ArticlePhysiological genomics2009
Lasp1 gene disruption is linked to enhanced cell migration and tumor formation.
Article in Physiological genomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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
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
15 citing papers in PubMed, 21 citations in OpenAlex.
- E7-mediated repression of miR-203 promotes LASP1-dependent proliferation in HPV-positive cervical cancer.Oncogene · 2024Article
- Gene network revealsFrontiers in neurology · 2023Article
- Lasp1 regulates adherens junction dynamics and fibroblast transformation in destructive arthritis.Nature communications · 2021Article
- Emerging roles for LPP in metastatic cancer progression.Journal of cell communication and signaling · 2018Review
- Cancer-associated fibroblasts regulate endothelial adhesion protein LPP to promote ovarian cancer chemoresistance.The Journal of clinical investigation · 2018Article
- Proteomic comparison of the EWS-FLI1 expressing cells EF with NIH-3T3 and actin remodeling effect of (R/W)EuPA open proteomics · 2016Article
- An update on the LIM and SH3 domain protein 1 (LASP1): a versatile structural, signaling, and biomarker protein.Oncotarget · 2015Review
- Proteomic analysis on effectors involved in BMP-2-induced osteogenic differentiation of beagle bone marrow mesenchymal stem cells.Proteome science · 2014Article
- A complex containing LPP and α-actinin mediates TGFβ-induced migration and invasion of ErbB2-expressing breast cancer cells.Journal of cell science · 2013Article
- Nuclear import of LASP-1 is regulated by phosphorylation and dynamic protein-protein interactions.Oncogene · 2013Article
- Investigating lasp-2 in cell adhesion: new binding partners and roles in motility.Molecular biology of the cell · 2013Article
- Article
- Acid secretion-associated translocation of KCNJ15 in gastric parietal cells.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- The Nebulin family: an actin support group.Trends in cell biology · 2011Review
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Lasp1 is an actin-binding, signaling pathway-regulated phosphoprotein that is overexpressed in several cancers. siRNA knockdown in cell lines retards cell migration, suggesting the possibility that Lasp1 upregulation influences cancer metastasis. Herein, we utilized a recently developed gene knockout model to assess the role of Lasp1 in modulating nontransformed cell functions. Wound healing and tumor initiation progressed more rapidly in Lasp1(-/-) mice compared with Lasp1(+/+) controls. Embryonic fibroblasts (MEFs) derived from Lasp1(-/-) mice also migrated more rapidly in vitro. These MEFs characteristically possessed increased focal adhesion numbers and displayed more rapid attachment compared with wild-type MEFs. Differential microarray analyses revealed alterations in message expression for proteins implicated in cell migration, adhesion, and cytoskeletal organization. Notably, the focal adhesion protein, lipoma preferred partner (LPP), a zyxin family member and putative Lasp1 binding protein, was increased about twofold. Because LPP gene disruption reduces cell migration, we hypothesize that LPP plays a role in enhancing the migratory capacity of Lasp1(-/-) MEFs, perhaps by modifying the subcellular localization of other motility-associated proteins. The striking contrast in the functional effects of loss of Lasp1 in innate cells compared with cell lines reveals distinct differences in mechanisms of motility and attachment in these models.
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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.