A Hopeful Natural Product, Pristimerin, Induces Apoptosis, Cell Cycle Arrest, and Autophagy in Esophageal Cancer Cells

Esophageal cancer is one of the most common malignant digestive diseases worldwide. Although many approaches have been established for the treatment of esophageal cancer, the survival outcome has not improved. Pristimerin is a quinone methide triterpenoid with anticancer, antiangiogenic, anti-inflam...

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Published inAnalytical cellular pathology (Amsterdam) Vol. 2019; no. 2019; pp. 1 - 10
Main Authors Huang, Peng, Zhang, Yan-Qiao, Sun, Li-Ying
Format Journal Article
LanguageEnglish
Published Cairo, Egypt Hindawi Publishing Corporation 01.01.2019
Hindawi
Wiley
Subjects
Animals
Antineoplastic Agents - pharmacokinetics
Apoptosis - drug effects
Autophagy - drug effects
Biological Products - pharmacokinetics
Cell Cycle Checkpoints - drug effects
Cell Line, Tumor
Esophageal Neoplasms - drug therapy
Esophageal Neoplasms - metabolism
Esophageal Neoplasms - pathology
Humans
Mice
Mice, Inbred BALB C
Triterpenes - pharmacokinetics
Online AccessGet full text
ISSN2210-7177
2210-7185
2210-7185
DOI10.1155/2019/6127169

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Abstract Esophageal cancer is one of the most common malignant digestive diseases worldwide. Although many approaches have been established for the treatment of esophageal cancer, the survival outcome has not improved. Pristimerin is a quinone methide triterpenoid with anticancer, antiangiogenic, anti-inflammatory, and antiprotozoal activities. However, the role of pristimerin in cancers such as esophageal cancer is unclear. In this study, we investigated the role and mechanisms of action of pristimerin in esophageal cancer. First, we found that pristimerin can induce apoptosis in esophageal cancer in vivo and in vitro. CCK-8 and clonogenic assays showed that pristimerin decreased the growth of Eca109 cells. In addition, we found that pristimerin decreased the protein expression of CDK2, CDK4, cyclin E, and BCL-2 and increased the expression of CDKN1B. Meanwhile, pristimerin elevated the ratio of LC3-II/LC3-I. Otherwise, downregulation of CDKN1B can reduce the esophageal cancer tumor growth induced by pristimerin. In conclusion, our findings revealed an important role of pristimerin in esophageal cancer and suggest that pristimerin might be a potential therapeutic agent for this cancer.
AbstractList Esophageal cancer is one of the most common malignant digestive diseases worldwide. Although many approaches have been established for the treatment of esophageal cancer, the survival outcome has not improved. Pristimerin is a quinone methide triterpenoid with anticancer, antiangiogenic, anti-inflammatory, and antiprotozoal activities. However, the role of pristimerin in cancers such as esophageal cancer is unclear. In this study, we investigated the role and mechanisms of action of pristimerin in esophageal cancer. First, we found that pristimerin can induce apoptosis in esophageal cancer in vivo and in vitro. CCK-8 and clonogenic assays showed that pristimerin decreased the growth of Eca109 cells. In addition, we found that pristimerin decreased the protein expression of CDK2, CDK4, cyclin E, and BCL-2 and increased the expression of CDKN1B. Meanwhile, pristimerin elevated the ratio of LC3-II/LC3-I. Otherwise, downregulation of CDKN1B can reduce the esophageal cancer tumor growth induced by pristimerin. In conclusion, our findings revealed an important role of pristimerin in esophageal cancer and suggest that pristimerin might be a potential therapeutic agent for this cancer.
Esophageal cancer is one of the most common malignant digestive diseases worldwide. Although many approaches have been established for the treatment of esophageal cancer, the survival outcome has not improved. Pristimerin is a quinone methide triterpenoid with anticancer, antiangiogenic, anti-inflammatory, and antiprotozoal activities. However, the role of pristimerin in cancers such as esophageal cancer is unclear. In this study, we investigated the role and mechanisms of action of pristimerin in esophageal cancer. First, we found that pristimerin can induce apoptosis in esophageal cancer in vivo and in vitro . CCK-8 and clonogenic assays showed that pristimerin decreased the growth of Eca109 cells. In addition, we found that pristimerin decreased the protein expression of CDK2, CDK4, cyclin E, and BCL-2 and increased the expression of CDKN1B. Meanwhile, pristimerin elevated the ratio of LC3-II/LC3-I. Otherwise, downregulation of CDKN1B can reduce the esophageal cancer tumor growth induced by pristimerin. In conclusion, our findings revealed an important role of pristimerin in esophageal cancer and suggest that pristimerin might be a potential therapeutic agent for this cancer.
