scholarly journals Correction: Co-targeting translation and proteasome rapidly kills colon cancer cells with mutant RAS/RAF via ER stress

Oncotarget ◽  
2018 ◽  
Vol 9 (6) ◽  
pp. 7271-7271
Author(s):  
Xiangyun Li ◽  
Mei Li ◽  
Hang Ruan ◽  
Wei Qiu ◽  
Xiang Xu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Er Stress ◽  
Cancer Cells ◽  
Colon Cancer Cells

γ-Synuclein is Closely Involved in Autophagy that Protects Colon Cancer Cell from Endoplasmic Reticulum Stress

2021 ◽  
Vol 21 ◽  
Author(s):  
Qing Ye ◽  
Yuanfei Peng ◽  
Feng Huang ◽  
Jinhu Chen ◽  
Yangmei Xu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Western Blot ◽  
Er Stress ◽  
Cancer Cells ◽  
Early Stage ◽  
Colon Cancer Cell ◽  
Colon Cancer Cells ◽  
Rt Pcr ◽  
Jnk Pathway ◽  
Hct116 Cells

Background: In previous studies, we provided evidence suggesting the involvement of γ-synuclein in growth, invasion, and metastasis of colon cancer cells in vitro and in vivo. Among γ-synuclein downstream genes, the microtubule-associated protein 1 light chain 3 (LC3), an autophagy gene, was screened by gene expression profile chip analysis. Objective: We planned to investigate the functional effects of γ-synuclein on autophagy induced by ER stress in colon cancer cells. Methods: We investigated the functional effects of γ-synuclein on autophagy and apoptosis induced by Thapsigargin (TG), ER stressinducing agent, in colon cancer cell lines using immunofluorescence staining, RT-PCR, western blot, CCK8 test, flow cytometry analysis, and transmission electron microscopy. To further determine how γ-synuclein regulated autophagy and apoptosis, PD98059 (ERK inhibitor), SP600125 (ERK inhibitor), anisomycin (JNK activator), and c-Jun siRNA were used respectively in γ-synuclein siRNA transfected HCT116 cells. Then, autophagy proteins, apoptosis proteins, and pathway proteins were detected by western blot analysis. The expression of autophagy genes was assessed by RT-PCR. Results: Our data showed that ER stress-induced colon cancer cells autophagy mainly in the early stage (0-24h) and apoptosis mainly in the late stage (24-48h). ER stress up-regulated γ-synuclein gene and protein expression in colon cancer cells, accompanied by autophagy. γ-synuclein protected HCT116 cells by enhancing autophagy in the early stage (0-24h) through activation of ERK and JNK pathway and inhibiting apoptosis in the late stage (24-48h) through inhibition of the JNK pathway. γ-synuclein could promote autophagy via the JNK pathway activation of ATG genes, LC3, Beclin 1, and ATG7. γ-synuclein may play a role in the transition between autophagy and apoptosis in our model. Conclusion: Overall, we provided the first experimental evidence to show that γ-synuclein may play an important role in autophagy that protects colon cancer cells from ER stress. Therefore, our data suggest a new molecular mechanism for γ-synuclein-mediated CRC progression.

scholarly journals Arachidonic acid induces ER stress and apoptosis in HT-29 human colon cancer cells

2020 ◽  
Vol 24 (5) ◽  
pp. 260-266
Author(s):  
Sijeong Bae ◽  
Min-Kyoung Kim ◽  
Hong Seok Kim ◽  
Young-Ah Moon
Keyword(s):  
Colon Cancer ◽  
Arachidonic Acid ◽  
Er Stress ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells ◽  
Ht 29

scholarly journals Inhibition of HSP90 by AUY922 Preferentially Kills Mutant KRAS Colon Cancer Cells by Activating Bim through ER Stress

2016 ◽  
Vol 15 (3) ◽  
pp. 448-459 ◽  
Author(s):  
Chun Yan Wang ◽  
Su Tang Guo ◽  
Jia Yu Wang ◽  
Fen Liu ◽  
Yuan Yuan Zhang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Er Stress ◽  
Cancer Cells ◽  
Colon Cancer Cells

scholarly journals The Novel Curcumin Derivative 1g Induces Mitochondrial and ER-Stress-Dependent Apoptosis in Colon Cancer Cells by Induction of ROS Production

2020 ◽  
Author(s):  
Hao Wang ◽  
Jia-Lin Sun ◽  
Ying-Xing Xu ◽  
Zhong-Guo Sui
Keyword(s):  
Colon Cancer ◽  
Membrane Potential ◽  
Er Stress ◽  
Cancer Cells ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Colon Cancer Cells ◽  
Ros Scavenging ◽  
Stress Dependent

Abstract Background: A novel curcumin (Cur) derivative 1g can inhibit the proliferation of colon cancer in vitro and in vivo. The purpose of this study was to explore the role of 1g in inducing apoptosis of colon cancer cells, especially mitochondrial apoptosis and endoplasmic reticulum (ER)-stress caused by reactive oxygen species (ROS).Methods: Bioinformatics was used to analyze differentially expressed mrnas. Gene expression was measured by using qRT-PCR and protein expression was measured by using western blotting. Cell apoptosis, cycle, mitochondrial membrane potential and ROS were analyzed by flow cytometry. Experiments on transplanted tumors in animals.Results: The mechanism of this effect was a change in mitochondrial membrane potential caused by 1g that increased its pro-apoptotic activity. In addition, 1g produced ROS, induced G1 checkpoint blockade, and enhanced ER-stress in colon cancer cells. On the contrary, pretreatment with the ROS scavenging agent N-acetyl-l-cysteine (NAC) inhibited the mitochondrial dysfunction caused by 1g and reversed ER-stress, cell cycle stagnation, and apoptosis. Additionally, pretreatment with the p-PERK inhibitor GSK2606414 significantly reduced ER-stress and reversed the apoptosis induced by colon cancer cells.Conclusions: This study not only found that 1g inherits the safety of Cur and has a more inhibitory effect on colon cancer cells than Cur, but also revealed that excessive production of ROS is one of the mechanisms of anti-tumor action.

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