Evidence map›Paper›PMID 22880071›Full record

ArticlePloS one2012

Spontaneous cancer-stromal cell fusion as a mechanism of prostate cancer androgen-independent progression.

Ruoxiang Wang, Xiaojuan Sun, Christopher Y Wang, Peizhen Hu, Chia-Yi Chu, Shurong Liu, Haiyen E Zhau, Leland W K Chung

Abstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed.

  1. Review
  2. How Do Cancer Cells Fuse and Why?Advances in experimental medicine and biology · 2026
    Review
  3. Review
  4. Cell Fusion and Syncytia Formation in Cancer.Results and problems in cell differentiation · 2024
    Review
  5. Microfluidic-based human prostate-cancer-on-chip.Frontiers in bioengineering and biotechnology · 2024
    Article
  6. Article
  7. Generation of Cancer Stem/Initiating Cells by Cell-Cell Fusion.International journal of molecular sciences · 2022
    Review
  8. Review
  9. Tumor Hybrid Cells: Nature and Biological Significance.Frontiers in cell and developmental biology · 2022
    Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Kinins in Glioblastoma Microenvironment.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2019
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Ruoxiang WangDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, United States of America. ruoxiang.wang@cshs.org
Xiaojuan Sun
Christopher Y Wang
Peizhen Hu
Chia-Yi Chu
Shurong Liu
Haiyen E Zhau
Leland W K Chung

Funding

Prostate Cancer Bone Metastasis: Biology and TargetingP01CA098912 · NCI · EMORY UNIVERSITY · PI ZAYZAFOON, MAJD · 2003 to 2019
$24.0M
MSM/WCI Partnership To Investigate Mechanisms of Prostate Cancer: Planning StageP20CA132388 · NCI · EMORY UNIVERSITY · PI MARSHALL, FRAY F. · 2007 to 2009
$407k
Functional characterization of PrLZ in prostate cancerR21CA112330 · NCI · EMORY UNIVERSITY · PI WANG, RUOXIANG · 2005 to 2006
$260k
NCI NIH HHS CA132388NCI NIH HHS CA98912-02NCI NIH HHS P01 CA098912NCI NIH HHS P20 CA132388NCI NIH HHS PC040578NCI NIH HHS R21 CA112330NCI NIH HHS R21CA112330
6 · The paper itself

Abstract

We have previously shown that human prostate cancer cells are capable of acquiring malignant attributes through interaction with stromal cells in the tumor microenvironment, while the interacting stromal cells can also become affected with both phenotypic and genotypic alterations. This study used a co-culture model to investigate the mechanism underlying the co-evolution of cancer and stromal cells. Red fluorescent androgen-dependent LNCaP prostate cancer cells were cultured with a matched pair of normal and cancer-associated prostate myofibroblast cells to simulate cancer-stromal interaction, and cellular changes in the co-culture were documented by tracking the red fluorescence. We found frequent spontaneous fusions between cancer and stromal cells throughout the co-culture. In colony formation assays assessing the fate of the hybrid cells, most of the cancer-stromal fusion hybrids remained growth-arrested and eventually perished. However, some of the hybrids survived to form colonies from the co-culture with cancer-associated stromal cells. These derivative clones showed genomic alterations together with androgen-independent phenotype. The results from this study reveal that prostate cancer cells are fusogenic, and cancer-stromal interaction can lead to spontaneous fusion between the two cell types. While a cancer-stromal fusion strategy may allow the stromal compartment to annihilate invading cancer cells, certain cancer-stromal hybrids with increased survival capability may escape annihilation to form a derivative cancer cell population with an altered genotype and increased malignancy. Cancer-stromal fusion thus lays a foundation for an incessant co-evolution between cancer and the cancer-associated stromal cells in the tumor microenvironment.

Indexed as

Disease ProgressionAndrogensCell FusionCell Line, TumorCell ShapeCell TrackingClone CellsCoculture TechniquesGenotypeHumansMalePhenotypeProstatic NeoplasmsStromal CellsTime FactorsTumor Stem Cell AssayAndrogens

Identifiers

PMID22880071
PMCPMC3411834

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Registered trials

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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.