scholarly journals A Purified Resin Glycoside Fraction from Pharbitidis Semen Induces Paraptosis by Activating Chloride Intracellular Channel-1 in Human Colon Cancer Cells

2019 ◽  
Vol 18 ◽  
pp. 153473541882212 ◽  
Author(s):  
Dongrong Zhu ◽  
Chen Chen ◽  
Yuanzheng Xia ◽  
Ling-Yi Kong ◽  
Jianguang Luo
Keyword(s):  
Colon Cancer ◽  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Cytotoxic Effect ◽  
Human Colon ◽  
Colon Cancer Cell ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Resin Glycoside ◽  
Intracellular Channel

Pharbitidis Semen has worldwide recognition in traditional medicine for the treatment of several illnesses apart from its purgative properties, and it is also reported to show anticancer effect. However, limited pharmacological studies are available on the extract or resin glycosides fraction of Pharbitidis Semen. The purpose of this study was to determine the mechanism of the colon cancer cell cytotoxic effect of a purified resin glycoside fraction from Pharbitidis Semen (RFP). Our results showed that the RFP-induced cell death was mediated by the caspase-independent and autophagy-protective paraptosis, a type of cell death that is characterized by the accumulation of cytoplasmic vacuoles and mitochondria swelling. RFP significantly stimulated endoplasmic reticulum stress, inhibited proteasome-dependent degradation, and activated the MAPK signaling pathway in human colon cancer cell lines. Furthermore, we found that RFP activated chloride intracellular channel-1 (CLIC1) and increased the intracellular Cl− concentration. Blockage of CLIC1 by DIDS (disodium 4,4′-diisothiocyanato-2,2′-stilbenedisulfonate hydrate) attenuated cell death, cytoplasmic vacuolization, and endoplasmic reticulum stress, suggesting that CLIC1 acts as a critical early signal in RFP-induced paraptosis. In conclusion, results obtained indicated that the cytotoxic effect of RFP in colon cancer cells was the outcome of paraptosis mediated by activation of CLIC1.

Brosimone I, an isoprenoid-substituted flavonoid, induces cell cycle G1phase arrest and apoptosis through ROS-dependent endoplasmic reticulum stress in HCT116 human colon cancer cells

2019 ◽  
Vol 10 (5) ◽  
pp. 2729-2738 ◽  
Author(s):  
Yueliang Zhao ◽  
Yue Zhou ◽  
Mingfu Wang
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Endoplasmic Reticulum ◽  
Cell Growth ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Cell Growth Inhibition ◽  
Human Colon Cancer ◽  
Artocarpus Heterophyllus ◽  
Human Colon Cancer Cells

Brosimone I, an isoprenoid-substituted flavonoid fromArtocarpus heterophyllus, induces cell growth inhibition through the induction of ROS-mediated increased cytosolic Ca2+, ER stress, and the activation of the CaMKK-AMPK pathway.

Incomplete processing of progastrin expressed by human colon cancer cells: role of noncarboxyamidated gastrins

1994 ◽  
Vol 266 (3) ◽  
pp. G459-G468 ◽  
Author(s):  
P. Singh ◽  
Z. Xu ◽  
B. Dai ◽  
S. Rajaraman ◽  
N. Rubin ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Human Colon ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Colon Cancer Cell Lines

