ArticleScientific reports2019
A new model isolates glioblastoma clonal interactions and reveals unexpected modes for regulating motility, proliferation, and drug resistance.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Strength through diversity: how cancers thrive when clones cooperate.Molecular oncology · 2026Review
- Polyploid giant cancer cells (PGCC): short-term return to multicellularity.Biological research · 2025Article
- Signaling dynamics in coexisting monoclonal cell subpopulations unveil mechanisms of resistance to anti-cancer compounds.Cell communication and signaling : CCS · 2024Article
- Comparative single-cell RNA-sequencing profiling of BMP4-treated primary glioma cultures reveals therapeutic markers.Neuro-oncology · 2022Article
- If Artificial In Vitro Microenvironment Can Influence Tumor Drug Resistance Network via Modulation of lncRNA Expression?-Comparative Analysis of Glioblastoma-Derived Cell Culture Models and Initial Tumors In Vivo.Cellular and molecular neurobiology · 2022Article
- Morphological Phenotyping of Organotropic Brain- and Bone-Seeking Triple Negative Metastatic Breast Tumor Cells.Frontiers in cell and developmental biology · 2022Article
- Genetic diversity through social heterosis can increase virulence in RNA viral infections and cancer progression.Royal Society open science · 2021Article
- Group Behavior and Emergence of Cancer Drug Resistance.Trends in cancer · 2021Review
- Deciphering neural heterogeneity through cell lineage tracing.Cellular and molecular life sciences : CMLS · 2021Review
- Review
- Unveiling functional heterogeneity in breast cancer multicellular tumor spheroids through single-cell RNA-seq.Scientific reports · 2020Article
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Authors and funding
7 authors.
Funding
Abstract
Tumor clonal heterogeneity drives treatment resistance. But robust models are lacking that permit eavesdropping on the basic interaction network of tumor clones. We developed an in vitro, functional model of clonal cooperation using U87MG glioblastoma cells, which isolates fundamental clonal interactions. In this model pre-labeled clones are co-cultured to track changes in their individual motility, growth, and drug resistance behavior while mixed. This highly reproducible system allowed us to address a new class of fundamental questions about clonal interactions. We demonstrate that (i) a single clone can switch off the motility of the entire multiclonal U87MG cell line in 3D culture, (ii) maintenance of clonal heterogeneity is an intrinsic and influential cancer cell property, where clones coordinate growth rates to protect slow growing clones, and (iii) two drug sensitive clones can develop resistance de novo when cooperating. Furthermore, clonal communication for these specific types of interaction did not require diffusible factors, but appears to depend on cell-cell contact. This model constitutes a straightforward but highly reliable tool for isolating the complex clonal interactions that make up the fundamental "hive mind" of the tumor. It uniquely exposes clonal interactions for future pharmacological and biochemical studies.
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