scholarly journals Adenylosuccinate lyase is oncogenic in colorectal cancer by causing mitochondrial dysfunction and independent activation of NRF2 and mTOR-MYC-axis

Theranostics ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 4011-4029
Author(s):  
Stephanie Taha-Mehlitz ◽  
Gaia Bianco ◽  
Mairene Coto-Llerena ◽  
Venkatesh Kancherla ◽  
Glenn R. Bantug ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Mitochondrial Dysfunction ◽  
Adenylosuccinate Lyase

scholarly journals Colorectal Cancer Apoptosis Induced by Dietary δ-Valerobetaine Involves PINK1/Parkin Dependent-Mitophagy and SIRT3

2021 ◽  
Vol 22 (15) ◽  
pp. 8117
Author(s):  
Nunzia D’Onofrio ◽  
Elisa Martino ◽  
Luigi Mele ◽  
Antonino Colloca ◽  
Martina Maione ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Mitochondrial Dysfunction ◽  
Cancer Cells ◽  
Current Knowledge ◽  
Apoptotic Cell ◽  
Critical Role ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Protein Levels

Understanding the mechanisms of colorectal cancer progression is crucial in the setting of strategies for its prevention. δ-Valerobetaine (δVB) is an emerging dietary metabolite showing cytotoxic activity in colon cancer cells via autophagy and apoptosis. Here, we aimed to deepen current knowledge on the mechanism of δVB-induced colon cancer cell death by investigating the apoptotic cascade in colorectal adenocarcinoma SW480 and SW620 cells and evaluating the molecular players of mitochondrial dysfunction. Results indicated that δVB reduced cell viability in a time-dependent manner, reaching IC50 after 72 h of incubation with δVB 1.5 mM, and caused a G2/M cell cycle arrest with upregulation of cyclin A and cyclin B protein levels. The increased apoptotic cell rate occurred via caspase-3 activation with a concomitant loss in mitochondrial membrane potential and SIRT3 downregulation. Functional studies indicated that δVB activated mitochondrial apoptosis through PINK1/Parkin pathways, as upregulation of PINK1, Parkin, and LC3B protein levels was observed (p < 0.0001). Together, these findings support a critical role of PINK1/Parkin-mediated mitophagy in mitochondrial dysfunction and apoptosis induced by δVB in SW480 and SW620 colon cancer cells.

Liensinine perchlorate inhibits colorectal cancer tumorigenesis by inducing mitochondrial dysfunction and apoptosis

2018 ◽  
Vol 9 (11) ◽  
pp. 5536-5546 ◽  
Author(s):  
Yang Wang ◽  
Yang-Jia Li ◽  
Xiao-Hui Huang ◽  
Can-Can Zheng ◽  
Xing-Feng Yin ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Quantitative Proteomics ◽  
Food Source ◽  
Colorectal Cancer Cell ◽  
Functional Screen ◽  
Cancer Cell Apoptosis

Functional screen and quantitative proteomics reveal that food-source liensinine induces colorectal cancer cell apoptosisviathe JNK-mitochondrial dysfunction signaling pathway.

scholarly journals Parthenolide suppresses tumor growth in a xenograft model of colorectal cancer cells by inducing mitochondrial dysfunction and apoptosis

2012 ◽  
Vol 41 (4) ◽  
pp. 1547-1553 ◽  
Author(s):  
SE-LIM KIM ◽  
KIEU THE THU TRANG ◽  
SEONG HUN KIM ◽  
IN HEE KIM ◽  
SEUNG OK LEE ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Mitochondrial Dysfunction ◽  
Cancer Cells ◽  
Xenograft Model ◽  
Colorectal Cancer Cells

scholarly journals Effects of obesity and weight loss on mitochondrial structure and function and implications for colorectal cancer risk

2019 ◽  
Vol 78 (3) ◽  
pp. 426-437 ◽  
Author(s):  
S. P. Breininger ◽  
F. C. Malcomson ◽  
S. Afshar ◽  
D. M. Turnbull ◽  
L. Greaves ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Weight Loss ◽  
Mitochondrial Dysfunction ◽  
Human Subjects ◽  
Human Colon ◽  
Structure And Function ◽  
Model Systems ◽  
Intentional Weight Loss ◽  
Mitochondrial Structure ◽  
And Function

Colorectal cancer (CRC) is the third most common cancer globally. CRC risk is increased by obesity, and by its lifestyle determinants notably physical inactivity and poor nutrition. Obesity results in increased inflammation and oxidative stress which cause genomic damage and contribute to mitochondrial dysregulation and CRC risk. The mitochondrial dysfunction associated with obesity includes abnormal mitochondrial size, morphology and reduced autophagy, mitochondrial biogenesis and expression of key mitochondrial regulators. Although there is strong evidence that increased adiposity increases CRC risk, evidence for the effects of intentional weight loss on CRC risk is much more limited. In model systems, energy depletion leads to enhanced mitochondrial integrity, capacity, function and biogenesis but the effects of obesity and weight loss on mitochondria in the human colon are not known. We are using weight loss following bariatric surgery to investigate the effects of altered adiposity on mitochondrial structure and function in human colonocytes. In summary, there is strong and consistent evidence in model systems and more limited evidence in human subjects that over-feeding and/or obesity result in mitochondrial dysfunction and that weight loss might mitigate or reverse some of these effects.

Flavonoid-rich extracts from okra flowers exert antitumor activity in colorectal cancer through induction of mitochondrial dysfunction-associated apoptosis, senescence and autophagy

2020 ◽  
Vol 11 (12) ◽  
pp. 10448-10466
Author(s):  
Yuanle Deng ◽  
Sha Li ◽  
Meng Wang ◽  
Xiaotong Chen ◽  
Li Tian ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Antitumor Activity ◽  
Mitochondrial Dysfunction

AFE activates p53, acting on apoptosis, autophagy, senescence, and metastasis, and induces mitochondrial dysfunction.

scholarly journals 3’-hydroxy-4’-methoxy-β-methyl-β-nitrostyrene inhibits tumorigenesis in colorectal cancer cells through ROS-mediated DNA damage and mitochondrial dysfunction

Oncotarget ◽  
2017 ◽  
Vol 8 (11) ◽  
pp. 18106-18117 ◽  
Author(s):  
Chun-Hao Tsai ◽  
Amos C. Hung ◽  
Yuan-Yin Chen ◽  
Ya-Wen Chiu ◽  
Pei-Wen Hsieh ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Mitochondrial Dysfunction ◽  
Cancer Cells ◽  
Colorectal Cancer Cells
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