ArticleScientific reports2019
Activation of the PERK-ATF4 pathway promotes chemo-resistance in colon cancer cells.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed.
- Single-nuclei UPR profiling by flow cytometry reveals bortezomib resistance mechanisms in multiple myeloma.EMBO molecular medicine · 2026Article
- ASCC3 promotes chemosensitivity in colorectal cancer cells.Scientific reports · 2026Article
- From stress to homeostasis: Mass spectrometry-based insights into the unfolded protein response (UPR) and proteostasis.Advances in biological regulation · 2026Review
- Network-level reprogramming of cell death pathways in colorectal cancer cells by combined thymoquinone and 5-fluorouracil treatment.Frontiers in molecular biosciences · 2026Article
- Mutation and Microsatellite Instability (MSI) Affect the Differential Gene Expression of Folic Acid and 5-Flourouracil Metabolism-Related Genes in Colorectal Carcinoma.Current oncology (Toronto, Ont.) · 2025Article
- Genes-first and phenotypes-first paths to treatment resistance in hematological malignancies.Cell death & disease · 2025Review
- Review
- ATF4 promotes glutaminolysis and glycolysis in colorectal cancer by transcriptionally inducing SLC1A5.Acta biochimica et biophysica Sinica · 2025Article
- Impact of proteostasis workload on sensitivity to proteasome inhibitors in multiple myeloma.Clinical and experimental medicine · 2025Review
- CRISPR/Cas9 system: a novel approach to overcome chemotherapy and radiotherapy resistance in cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Fine-Tuning of ATF4 DNA Binding Activity by a Secondary Basic Motif Unique to the ATF-X Subfamily of bZip Transcription Factors.Biochemistry · 2025Article
- Endoplasmic Reticulum Stress: Triggers Microenvironmental Regulation and Drives Tumor Evolution.Cancer medicine · 2025Review
- 14-3-3σ restricts YY1 to the cytoplasm, promoting therapy resistance, and tumor progression in colorectal cancer.International journal of cancer · 2025Article
- Acquired resistance to molecularly targeted therapies for cancer.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- ATF4 inhibits tumor development and mediates p-GCN2/ASNS upregulation in colon cancer.Scientific reports · 2024Article
- Mammalian integrated stress responses in stressed organelles and their functions.Acta pharmacologica Sinica · 2024Review
- NCI 159456 PERK Inhibitor as a Targeted Therapy for Lung Cancer: An In Vitro Study.Biomedicines · 2024Article
- Endoplasmic reticulum stress and therapeutic strategies in metabolic, neurodegenerative diseases and cancer.Molecular medicine (Cambridge, Mass.) · 2024Review
- Sublethal engagement of apoptotic pathways in residual cancer.Trends in cell biology · 2024Review
- Control of immune cell function by the unfolded protein response.Nature reviews. Immunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colon cancer is a major health problem worldwide. While chemotherapy remains a main approach for treating late-stage colon cancer patients, most, if not all, of them will develop drug resistance and die of uncontrollable disease progression eventually. Therefore, identification of mechanism of drug resistance and development of overcoming strategy hold great significance in management of colon cancer. In this study, we discovered that activation of the PERK branch of the unfolded protein response (UPR) pathways is required for colon cancer cells to survive treatment of 5-Fluorouracil (5-FU), one of the first-line chemotherapeutics for late-stage colon cancer patients. Genetic and pharmacological inhibition of PERK or its downstream factors greatly sensitize colon cancer cells to 5-FU. Most importantly, in vivo use of PERK inhibitor synergizes with 5-FU in suppressing the growth of colon cancer cells in mouse models. In summary, our findings established a promising way to overcome resistance to chemotherapy in colon cancer.
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.