ArticleCell cycle (Georgetown, Tex.)2023
3,5-diCQA suppresses colorectal cancer cell growth through ROS/AMPK/mTOR mediated mitochondrial dysfunction and ferroptosis.
Article in Cell cycle (Georgetown, Tex.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- Analysis of the correlation between systemic oxidative stress and clinical characteristics for the prognosis in neuroblastoma.Neurosurgical review · 2026Article
- ANGPTL8 accelerates bone loss in diabetic mice by promoting osteoclastic differentiation and inhibiting osteoblastic differentiation through AMPK pathway-mediated metabolic reprogramming.Cellular and molecular life sciences : CMLS · 2026Article
- Caffeoylquinic Acids From Lonicera japonica Thunb. as Hypoglycemic Agents: Network Pharmacology and Pharmacological Validation.Journal of diabetes research · 2026Article
- NRF2 as a ferroptosis gatekeeper in colorectal cancer: implications for therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- From mitochondrial dysregulation to ferroptosis: Exploring new strategies and challenges in radioimmunotherapy (Review).International journal of oncology · 2025Review
- Damnacanthus giganteus extract block diffuse large b-cell lymphoma proliferation and EMT by regulating mitochondrial dysfunction and glycolysis.Hereditas · 2025Article
- Liensinine reshapes the immune microenvironment and enhances immunotherapy by reprogramming metabolism through the AMPK-HIF-1α axis in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2025Article
- Magnolia kobus DC. suppresses neointimal hyperplasia by regulating ferroptosis and VSMC phenotypic switching in a carotid artery ligation mouse model.Chinese medicine · 2025Article
- Article
- CircMAN1A2_009 facilitates YBX1 nuclear localization to induce GLO1 activation for cervical adenocarcinoma cell growth.Cancer science · 2024Article
- Exploring the immunometabolic potential of Danggui Buxue Decoction for the treatment of IBD-related colorectal cancer.Chinese medicine · 2024Review
- Beyond Mortality: Exploring the Influence of Plant Phenolics on Modulating Ferroptosis-A Systematic Review.Antioxidants (Basel, Switzerland) · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
3,5-diCQA has been shown to have anti-tumor effect by decreasing cancer cell growth. However, the molecular mechanism by which 3,5-diCQA impacts colorectal cancer (CRC) cells is unknown. This study discovered that 3,5-diCQA had a suppressive effect on CRC cells, mainly in the inhibition of proliferation, migration, and the enhancement of apoptosis in HCT116 and SW480 cells. Additionally, 3,5-diCQA was found to cause cell cycle arrest in CRC cells. Meanwhile, we found that 3,5-diCQA activates the AMPK pathway through the generation of ROS, mediates mitochondrial damage, and reduces mitochondrial aerobic glycolysis and oxidative phosphorylation levels. 3,5-diCQA promoted oxidative damage and ferroptosis in CRC cells. Hence, we added ROS inhibitor NAC and found that the NAC reversed the effects of 3,5-diCQA on proliferation, apoptosis, ROS generation, and ferroptosis in CRC cells. Moreover, 3,5-diCQA was also shown to suppress the development of CRC tumor in a tumor-forming model of nude mice. In conclusion, we found that 3,5-diCQA enhances the oxidative damage and ferroptosis while reducing proliferation and migration of CRC cells, depending on mitochondrial dysfunction caused by the ROS/AMPK/mTOR pathway.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.