Esophageal cancer is one of the most common malignant digestive diseases worldwide. Although many approaches have been established for the treatment of esophageal cancer, the survival outcome has not improved. Pristimerin is a quinone methide triterpenoid with anticancer, antiangiogenic, anti-inflammatory, and antiprotozoal activities. However, the role of pristimerin in cancers such as esophageal cancer is unclear. In this study, we investigated the role and mechanisms of action of pristimerin in esophageal cancer. First, we found that pristimerin can induce apoptosis in esophageal cancer in vivo and in vitro. CCK-8 and clonogenic assays showed that pristimerin decreased the growth of Eca109 cells. In addition, we found that pristimerin decreased the protein expression of CDK2, CDK4, cyclin E, and BCL-2 and increased the expression of CDKN1B. Meanwhile, pristimerin elevated the ratio of LC3-II/LC3-I. Otherwise, downregulation of CDKN1B can reduce the esophageal cancer tumor growth induced by pristimerin. In conclusion, our findings revealed an important role of pristimerin in esophageal cancer and suggest that pristimerin might be a potential therapeutic agent for this cancer.Esophageal cancer is one of the most common malignant digestive diseases worldwide. Although many approaches have been established for the treatment of esophageal cancer, the survival outcome has not improved. Pristimerin is a quinone methide triterpenoid with anticancer, antiangiogenic, anti-inflammatory, and antiprotozoal activities. However, the role of pristimerin in cancers such as esophageal cancer is unclear. In this study, we investigated the role and mechanisms of action of pristimerin in esophageal cancer. First, we found that pristimerin can induce apoptosis in esophageal cancer in vivo and in vitro. CCK-8 and clonogenic assays showed that pristimerin decreased the growth of Eca109 cells. In addition, we found that pristimerin decreased the protein expression of CDK2, CDK4, cyclin E, and BCL-2 and increased the expression of CDKN1B. Meanwhile, pristimerin elevated the ratio of LC3-II/LC3-I. Otherwise, downregulation of CDKN1B can reduce the esophageal cancer tumor growth induced by pristimerin. In conclusion, our findings revealed an important role of pristimerin in esophageal cancer and suggest that pristimerin might be a potential therapeutic agent for this cancer.
Esophageal cancer is one of the most common malignant digestive diseases worldwide. Although many approaches have been established for the treatment of esophageal cancer, the survival outcome has not improved. Pristimerin is a quinone methide triterpenoid with anticancer, antiangiogenic, anti-inflammatory, and antiprotozoal activities. However, the role of pristimerin in cancers such as esophageal cancer is unclear. In this study, we investigated the role and mechanisms of action of pristimerin in esophageal cancer. First, we found that pristimerin can induce apoptosis in esophageal cancer and . CCK-8 and clonogenic assays showed that pristimerin decreased the growth of Eca109 cells. In addition, we found that pristimerin decreased the protein expression of CDK2, CDK4, cyclin E, and BCL-2 and increased the expression of CDKN1B. Meanwhile, pristimerin elevated the ratio of LC3-II/LC3-I. Otherwise, downregulation of CDKN1B can reduce the esophageal cancer tumor growth induced by pristimerin. In conclusion, our findings revealed an important role of pristimerin in esophageal cancer and suggest that pristimerin might be a potential therapeutic agent for this cancer.
Author Sun, Li-Ying
Huang, Peng
Zhang, Yan-Qiao
AuthorAffiliation 1 Department of Gastrointestinal Oncology, Harbin Medical University Cancer Hospital, Harbin 150081, China
2 Department of Gastroenterology, The First Affiliated Hospital of Harbin Medical University, Harbin 150081, China
AuthorAffiliation_xml – name: 2 Department of Gastroenterology, The First Affiliated Hospital of Harbin Medical University, Harbin 150081, China
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Cites_doi 10.1248/bpb.b12-00685
10.1016/j.taap.2013.10.025
10.1101/cshperspect.a008714
10.1016/j.cellsig.2013.11.028
10.4161/cbt.19589
10.3892/mmr.2018.9488
10.3892/ijo.2014.2325
10.1159/000430350
10.1007/s00595-014-0841-4
10.3892/mmr.2015.4410
10.1111/dote.12170
10.1016/bs.ctdb.2015.07.012
10.1007/s11748-013-0246-0
10.1016/j.ijbiomac.2015.01.060
10.1016/j.bcp.2010.12.015
10.4161/auto.5921
10.1590/s0102-67202014000400003
