ArticleMolecular and cellular biology1994
Effects of c-myc expression on cell cycle progression.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
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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.
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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.
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Who cites it
57 citing papers in PubMed, 141 citations in OpenAlex.
- Zinc Finger Protein 143 Bidirectionally Regulates the Proliferation of Hepatocytes and Hepatocellular Carcinoma Cells via c-Myc.Cell biochemistry and function · 2026Article
- Gene Expression Alterations Associated With Resveratrol-Induced Antiproliferative Effects and S-Phase Cell Cycle Arrest in Osteosarcoma Cancer Cells.Journal of cellular and molecular medicine · 2026Article
- Re-expression of embryonic stem cell markers in malignant tissue: an observational study in pancreatic cancer.Anatomy & cell biology · 2026Article
- c-Myc knockdown restores tamoxifen sensitivity in triple-negative breast cancer by reactivating the expression of ERα: the central role of miR-152 and miR-148a.Breast cancer (Tokyo, Japan) · 2025Article
- Temporal myc dynamics permit mitotic bypass, promoting polyploid phenotypes.Cancer letters · 2025Review
- MYC Oncogene: A Druggable Target for Treating Cancers with Natural Products.Aging and disease · 2024Review
- Defective bone repletion in aged Balb/cBy mice was caused by impaired osteoblastic differentiation.Journal of bone and mineral metabolism · 2022Article
- ML323, a USP1 inhibitor triggers cell cycle arrest, apoptosis and autophagy in esophageal squamous cell carcinoma cells.Apoptosis : an international journal on programmed cell death · 2022Article
- Lipid phosphate phosphatase-2 promotes tumor growth through increased c-Myc expression.Theranostics · 2022Article
- MYC: a multipurpose oncogene with prognostic and therapeutic implications in blood malignancies.Journal of hematology & oncology · 2021Review
- The Role of Non-Coding RNAs in the Regulation of the Proto-Oncogene MYC in Different Types of Cancer.Biomedicines · 2021Review
- Bisphenol S and Epidermal Growth Factor Receptor Signaling in Human Placental Cytotrophoblasts.Environmental health perspectives · 2021Article
- Suprabasin-derived bioactive peptides identified by plasma peptidomics.Scientific reports · 2021Article
- MYC dysfunction modulates stemness and tumorigenesis in breast cancer.International journal of biological sciences · 2021Article
- Loss of Fbxw7 triggers mammary tumorigenesis associated with E2F/c-Myc activation and Trp53 mutation.Neoplasia (New York, N.Y.) · 2020Article
- Alterations of oncogenes expression in NK cells in patients with cancer.Immunity, inflammation and disease · 2017Article
- Morusin inhibits cell proliferation and tumor growth by down-regulating c-Myc in human gastric cancer.Oncotarget · 2017Article
- MYC-Driven Pathways in Breast Cancer Subtypes.Biomolecules · 2017Review
- Wnt9a Is Required for the Aortic Amplification of Nascent Hematopoietic Stem Cells.Cell reports · 2016Article
- The T-Box factor TBX3 is important in S-phase and is regulated by c-Myc and cyclin A-CDK2.Cell cycle (Georgetown, Tex.) · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We used targeted homologous recombination to disrupt one c-myc gene copy in a diploid fibroblast cell line and found that a twofold reduction in Myc expression resulted in lower exponential growth rates and a lengthening of the G0-to-S-phase transition (M. Shichiri, K. D. Hanson and J. M. Sedivy, Cell Growth Differ. 4:93-104, 1993). Myc is a transcription factor, and the number of target genes whose regulation could result in differential growth rates may be very large. We have approached this problem by examining effects of reduced c-myc expression in three broad areas: (i) secretion of growth factors, (ii) expression of growth factor receptors, and (iii) intracellular signal transduction between Myc and components of the intrinsic cell cycle clock. We have found no evidence that differential medium conditioning can account for the growth phenotypes. Likewise, the expression of receptors for platelet-derived growth factor, epidermal growth factor, basic fibroblast growth factor, and insulin-like growth factor I was the same in diploid and heterozygous cells (platelet-derived growth factor, epidermal growth factor, fibroblast growth factor, and insulin-like growth factor are the sole growth factors required by these cells for growth in serum-free medium). In contrast, expression of cyclin E, cyclin A, and Rb phosphorylation were delayed when quiescent c-myc heterozygous cells were stimulated to enter the cell cycle. Expression of cyclin D1, cyclin D3, and Cdk2 was not affected. The timing of cyclin E induction was the earliest observable effect of reduced Myc expression. Our data indicate that Myc contributes to regulation of proliferation by a cell-autonomous mechanism that involves the modulation of cyclin E expression and, consequently, progression through the restriction point of the cell cycle.
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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.