ArticleJournal of translational medicine2012
Blockade of phospholipid scramblase 1 with its N-terminal domain antibody reduces tumorigenesis of colorectal carcinomas in vitro and in vivo.
Article in Journal of translational medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Pooled it
- Isolation and functional properties of highly-purified N-terminal domain of human NaPi2b by scalable "resin overload" technique.Analytical biochemistry · 2025Article
- The RELT Family of Proteins: An Increasing Awareness of Their Importance for Cancer, the Immune System, and Development.Biomedicines · 2023Review
- Phospholipid scramblase 1: a protein with multiple functions via multiple molecular interactors.Cell communication and signaling : CCS · 2022Review
- Phospholipid Scramblases: Role in Cancer Progression and Anticancer Therapeutics.Frontiers in genetics · 2022Review
- RNA interference-mediated downregulation of phospholipid scramblase 1 expression in primary liver cancerOncology letters · 2020Article
- Article
- ANO6 promotes cell proliferation and invasion in glioma through regulating the ERK signaling pathway.OncoTargets and therapy · 2019Article
- CD95/Fas Increases Stemness in Cancer Cells by Inducing a STAT1-Dependent Type I Interferon Response.Cell reports · 2017Article
- Article
- Effects of folylpolyglutamate synthase modulation on global and gene-specific DNA methylation and gene expression in human colon and breast cancer cells.The Journal of nutritional biochemistry · 2016Article
- Induction of PLSCR1 in a STING/IRF3-dependent manner upon vector transfection in ovarian epithelial cells.PloS one · 2015Article
- N-terminal proline-rich domain is required for scrambling activity of human phospholipid scramblases.The Journal of biological chemistry · 2014Article
- The role of TMEM16A (ANO1) and TMEM16F (ANO6) in cell migration.Pflugers Archiv : European journal of physiology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMembrane-bound phospholipid scramblase 1 (PLSCR1) is involved in both lipid trafficking and cell signaling. Previously, we showed that PLSCR1 is overexpressed in many colorectal carcinomas (CRCs). In the present study, we investigated the tumorigenic role of PLSCR1 in CRC and suggest that it is a potential therapeutic target.
methodsTo identify PLSCR1 as a therapeutic target, we studied the tumorigenic properties of CRC cell lines treated with a monoclonal antibody (NP1) against the N-terminus of PLSCR1 in vitro and in vivo. We also investigated cell cycle status and epidermal growth factor receptor-related pathways and downstream effectors of PLSCR1 after blocking its function with NP1.
resultsTreating CRC cells with NP1 in vitro and in vivo decreased cell proliferation, anchorage-independent growth, migration, and invasion. Adding NP1 to the CRC cell line HT29 caused arrest at G1/S. Treating HT29 cells with NP1 significantly decreased the expression of cyclin D1 and phosphorylation levels of Src, the adaptor protein Shc, and Erks. The reduced level of cyclin D1 led to an increase in the activated form of the tumor suppressor retinoblastoma protein via dephosphorylation. These actions led to attenuation of tumorigenesis.
conclusionsTherefore, PLSCR1 may serve as a potential therapeutic target for CRC.
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