ArticlePloS one2013
Chlamydia induces anchorage independence in 3T3 cells and detrimental cytological defects in an infection model.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Pooled it
- Evaluation of Vimentin as a Marker of Cervical Carcinogenesis in Women Infected with Human Papillomavirus andInternational journal of hematology-oncology and stem cell research · 2025Article
- Genital infections in high-risk human papillomavirus positive Paraguayan women aged 30-64 with and without cervical lesions.PloS one · 2024Article
- When Bacteria and Viruses Collide: A Tale ofViruses · 2023Review
- TheProceedings of the National Academy of Sciences of the United States of America · 2023Article
- In Search of a Mechanistic Link between Chlamydia trachomatis-Induced Cellular Pathophysiology and Oncogenesis.Infection and immunity · 2023Review
- Deregulation of the cyclin-dependent kinase inhibitor p27 as a putative candidate for transformation inAIMS microbiology · 2023Article
- Review
- Chlamydia and HPV induce centrosome amplification in the host cell through additive mechanisms.Cellular microbiology · 2021Article
- Review
- Article
- Sulforaphane promotes chlamydial infection by suppressing mitochondrial protein oxidation and activation of complement C3.Protein science : a publication of the Protein Society · 2019Article
- Characterization of the Growth ofFrontiers in cellular and infection microbiology · 2017Article
- Subversion of host genome integrity by bacterial pathogens.Nature reviews. Molecular cell biology · 2016Review
- Review
- Chlamydia cell biology and pathogenesis.Nature reviews. Microbiology · 2016Review
- Multinucleation during C. trachomatis infections is caused by the contribution of two effector pathways.PloS one · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Chlamydia are gram negative, obligate intracellular bacterial organisms with different species causing a multitude of infections in both humans and animals. Chlamydia trachomatis is the causative agent of the sexually transmitted infection (STI) Chlamydia, the most commonly acquired bacterial STI in the United States. Chlamydial infections have also been epidemiologically linked to cervical cancer in women co-infected with the human papillomavirus (HPV). We have previously shown chlamydial infection results in centrosome amplification and multipolar spindle formation leading to chromosomal instability. Many studies indicate that centrosome abnormalities, spindle defects, and chromosome segregation errors can lead to cell transformation. We hypothesize that the presence of these defects within infected dividing cells identifies a possible mechanism for Chlamydia as a cofactor in cervical cancer formation. Here we demonstrate that infection with Chlamydia trachomatis is able to transform 3T3 cells in soft agar resulting in anchorage independence and increased colony formation. Additionally, we show for the first time Chlamydia infects actively replicating cells in vivo. Infection of mice with Chlamydia results in significantly increased cell proliferation within the cervix, and in evidence of cervical dysplasia. Confocal examination of these infected tissues also revealed elements of chlamydial induced chromosome instability. These results contribute to a growing body of data implicating a role for Chlamydia in cervical cancer development and suggest a possible molecular mechanism for this effect.
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Registered trials
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