scholarly journals Sensitivity of allyl isothiocyanate to induce apoptosis via ER stress and the mitochondrial pathway upon ROS production in colorectal adenocarcinoma cells

2020 ◽  
Author(s):  
Jo‑Hua Chiang ◽  
Fuu‑Jen Tsai ◽  
Yuan‑Man Hsu ◽  
Mei‑Chin Yin ◽  
Hong‑Yi Chiu ◽  
...  
Keyword(s):  
Er Stress ◽  
Colorectal Adenocarcinoma ◽  
Allyl Isothiocyanate ◽  
Mitochondrial Pathway ◽  
Ros Production ◽  
Adenocarcinoma Cells

A serine protease extracted from Trichosanthes kirilowii induces apoptosis via the PI3K/AKT-mediated mitochondrial pathway in human colorectal adenocarcinoma cells

2016 ◽  
Vol 7 (2) ◽  
pp. 843-854 ◽  
Author(s):  
Li Song ◽  
Jiao Chang ◽  
Zhuoyu Li
Keyword(s):  
Colorectal Cancer ◽  
Serine Protease ◽  
Colorectal Adenocarcinoma ◽  
Mitochondrial Pathway ◽  
Adenocarcinoma Cells ◽  
Trichosanthes Kirilowii ◽  
Dependent Pathway ◽  
Cancer Activity ◽  
Novel Protein

A novel protein TKP extracted from T. kirilowii fruit exerted potential anti-colorectal cancer activity by inducing apoptosis, which was regulated by the PI3K/AKT-mediated mitochondria-dependent pathway.

α-Tocopherol attenuates the cytotoxic effect of δ-tocotrienol in human colorectal adenocarcinoma cells

2010 ◽  
Vol 397 (2) ◽  
pp. 214-219 ◽  
Author(s):  
Akira Shibata ◽  
Kiyotaka Nakagawa ◽  
Phumon Sookwong ◽  
Tsuyoshi Tsuduki ◽  
Akira Asai ◽  
...  
Keyword(s):  
Cytotoxic Effect ◽  
Colorectal Adenocarcinoma ◽  
Adenocarcinoma Cells

scholarly journals Aqueous Fraction of Nephelium ramboutan-ake Rind Induces Mitochondrial-Mediated Apoptosis in HT-29 Human Colorectal Adenocarcinoma Cells

Molecules ◽  
2012 ◽  
Vol 17 (6) ◽  
pp. 6633-6657 ◽  
Author(s):  
Chim Kei Chan ◽  
Bey Hing Goh ◽  
Muhamad Noor Alfarizal Kamarudin ◽  
Habsah Abdul Kadir
Keyword(s):  
Colorectal Adenocarcinoma ◽  
Aqueous Fraction ◽  
Adenocarcinoma Cells ◽  
Ht 29

scholarly journals Modulating Properties of Piroxicam, Meloxicam and Oxicam Analogues against Macrophage-Associated Chemokines in Colorectal Cancer

Molecules ◽  
2021 ◽  
Vol 26 (23) ◽  
pp. 7375
Author(s):  
Paulina Lewandowska ◽  
Izabela Szczuka ◽  
Iwona Bednarz-Misa ◽  
Berenika M. Szczęśniak-Sięga ◽  
Katarzyna Neubauer ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colorectal Adenocarcinoma ◽  
Normal Mucosa ◽  
Colorectal Tumors ◽  
Adjacent Tissue ◽  
Inflammatory Drug ◽  
Chemokine Expression ◽  
Adenocarcinoma Cells ◽  
Thiazine Ring ◽  
N Stage