10.1186/s41043-015-0019-8
10.3892/or.2015.3708
10.1016/j.phymed.2018.01.008
10.1016/j.cell.2012.12.031
10.1007/s00595-013-0713-3
10.4161/auto.6.1.10220
10.1073/pnas.0703976104
10.1186/s12885-015-1915-4
10.1371/journal.pone.0131560
10.1016/j.abb.2014.05.029
10.1371/journal.pone.0043826
10.1002/ijc.21056
10.1080/15384101.2015.1078034
10.3748/wjg.v19.i34.5598
10.3748/wjg.v21.i26.7933
10.3892/or.2015.4252
10.1245/s10434-013-3343-5
10.1016/j.exphem.2014.11.002
10.1038/nrgastro.2014.70
10.1016/j.neuint.2017.04.009
10.1016/j.phymed.2018.03.033
10.1016/j.biopha.2013.01.013
10.1038/nrm2308
10.1038/nrd.2016.253
10.1097/cad.0000000000000089
10.1007/s11010-010-0709-x
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References 22
44
23
45
24
25
26
27
28
29
(1) 2017; 95
30
31
10
32
11
33
12
34
13
35
14
36
15
37
16
38
17
39
18
19
2
3
4
5
(9) 2014; 7
6
7
8
40
41
20
42
21
43
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  doi: 10.1248/bpb.b12-00685
– ident: 41
  doi: 10.1016/j.taap.2013.10.025
– ident: 21
  doi: 10.1101/cshperspect.a008714
– ident: 44
  doi: 10.1016/j.cellsig.2013.11.028
– ident: 31
  doi: 10.4161/cbt.19589
– ident: 28
  doi: 10.3892/mmr.2018.9488
– ident: 32
  doi: 10.3892/ijo.2014.2325
– volume: 7
  start-page: 6015
  issue: 9
  year: 2014
  ident: 9
  publication-title: International Journal of Clinical and Experimental Pathology
– ident: 18
  doi: 10.1159/000430350
– ident: 6
  doi: 10.1007/s00595-014-0841-4
– ident: 11
  doi: 10.3892/mmr.2015.4410
– ident: 17
  doi: 10.1111/dote.12170
– ident: 43
  doi: 10.1016/bs.ctdb.2015.07.012
– ident: 5
  doi: 10.1007/s11748-013-0246-0
– ident: 34
  doi: 10.1016/j.ijbiomac.2015.01.060
– ident: 14
  doi: 10.1016/j.bcp.2010.12.015
– ident: 37
  doi: 10.4161/auto.5921
– volume: 95
  start-page: 22
  issue: 1
  year: 2017
  ident: 1
  publication-title: American Family Physician
– ident: 15
  doi: 10.1590/s0102-67202014000400003
– ident: 10
  doi: 10.1186/s41043-015-0019-8
– ident: 19
  doi: 10.3892/or.2015.3708
– ident: 30
  doi: 10.1016/j.phymed.2018.01.008
– ident: 25
  doi: 10.1016/j.cell.2012.12.031
– ident: 12
  doi: 10.1007/s00595-013-0713-3
– ident: 38
  doi: 10.4161/auto.6.1.10220
– ident: 26
  doi: 10.1073/pnas.0703976104
– ident: 36
  doi: 10.1186/s12885-015-1915-4
– ident: 7
  doi: 10.1371/journal.pone.0131560
– ident: 35
  doi: 10.1016/j.abb.2014.05.029
– ident: 27
  doi: 10.1371/journal.pone.0043826
– ident: 39
  doi: 10.1002/ijc.21056
– ident: 40
  doi: 10.1080/15384101.2015.1078034
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  doi: 10.3748/wjg.v19.i34.5598
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  doi: 10.3748/wjg.v21.i26.7933
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  doi: 10.3892/or.2015.4252
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  doi: 10.1245/s10434-013-3343-5
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  doi: 10.1016/j.exphem.2014.11.002
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  doi: 10.1038/nrgastro.2014.70
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  doi: 10.1016/j.neuint.2017.04.009
– ident: 29
  doi: 10.1016/j.phymed.2018.03.033
– ident: 13
  doi: 10.1016/j.biopha.2013.01.013
– ident: 23
  doi: 10.1038/nrm2308
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  doi: 10.1038/nrd.2016.253
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Snippet Esophageal cancer is one of the most common malignant digestive diseases worldwide. Although many approaches have been established for the treatment of...
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SubjectTerms Animals
Antineoplastic Agents - pharmacokinetics
Apoptosis - drug effects
Autophagy - drug effects
Biological Products - pharmacokinetics
Cell Cycle Checkpoints - drug effects
Cell Line, Tumor
Esophageal Neoplasms - drug therapy
Esophageal Neoplasms - metabolism
Esophageal Neoplasms - pathology
Humans
Mice
Mice, Inbred BALB C
Triterpenes - pharmacokinetics
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Title A Hopeful Natural Product, Pristimerin, Induces Apoptosis, Cell Cycle Arrest, and Autophagy in Esophageal Cancer Cells
URI https://search.emarefa.net/detail/BIM-1117862
https://dx.doi.org/10.1155/2019/6127169
https://www.ncbi.nlm.nih.gov/pubmed/31218209
https://www.proquest.com/docview/2244146194
https://pubmed.ncbi.nlm.nih.gov/PMC6536960
https://doaj.org/article/602121d540c54d3eb32db6222f9eaea0
Volume 2019
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