scholarly journals Trypsin‐Instructed Self‐Assembly on Endoplasmic Reticulum for Selectively Inhibiting Cancer Cells

2020 ◽  
pp. 2000416
Author(s):  
Beom Jin Kim ◽  
Yu Fang ◽  
Hongjian He ◽  
Bing Xu
Keyword(s):  
Endoplasmic Reticulum ◽  
Cancer Cells ◽  
Self Assembly

scholarly journals Tandem Molecular Self-Assembly Selectively Inhibits Lung Cancer Cells by Inducing Endoplasmic Reticulum Stress

Research ◽  
2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Debin Zheng ◽  
Yumiao Chen ◽  
Sifan Ai ◽  
Renshu Zhang ◽  
Zhengfeng Gao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Cancer Cells ◽  
Self Assembly ◽  
A549 Cells ◽  
Cancer Diagnostics ◽  
Lung Cancer Cells ◽  
Great Promise ◽  
Selective Formation

The selective formation of nanomaterials in cancer cells and tumors holds great promise for cancer diagnostics and therapy. Until now, most strategies rely on a single trigger to control the formation of nanomaterials in situ. The combination of two or more triggers may provide for more sophisticated means of manipulation. In this study, we rationally designed a molecule (Comp. 1) capable of responding to two enzymes, alkaline phosphatase (ALP), and reductase. Since the A549 lung cancer cell line showed elevated levels of extracellular ALP and intracellular reductase, we demonstrated that Comp. 1 responded in a stepwise fashion to those two enzymes and displayed a tandem molecular self-assembly behavior. The selective formation of nanofibers in the mitochondria of the lung cancer cells led to the disruption of the mitochondrial membrane, resulting in an increased level of reactive oxygen species (ROS) and the release of cytochrome C (Cyt C). ROS can react with proteins, resulting in endoplasmic reticulum (ER) stress and the unfolded protein response (UPR). This severe ER stress led to disruption of the ER, formation of vacuoles, and ultimately, apoptosis of the A549 cells. Therefore, Comp. 1 could selectively inhibit lung cancer cells in vitro and A549 xenograft tumors in vivo. Our study provides a novel strategy for the selective formation of nanomaterials in lung cancer cells, which is powerful and promising for the diagnosis and treatment of lung cancer.

Supramolecular self-assembly of triazine-based small molecules: targeting the endoplasmic reticulum in cancer cells

Nanoscale ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 3326-3335 ◽  
Author(s):  
Chandramouli Ghosh ◽  
Aditi Nandi ◽  
Sudipta Basu
Keyword(s):  
Endoplasmic Reticulum ◽  
Small Molecules ◽  
Cancer Cells ◽  
Self Assembly ◽  
Self Assembled

We developed supramolecular self-assembled nanoparticles for targeting the endoplasmic reticulum (ER) in cancer cells.

scholarly journals Dehydrodiisoeugenol inhibits colorectal cancer growth by endoplasmic reticulum stress-induced autophagic pathways

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Changhong Li ◽  
Kui Zhang ◽  
Guangzhao Pan ◽  
Haoyan Ji ◽  
Chongyang Li ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Endoplasmic Reticulum ◽  
Cell Growth ◽  
Er Stress ◽  
Cancer Cells ◽  
Tumor Xenograft ◽  
Anticancer Activities ◽  
Colorectal Cancer Cells

Abstract Background Dehydrodiisoeugenol (DEH), a novel lignan component extracted from nutmeg, which is the seed of Myristica fragrans Houtt, displays noticeable anti-inflammatory and anti-allergic effects in digestive system diseases. However, the mechanism of its anticancer activity in gastrointestinal cancer remains to be investigated. Methods In this study, the anticancer effect of DEH on human colorectal cancer and its underlying mechanism were evaluated. Assays including MTT, EdU, Plate clone formation, Soft agar, Flow cytometry, Electron microscopy, Immunofluorescence and Western blotting were used in vitro. The CDX and PDX tumor xenograft models were used in vivo. Results Our findings indicated that treatment with DEH arrested the cell cycle of colorectal cancer cells at the G1/S phase, leading to significant inhibition in cell growth. Moreover, DEH induced strong cellular autophagy, which could be inhibited through autophagic inhibitors, with a rction in the DEH-induced inhibition of cell growth in colorectal cancer cells. Further analysis indicated that DEH also induced endoplasmic reticulum (ER) stress and subsequently stimulated autophagy through the activation of PERK/eIF2α and IRE1α/XBP-1 s/CHOP pathways. Knockdown of PERK or IRE1α significantly decreased DEH-induced autophagy and retrieved cell viability in cells treated with DEH. Furthermore, DEH also exhibited significant anticancer activities in the CDX- and PDX-models. Conclusions Collectively, our studies strongly suggest that DEH might be a potential anticancer agent against colorectal cancer by activating ER stress-induced inhibition of autophagy.

scholarly journals MTOR-independent autophagy induced by interrupted endoplasmic reticulum-mitochondrial Ca2+ communication: a dead end in cancer cells

Autophagy ◽  
2018 ◽  
Vol 15 (2) ◽  
pp. 358-361 ◽  
Author(s):  
Ulises Ahumada-Castro ◽  
Eduardo Silva-Pavez ◽  
Alenka Lovy ◽  
Evelyn Pardo ◽  
Jordi Molgό ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cancer Cells ◽  
Dead End
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