The mechanisms underlying the antineoplastic effects of oxicams have not been fully elucidated. We aimed to assess the effect of classic and novel oxicams on the expression/secretion of macrophage-associated chemokines (RTqPCR/Luminex xMAP) in colorectal adenocarcinoma cells, and on the expression of upstream the non-steroidal anti-inflammatory drug (NSAID)-activated genes NAG1, NFKBIA, MYD88, and RELA, as well as at the chemokine profiling in colorectal tumors. Meloxicam downregulated CCL4 9.9-fold, but otherwise the classic oxicams had a negligible/non-significant effect. Novel analogues with a thiazine ring substituted with arylpiperazine and benzoyl moieties significantly modulated chemokine expression to varying degree, upregulated NAG1 and NFKBIA, and downregulated MYD88. They inhibited CCL3 and CCL4, and their effect on CCL2 and CXCL2 depended on the dose and exposure. The propylene linker between thiazine and piperazine nitrogens and one arylpiperazine fluorine substituent characterized the most effective analogue. Only CCL19 and CXCL2 were not upregulated in tumors, nor was CXCL2 in tumor-adjacent tissue compared to normal mucosa. Compared to adjacent tissue, CCL4 and CXCL2 were upregulated, while CCL2, CCL8, and CCL19 were downregulated in tumors. Tumor CCL2 and CCL7 increased along with advancing T and CCL3, and CCL4 along with the N stage. The introduction of arylpiperazine and benzoyl moieties into the oxicam scaffold yields effective modulators of chemokine expression, which act by upregulating NAG1 and interfering with NF-κB signaling.

scholarly journals Effect of Pectin on the Expression of Proteins Associated with Mitochondrial Biogenesis and Cell Senescence in HT29-Human Colorectal Adenocarcinoma Cells

2019 ◽  
Vol 24 (2) ◽  
pp. 187-196
Author(s):  
José Javier Zamorano-León ◽  
Sandra Ballesteros ◽  
Natalia de las Heras ◽  
Luis Alvarez-Sala ◽  
Mariano de la Serna-Soto ◽  
...  
Keyword(s):  
Mitochondrial Biogenesis ◽  
Colorectal Adenocarcinoma ◽  
Cell Senescence ◽  
Adenocarcinoma Cells

scholarly journals CD437 induces apoptosis in ovarian adenocarcinoma cells via ER stress signaling

2008 ◽  
Vol 366 (3) ◽  
pp. 840-847 ◽  
Author(s):  
Yumi Watanabe ◽  
Hiroyuki Tsuchiya ◽  
Tomohiko Sakabe ◽  
Saori Matsuoka ◽  
Yuji Akechi ◽  
...  
Keyword(s):  
Er Stress ◽  
Stress Signaling ◽  
Ovarian Adenocarcinoma ◽  
Adenocarcinoma Cells

Abstract 393: Reticulon-4B Protects Against Endoplasmic Reticulum Stress Induced Platelet Apoptosis and Hyperactivation in Diabetes

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Yan Wang ◽  
Wai Ho Tang ◽  
Xinbo Zhang ◽  
Jing Du ◽  
John Hwa ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Protein Trafficking ◽  
Surface Expression ◽  
Diabetic Mouse ◽  
Mitochondrial Damage ◽  
Ros Production ◽  
Mitochondria Membrane Potential ◽  
Platelet Apoptosis

Background: Hyperglycemia triggered endoplasmic reticulum (ER) stress is one of the major causes for platelet hyperactivation and apoptosis in diabetes mellitus (DM). Reticulon-4B (aka Nogo-B) mainly localizes to the ER, and has been shown to influence the ER morphology, ER-Golgi trafficking, apoptotic balance, vesicle formation and protein trafficking in cells. The present study is aimed to investigate the role of Nogo-B on platelet function in DM. Methods and Results: Nogo-B is highly expressed in platelets from healthy individual. Platelets from DM patients and diabetic mice have decreased Nogo-B level. Using Streptozotocin (STZ) induced diabetic mouse model, we show that loss of Nogo (Nogo-/- mice) decreased platelet number, increased mean platelet volume and prolonged bleeding time compared to wild-type (WT) mice. Platelets from Nogo-/- mice were hyperactive with higher JONA and P-selectin surface expression compared to WT mice. Loss of Nogo increased thrombin and collagen induced platelet aggregation. Furthermore, platelets from diabetic Nogo-/- mice show elevated reactive oxygen species (ROS) production, decreased mitochondria membrane potential and increased apoptosis, which can be rescued by antioxidant N-acetyl-L-cysteine. Mechanistically, we show Nogo-B prevented sequestration of antiapoptotic proteins Bcl-xL and Bcl-2 induced by hyperglycemia, subsequently protected against platelet mitochondrial damage, ROS production, caspase-3 activation and apoptosis. Conclusion: These findings demonstrate that Nogo-B protects against ER stress induced platelet apoptosis and hyperactivation in DM by regulating Bcl-xL and Bcl-2 sequestration and mitochondrial damage. This novel pathway may provide therapeutic targets for thrombotic complications in diabetes mellitus.

