2020
DOI: 10.1155/2020/6571674
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Cucurbitacin D Induces G2/M Phase Arrest and Apoptosis via the ROS/p38 Pathway in Capan‐1 Pancreatic Cancer Cell Line

Abstract: Pancreatic cancer has a poor prognosis with a five-year survival rate of less than 10%. Moreover, chemotherapy is mostly rendered ineffective owing to chemotherapy resistance and cytotoxicity. Therefore, the development of effective therapeutic strategies and novel drugs against pancreatic cancer is an urgent need. Cucurbitacin D (CuD), a plant steroid derived from Trichosanthes kirilowii, is an anticancer agent effective against various cancer cell lines. However, the anticancer activity and molecular mechani… Show more

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Cited by 13 publications
(13 citation statements)
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“…Quinalizarin, an anthraquinone component isolated from Rubiaceae, has been demonstrated to link ROS generation to MAPK, STAT3, and mitochondrial dynamics and inheritance during cell division, as well as the development and disease NF-κB signaling pathways, leading the MCF7 breast cancer cell line and A549 lung cancer cell line to cell-cycle arrest and caspase-dependent apoptosis [ 102 , 103 ]. Cucurbitacin (CuD), a common phytochemical derived from Trichosanthes kirilowii, was used in Capan-1 pancreatic cancer cell line, demonstrating that the drug-induced ROS production induced G2/M cell-cycle arrest and mediated the p38/MAPK pathway, promoting cell death ( Figure 2 and Figure 3 ) [ 104 ].…”
Section: Hints For Anticancer Therapy: Exploitation Of Mitochondrial Rosmentioning
confidence: 99%
“…Quinalizarin, an anthraquinone component isolated from Rubiaceae, has been demonstrated to link ROS generation to MAPK, STAT3, and mitochondrial dynamics and inheritance during cell division, as well as the development and disease NF-κB signaling pathways, leading the MCF7 breast cancer cell line and A549 lung cancer cell line to cell-cycle arrest and caspase-dependent apoptosis [ 102 , 103 ]. Cucurbitacin (CuD), a common phytochemical derived from Trichosanthes kirilowii, was used in Capan-1 pancreatic cancer cell line, demonstrating that the drug-induced ROS production induced G2/M cell-cycle arrest and mediated the p38/MAPK pathway, promoting cell death ( Figure 2 and Figure 3 ) [ 104 ].…”
Section: Hints For Anticancer Therapy: Exploitation Of Mitochondrial Rosmentioning
confidence: 99%
“…Among them, cucurbitacin B (approximately 250 µg/g) and CucD (approximately 50 µg/g) were present in the largest quantity [46]. In our study, we focused on CucD because of the cytotoxicity of cucurbitacin B and CucD, and anti-cancer effects in various cancer models have been reported in literature [65][66][67][68]. Despite the observed toxicity of both cucurbitacin B and CucD, the cell viability of endothelial cells of the pulmonary artery (CPAE) was measured after Tk extract inoculation to evaluate the safety of Tk, and Tk did not show any significant toxicity to CPAE (Supplementary Figure S1).…”
Section: Discussionmentioning
confidence: 96%
“…It also significantly decreased expression of Cyclin D1, Survivin, XIAP, Bcl2 and Mcl-1 [42]. In the pancreatic cancer cell line Capan-1, CuD induced cell-cycle arrest and death via the ROS/p38 pathway [43]. Cucurbitacin I-induced cell death in ovarian cancer (SKOV3) included apoptosis, as evidenced by upregulated caspase 3 and BAX and a decrease in Bcl2 [21].…”
Section: Apoptotic and Cell-cycle Arrestmentioning
confidence: 98%