ArticlePLoS biology2022
A DNA replication-independent function of pre-replication complex genes during cell invasion in C. elegans.
Article in PLoS biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- An automated high-resolution screening platform identifies regulators of anchor cell invasion inScience advances · 2026Article
- The replicative helicase CMG is required for the divergence of cell fates during asymmetric cell division in vivo.Nature communications · 2024Article
- The C. elegans anchor cell: A model to elucidate mechanisms underlying invasion through basement membrane.Seminars in cell & developmental biology · 2024Review
- Prolonging somatic cell proliferation through constitutive hox gene expression in C. elegans.Nature communications · 2023Article
- The Caenorhabditis elegans anchor cell transcriptome: ribosome biogenesis drives cell invasion through basement membrane.Development (Cambridge, England) · 2023Article
- Article
- Prereplication complex proteins get caught moonlighting.PLoS biology · 2022Article
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Authors and funding
11 authors at 2 institutions in 1 country.
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Abstract
Cell invasion is an initiating event during tumor cell metastasis and an essential process during development. A screen of C. elegans orthologs of genes overexpressed in invasive human melanoma cells has identified several components of the conserved DNA pre-replication complex (pre-RC) as positive regulators of anchor cell (AC) invasion. The pre-RC genes function cell-autonomously in the G1-arrested AC to promote invasion, independently of their role in licensing DNA replication origins in proliferating cells. While the helicase activity of the pre-RC is necessary for AC invasion, the downstream acting DNA replication initiation factors are not required. The pre-RC promotes the invasive fate by regulating the expression of extracellular matrix genes and components of the PI3K signaling pathway. Increasing PI3K pathway activity partially suppressed the AC invasion defects caused by pre-RC depletion, suggesting that the PI3K pathway is one critical pre-RC target. We propose that the pre-RC, or a part of it, acts in the postmitotic AC as a transcriptional regulator that facilitates the switch to an invasive phenotype.
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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.