ArticleProceedings of the National Academy of Sciences of the United States of America2002
Biological models and genes of tumor reversion: cellular reprogramming through tpt1/TCTP and SIAH-1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 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
123 citing papers in PubMed, 250 citations in OpenAlex.
- Extracellular vesicles shape tumourigenesis: from signalling networks to systemic progression.Cancer metastasis reviews · 2026Review
- Fortilin deficiency induces anti-atherosclerotic phenotypes in macrophages and protects hypercholesterolemic mice against atherosclerosis.Communications biology · 2025Article
- miRNAs from Zebrafish Embryo Extracts Inhibit Breast Cancer Invasiveness and Migration by Modulating miR-218-5p/PI3K Pathway.International journal of molecular sciences · 2025Article
- Fortilin binds CTNNA3 and protects it against phosphorylation, ubiquitination, and proteasomal degradation to guard cells against apoptosis.Communications biology · 2025Article
- Translationally Controlled Tumor Protein Enhances Angiogenesis in Ovarian Tumors by Activating Vascular Endothelial Growth Factor Receptor 2 Signaling.Biomolecules & therapeutics · 2025Article
- Translationally Controlled Tumor Protein (TCTP) and Growth Regulation in the Drosophila Model.Advances in experimental medicine and biology · 2025Article
- The multifaceted potential ofHeliyon · 2024Review
- Biological role and expression of translationally controlled tumor protein (TCTP) in tumorigenesis and development and its potential for targeted tumor therapy.Cancer cell international · 2024Review
- TCTP regulates genotoxic stress and tumorigenicity via intercellular vesicular signaling.EMBO reports · 2024Article
- The phenotypic reversion of cancer: Experimental evidences on cancer reversibility through epigenetic mechanisms (Review).Oncology reports · 2024Review
- Tumor Heterogeneity of STEAP4 in Malignant Progression of Oral Squamous Cell Carcinoma.Journal of Cancer · 2024Article
- Prognostic value of translationally controlled tumor protein in colon cancer.Molecular and clinical oncology · 2023Article
- Normalizing Input-Output Relationships of Cancer Networks for Reversion Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Tctp, a unique Ing5-binding partner, inhibits the chromatin binding of Enok inProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Critical transition and reversion of tumorigenesis.Experimental & molecular medicine · 2023Review
- Dissected subgroups predict the risk of recurrence of stage II colorectal cancer and select rational treatment.Frontiers in immunology · 2023Article
- Article
- Translationally controlled tumor protein: the mediator promoting cancer invasion and migration and its potential clinical prospects.Journal of Zhejiang University. Science. B · 2022Review
- Highly expressed genes in multiple myeloma cells - what can they tell us about the disease?European journal of haematology · 2022Article
- Fortilin interacts with TGF-β1 and prevents TGF-β receptor activation.Communications biology · 2022Article
63 more citing papers are in PubMed but not listed here.
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor reversion is the process by which some cancer cells lose their malignant phenotype. This study was aimed at defining some of the molecular and phenotypic properties of this process. Biological models of tumor reversion were isolated from human leukemia and breast cancer cell lines by using the H-1 parvovirus as a selective agent. Differential gene expression analysis was performed between the parental malignant cells and their revertants or alternatively between these parental cells and their SIAH-1 transfectant counterparts. These SIAH-1 transfectants have a suppressed malignant phenotype and were used as a control for a viral-free system. Two hundred sixty-three genes were found to be either activated or inhibited during the reversion process, as confirmed by Northern blot analysis or quantitative PCR. Of these, 32% were differentially expressed in all systems, irrespective of whether parvovirus-selected, SIAH-1 overexpressing, or p53 mutant or wild-type cell lines were used, suggesting the existence of a universal mechanism underlying tumor reversion. Translationally Controlled Tumor Protein (tpt1/TCTP) has the strongest differential expression, down-regulated in the reversion of U937- and SIAH-1-overexpressing cells. Inhibition of TCTP expression by anti-sense cDNA or small interfering RNA molecules results in suppression of the malignant phenotype and in cellular reorganization, similar to the effect of SIAH-1. Hence, tumor reversion can be defined at the molecular level, not just as the reversal of malignant transformation, but as a biological process in its own right involving a cellular reprogramming mechanism, overriding genetic changes in cancer, by triggering an alternative pathway leading to suppression of tumorigenicity.
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.