced apoptosis was found to be associated with glutathione (GSH) depletion, reactive oxygen species (ROS) generation, mitochondrial transmembrane potential dissipation, cardiolipin oxidation, upregulation of p53 and Bax, downregulation of Bcl‐2, cytochrome c release, activation of caspases (caspase 9 and 3), and cleavage of poly (ADP‐ribose) polymerase. This alantolactone‐induced apoptosis and GSH depletion were effectively inhibited or abrogated by a thiol antioxidant, N‐acetyl‐L‐cysteine, whereas other antioxidant (polyethylene glycol (PEG)‐catalase and PEG‐superoxide‐dismutase) did not prevent apoptosis and GSH depletion. Alantolactone treatment inhibited the translocation of NF‐κB into nucleus; however, NF‐κB inhibitor, SN50 failed to potentiate alantolactone‐induced apoptosis indicating that alantolactone induces NF‐κB‐independent apoptosis in glioma cells. These findings suggest that the sensitivity of tumor cells to alantolactone appears to results from GSH depletion and ROS production. Furthermore, our in vivo toxicity study demonstrated that alantolactone did not induce significant hepatotoxicity and nephrotoxicity in mice. Therefore, alantolactone may become a potential lead compound for future development of antiglioma therapy. © © 2012 IUBMB Life, 64(9): 783–794, 2012

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JSI-124 inhibits glioblastoma multiforme cell proliferation through G2/M cell cycle arrest and apoptosis augmentation

Cited by 79 publications

References 28 publications

Cucurbitacin I Induces Protective Autophagy in Glioblastoma in Vitro and in Vivo

Cucurbitacin I Induces Protective Autophagy in Glioblastoma in Vitro and in Vivo

Cucurbitacin I inhibits cell migration and invasion and enhances chemosensitivity in colon cancer

Alantolactone induces apoptosis in glioblastoma cells via GSH depletion, ROS generation, and mitochondrial dysfunction

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