Molecular Docking and In Vitro Anticancer Screening of Synthesized Arylthiazole linked 2H-indol-2-one Derivatives as VEGFR-2 Kinase Inhibitors

2021 ◽  
Vol 21 ◽  
Author(s):  
Nishtha Shalmali ◽  
Sandhya Bawa ◽  
Md Rahmat Ali ◽  
Sourav Kalra ◽  
Raj Kumar ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Anticancer Activity ◽  
Cell Lines ◽  
Cancer Cell ◽  
Active Sites ◽  
Colorectal Adenocarcinoma ◽  
Kinase Inhibitors ◽  
Adenocarcinoma Cells ◽  
Ic50 Values

Background: Indoline-2,3-dione comprises a leading course group of heterocycles endowed with appealing biological actions, including anticancer activity. There are significant justifications for exploring the anticancer activity of Schiff base derivatives of isatin as a vast number of reports have documented remarkable antiproliferative action of isatin nucleus against various cancer cell lines. Aims and Objectives: A series of arylthiazole linked 2H-indol-2-one derivatives (5a-t) was designed and synthesized as potential VEGFR-2 kinase inhibitors keeping the essential pharmacophoric features of standard drugs, like sunitinib, sorafenib, nintedanib, etc. They were evaluated for their in vitro anticancer activity. The aim of this study was to investigate and assess the anticancer potential of isatin-containing compounds along with their kinase inhibition activity. Methods: The title compounds were synthesized by reacting substituted isatins with para-substituted arylthiazoles using appropriate reaction conditions. Selected synthesized derivatives went under preliminary screening against a panel of 60 cancer cell lines at NCI, the USA, for single-dose and five dose assays. Molecular docking was performed to explore the binding and interactions with the active sites of the VEGFR-2 receptor (PDB Id: 3VHE). Derivatives 5a, 5b, 5c, 5d, 5g, 5h, and 5m were assessed for in vitro inhibition potency against Human VEGFR-2 using ELISA (Enzyme-Linked Immunosorbent Assay) kit. All the target compounds were determined against human colon cancer cell line SW480 (colorectal adenocarcinoma cells). Cellular apoptosis/necrosis was determined by flow cytometry using annexin V-FITC. DNA content of the cells was analyzed by flow cytometry and the cycle distribution was quantified. Results: Compounds 5a and 5g exhibited noteworthy inhibition during a five-dose assay against a panel of 60 cell lines with MID GI50 values of 1.69 and 1.54 µM, respectively. Also, both the lead compounds 5a and 5g demonstrated promising VEGFR-2 inhibitory activity with IC50 values of 5.43±0.95 and 9.63±1.32 µM, respectively. The aforesaid potent compounds were found effective against SW480 (colorectal adenocarcinoma cells) with IC50 values of 31.44 µM and 106.91 µM, respectively. Compound 5a was found to arrest the cell cycle at the G2/M phase, increasing apoptotic cell death. The docking study also supported VEGFR-2 inhibitory activity as both compounds 5a and 5g displayed promising binding and interactions with the active sites of VEGFR-2 receptor (PDB: 3VHE) with docking scores -9.355 and -7.758, respectively. All the compounds obeyed Lipinski’s rule of five. Conclusion: Indoline-2,3-dione and thiazole have huge potential to be considered a steer combination approach for developing promising kinase inhibitors as cancer therapeutics.

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