ReviewCancers2020
Targeting Protein Synthesis in Colorectal Cancer.
Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Study on the effects of rapamycin and the mTORC1/2 dual inhibitor OSI-027 on the metabolism of colon cancer cells based on UPLC-MS/MS metabolomics.Investigational new drugs · 2024Article
- Article
- Beneficial effects of alpha-1 antitrypsin therapy in a mouse model of colitis-associated colon cancer.BMC cancer · 2023Article
- Targeting Myc-driven stress addiction in colorectal cancer.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2023Review
- Quassinoid analogs exert potent antitumor activity via reversible protein biosynthesis inhibition in human colorectal cancer.Biochemical pharmacology · 2023Article
- CDK13 phosphorylates the translation machinery and promotes tumorigenic protein synthesis.Oncogene · 2023Article
- Targeting mitochondrial tyrosyl-tRNA synthetase YARS2 suppresses colorectal cancer progression.Cancer biology & therapy · 2022Article
- GCN2 inhibition sensitizes arginine-deprived hepatocellular carcinoma cells to senolytic treatment.Cell metabolism · 2022Article
- RNA polymerase I inhibition induces terminal differentiation, growth arrest, and vulnerability to senolytics in colorectal cancer cells.Molecular oncology · 2022Article
- Single-cell atlas of the aging mouse colon.iScience · 2022Article
- Therapy Trial Design in Vanishing White Matter: An Expert Consortium Opinion.Neurology. Genetics · 2022Review
- Targeting Myc-driven stress vulnerability in mutant KRAS colorectal cancer.Molecular biomedicine · 2022Article
- Role of PTEN, PI3K, and mTOR in Triple-Negative Breast Cancer.Life (Basel, Switzerland) · 2021Article
- NCOR1 Sustains Colorectal Cancer Cell Growth and Protects against Cellular Senescence.Cancers · 2021Article
- Lyme Neuroborreliosis: Mechanisms ofBrain sciences · 2021Review
- CIP2A regulates MYC translation (via its 5'UTR) in colorectal cancer.International journal of colorectal disease · 2021Article
- Article
- IntracellularFrontiers in cellular and infection microbiology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Under physiological conditions, protein synthesis controls cell growth and survival and is strictly regulated. Deregulation of protein synthesis is a frequent event in cancer. The majority of mutations found in colorectal cancer (CRC), including alterations in the WNT pathway as well as activation of RAS/MAPK and PI3K/AKT and, subsequently, mTOR signaling, lead to deregulation of the translational machinery. Besides mutations in upstream signaling pathways, deregulation of global protein synthesis occurs through additional mechanisms including altered expression or activity of initiation and elongation factors (e.g., eIF4F, eIF2α/eIF2B, eEF2) as well as upregulation of components involved in ribosome biogenesis and factors that control the adaptation of translation in response to stress (e.g., GCN2). Therefore, influencing mechanisms that control mRNA translation may open a therapeutic window for CRC. Over the last decade, several potential therapeutic strategies targeting these alterations have been investigated and have shown promising results in cell lines, intestinal organoids, and mouse models. Despite these encouraging in vitro results, patients have not clinically benefited from those advances so far. In this review, we outline the mechanisms that lead to deregulated mRNA translation in CRC and highlight recent progress that has been made in developing therapeutic strategies that target these mechanisms for tumor therapy.
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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.