ArticleOncotarget2016
CATS (FAM64A) abnormal expression reduces clonogenicity of hematopoietic cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
The trial behind it
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Who cites it
11 citing papers in PubMed, 27 citations in OpenAlex.
- FAM64A silencing inhibits the proliferation, migration, invasion, and epithelial-mesenchymal transition in ovarian cancer cells via activating Hippo pathway.Discover oncology · 2025Article
- Article
- Predictive value of PIMREG in the prognosis and response to immune checkpoint blockade of glioma patients.Frontiers in immunology · 2022Article
- Article
- Pan-Cancer Analysis of PIMREG as a Biomarker for the Prognostic and Immunological Role.Frontiers in genetics · 2021Article
- Article
- FAM64A Promotes Osteosarcoma Cell Growth and Metastasis and Is Mediated by miR-493.Journal of oncology · 2020Article
- FAM64A positively regulates STAT3 activity to promote Th17 differentiation and colitis-associated carcinogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Overexpression of PIMREG promotes breast cancer aggressiveness via constitutive activation of NF-κB signaling.EBioMedicine · 2019Article
- Aberrant FAM64A mRNA expression is an independent predictor of poor survival in pancreatic cancer.PloS one · 2019Article
- PIMREG, a Marker of Proliferation, Facilitates Aggressive Development of Cholangiocarcinoma Cells Partly Through Regulating Cell Cycle-Related Markers.Technology in cancer research & treatmentArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The CATS (FAM64A) protein interacts with CALM (PICALM) and the leukemic fusion protein CALM/AF10. CATS is highly expressed in leukemia, lymphoma and tumor cell lines and its protein levels strongly correlates with cellular proliferation in both malignant and normal cells. In order to obtain further insight into CATS function we performed an extensive analysis of CATS expression during differentiation of leukemia cell lines. While CATS expression decreased during erythroid, megakaryocytic and monocytic differentiation, a markedly increase was observed in the ATRA induced granulocytic differentiation. Lentivirus mediated silencing of CATS in U937 cell line resulted in somewhat reduced proliferation, altered cell cycle progression and lower migratory ability in vitro; however was not sufficient to inhibit tumor growth in xenotransplant model. Of note, CATS knockdown resulted in reduced clonogenicity of CATS-silenced cells and reduced expression of the self-renewal gene, GLI-1. Moreover, retroviral mediated overexpression of the murine Cats in primary bone marrow cells lead to decreased colony formation. Although our in vitro data suggests that CATS play a role in cellular processes important for tumorigenesis, such as cell cycle control and clonogenicity, these effects were not observed in vivo.
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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.