Gastrin is mitogenic for several colon cancers. To assess a possible autocrine role of gastrin in colon cancers, we examined human colon cancer cell lines for expression of gastrin mRNA and various forms of gastrin. Gastrin mRNA was not detected in the majority of colon cancer cell lines by Northern hybridization but was detected in all human colon cancer lines by the sensitive method of reverse transcriptase-polymerase chain reaction (PCR). Gastrin mRNA was quantitated by the competitive PCR method. The majority of cell lines expressed very low levels of gastrin mRNA (< 1-5 copies/cell); only one cell line expressed > 20 copies/cell. The mature carboxyamidated form of gastrin was not detected in any of the cell lines by radioimmunoassay or immunocytochemistry. Results suggested that either gastrin mRNA expressed by colon cancer cells was altered (mutated) or posttranslational processing of progastrin was incomplete. Gastrin cDNA from all the colon cancer cell lines had an identical sequence to the published sequence of human gastrin cDNA. Specific antibodies against precursor forms of gastrin were used, and significant concentrations of nonamidated (glycine-extended) and prepro forms of gastrin were measured in tumor extracts of representative colon cancer cell lines. The presence of precursor forms of gastrin suggested a lack of one or more of the processing enzymes and/or cofactors. Significant concentrations of the processing enzyme (peptidylglycine alpha-amidating monooxygenase) were detected in colon cancer cells by immunocytochemistry. Therefore, lack of other cofactors or enzymes may be contributing to incomplete processing of precursor forms of gastrin, which merits further investigation. Since low levels of gastrin mRNA were expressed by the majority of human colon cancer cell lines and progastrin was incompletely processed, it seems unlikely that gastrin can function as a viable autocrine growth factor for colon cancer cells. High concentrations of glycine-extended gastrin-17 (GG) (> 10(-6) M) were mitogenic for a gastrin-responsive human colon cancer (DLD-1) cell line in vitro. It remains to be seen if GG or other precursor forms of gastrin are similarly mitogenic in vivo, which may then lend credibility to a possible autocrine role of gastrinlike peptides in colon cancers.

scholarly journals INCB018424 induces apoptotic cell death through the suppression of pJAK1 in human colon cancer cells

Neoplasma ◽  
2014 ◽  
Vol 61 (01) ◽  
pp. 56-62 ◽  
Author(s):  
H. J. An ◽  
E. K. Choi ◽  
J. S. Kim ◽  
S. W. Hong ◽  
J. H. Moon ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Human Colon ◽  
Apoptotic Cell Death ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells

scholarly journals Luteolin induces apoptotic cell death via antioxidant activity in human colon cancer cells

2017 ◽  
Vol 51 (4) ◽  
pp. 1169-1178 ◽  
Author(s):  
Kyoung Ah Kang ◽  
Mei Jing Piao ◽  
Yea Seong Ryu ◽  
Yu Jae Hyun ◽  
Jeong Eon Park ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Antioxidant Activity ◽  
Cell Death ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Human Colon ◽  
Apoptotic Cell Death ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells

Opioid growth factor tonically inhibits human colon cancer cell proliferation in tissue culture

1996 ◽  
Vol 271 (3) ◽  
pp. R511-R518 ◽  
Author(s):  
I. S. Zagon ◽  
S. D. Hytrek ◽  
P. J. McLaughlin
Keyword(s):  
Colon Cancer ◽  
Tissue Culture ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cell ◽  
Human Colon Cancer Cell ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Opioid Growth Factor ◽  
Human Colon Cancer Cells

Native opioid peptides serve as growth factors in a number of normal and neoplastic cells and tissues, including the prevention and delayed growth of human colon cancer xenografts in nude mice. This study examined the hypothesis that opioids exert a direct inhibitory influence on tumor cell growth by the use of a tissue culture model. The naturally occurring pentapeptide [Met5]enkephalin depressed growth of HT-29 human colon cancer cells from 17 to 41% at 12-72 h after administration of 10(-6)M concentration; consistent with previously defined nomenclature, this peptide was termed opioid growth factor (OGF). OGF action exhibited a dose-response relationship, was reversible and not cytotoxic, and was opioid receptor mediated. Growth inhibition by OGF was not dependent on serum, and was noted in the two other human colon cancer cell lines examined WiDr and COLO 205. This peptide continually repressed growth because an increase in cell number was noted when cells were exposed to the potent opioid antagonist naltrexone or an antibody to OGF. Both OGF and its receptor, zeta (zeta), were found in colon cancer cells by immunocytochemistry, and receptor binding assays revealed a nuclear-associated receptor with a dissociation constant of 8.9 nM and a maximum binding capacity of 43 fmol/mg of protein. OGF was produced and secreted by the tumor cells. These results lead to the suggestion that OGF has a direct, tonic, inhibitory action on the growth of human colon cancer cells and contribute to our understanding of the mechanisms underlying the marked antitumor effect of this peptide in nude mice inoculated with human colon cancer cells.

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