ArticleOncogene1999
Suppression of src-induced transformed phenotype by expression of tropomyosin-1.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 63 citations in OpenAlex.
- Relevance Analysis of TPM2 and Clinicopathological Characteristics in Breast Cancer.International journal of general medicine · 2024Article
- The remodelling of actin composition as a hallmark of cancer.Translational oncology · 2021Review
- Myocardin-related transcription factor A (MRTF-A) activity-dependent cell adhesion is correlated to focal adhesion kinase (FAK) activity.Oncotarget · 2016Article
- Expression of tropomyosin 2 gene isoforms in human breast cancer cell lines.Oncology reports · 2016Article
- Hypoxia alters the recruitment of tropomyosins into the actin stress fibres of neuroblastoma cells.BMC cancer · 2015Article
- The Ras-ERK pathway modulates cytoskeleton organization, cell motility and lung metastasis signature genes in MDA-MB-231 LM2.Oncogene · 2014Article
- From the Cover: Neutralization of terminal differentiation in gliomagenesis.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Tropomyosin isoforms and reagents.Bioarchitecture · 2011Article
- New insights into the regulation of the actin cytoskeleton by tropomyosin.International review of cell and molecular biology · 2010Review
- Resensitization of breast cancer cells to anoikis by tropomyosin-1: role of Rho kinase-dependent cytoskeleton and adhesion.Oncogene · 2005Article
- Loss of expression of tropomyosin-1, a novel class II tumor suppressor that induces anoikis, in primary breast tumors.Oncogene · 2003Article
- Functional analysis of the actin-binding protein, tropomyosin 1, in neuroblastoma.British journal of cancer · 2003Article
- Calponin repeats regulate actin filament stability and formation of podosomes in smooth muscle cells.Molecular biology of the cell · 2003Article
- Overexpression of kinase suppressor of Ras upregulates the high-molecular-weight tropomyosin isoforms in ras-transformed NIH 3T3 fibroblasts.Molecular and cellular biology · 2003Article
- Opposing roles of the extracellular signal-regulated kinase and p38 mitogen-activated protein kinase cascades in Ras-mediated downregulation of tropomyosin.Molecular and cellular biology · 2002Article
- Article
- Post-transcriptional down-regulation of ROCKI/Rho-kinase through an MEK-dependent pathway leads to cytoskeleton disruption in Ras-transformed fibroblasts.Molecular biology of the cell · 2002Article
- Cytoskeletal organization in tropomyosin-mediated reversion of ras-transformation: Evidence for Rho kinase pathway.Oncogene · 2001Article
- TPM3-ALK and TPM4-ALK oncogenes in inflammatory myofibroblastic tumors.The American journal of pathology · 2000Article
- Interior decoration: tropomyosin in actin dynamics and cell migration.Cell adhesion & migrationReview
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 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Suppression of high M(r) tropomyosins (TMs) is a common feature of transformed cells. Previous work from this laboratory has demonstrated that the isoform 1 of TM, TM1, acts as an anti-oncogene in ras-transformed murine fibroblasts. In this study, we have investigated whether TM1 is a ras-specific suppressor, or a general suppressor protein of the cellular transformation. V-src transformed fibroblasts, which express decreased TM1, were transduced with a full-length cDNA to overexpress TM1. Both the control and the transduced cells expressed v-src kinase at comparable levels. TM1 expressing (src-T1) cells grew at a lower rate in monolayer, exhibited well spread, flat morphology than the control cells. Enhanced expression of TM1 resulted in improved microfilamental architecture. More significantly, src-T1 cells completely failed to grow under anchorage independent conditions. These data demonstrate that TM1 is as an anti-oncogene of functionally diverse oncogenes, and it is a class II tumor suppressor protein.
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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.