Chlamydia trachomatis modulates expression of tumor suppressor gene caveolin-1 and oncogene C-myc in the transformation zone of non-neoplastic cervical tissue

Schlott, Thilo; Eiffert, Helmut; Bohne, Wolfgang; Landgrebe, Jobst; Brunner, Edgar; Spielbauer, Bettina; Knight, Bryan

doi:10.1016/j.ygyno.2005.04.034

Cited by 20 publications

(14 citation statements)

References 54 publications

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“…C. trachomatis may promote the persistence of HPV infection (213,224). In vitro infection of fibroblasts and cervical tissue that were free of HPV showed decreased expression of the tumor suppressor gene caveolin-1 and increased expression of the proto-oncogene c-myc, indicating other possible ways that C. trachomatis may promote oncogenesis (218).…”

Section: Alterations Of Normal Host Responses Chronic Inflammationmentioning

confidence: 99%

Role of Bacteria in Oncogenesis

2010

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SUMMARY Although scientific knowledge in viral oncology has exploded in the 20th century, the role of bacteria as mediators of oncogenesis has been less well elucidated. Understanding bacterial carcinogenesis has become increasingly important as a possible means of cancer prevention. This review summarizes clinical, epidemiological, and experimental evidence as well as possible mechanisms of bacterial induction of or protection from malignancy.

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Section: Alterations Of Normal Host Responses Chronic Inflammationmentioning

confidence: 99%

Role of Bacteria in Oncogenesis

2010

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“…Additionally, the 5=-flanking region contains a CAAT sequence and a Sp1 consensus sequence (4). SRE-like elements are involved in the transcriptional response to stimuli, such as low-density lipoprotein-free cholesterol (LDL-FC) (89,114). Other transcription factors reported to regulate cav-1 expression include the forkhead (FKHR) family of transcription factors, FOXO3a (20, 105), C-myc (89,114), and NF-B (104).…”

Section: Caveolin-1mentioning

confidence: 99%

Caveolin-1: a critical regulator of lung injury

Jin

Lee

Minshall

et al. 2011

American Journal of Physiology-Lung Cellular and Molecular Phys

103

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Caveolin-1 (cav-1), a 22-kDa transmembrane scaffolding protein, is the principal structural component of caveolae. Cav-1 regulates critical cell functions including proliferation, apoptosis, cell differentiation, and transcytosis via diverse signaling pathways. Abundant in almost every cell type in the lung, including type I epithelial cells, endothelial cells, smooth muscle cells, fibroblasts, macrophages, and neutrophils, cav-1 plays a crucial role in the pathogenesis of acute lung injury (ALI). ALI and its severe form, acute respiratory distress syndrome (ARDS), are responsible for significant morbidity and mortality in intensive care units, despite improvement in ventilation strategies. The pathogenesis of ARDS is still poorly understood, and therapeutic options remain limited. In this article, we summarize recent data regarding the regulation and function of cav-1 in lung biology and pathology, in particular as it relates to ALI. We further discuss the potential molecular and cellular mechanisms by which cav-1 expression contributes to ALI. Investigating the cellular functions of cav-1 may provide new insights for understanding the pathogenesis of ALI and provide novel targets for therapeutic interventions in the future.

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“…Recently, it has been shown that human fibroblasts infected in vitro by CT responded to this infection with a reduction in the expression of tumor suppressor gene caveolin-1 and with the upregulation of the oncogene c-myc [13] . Only recently has HSV2 DNA been detected in CC samples by PCR [14,15] , but this was not confirmed in other studies [16,17] .…”

mentioning

confidence: 99%

“…Negative and positive controls were included in each PCR run. CT DNA was amplified by semi-nested PCR directed against the bacterial cryptic plasmid pCT which is highly conserved among CT serovars [13] .…”

mentioning

confidence: 99%

Co-Expression of HSV2 and <i>Chlamydia trachomatis</i> in HPV-Positive Cervical Cancer and Cervical Intraepithelial Neoplasia Lesions Is Associated with Aberrations in Key Intracellular Pathways

Paba¹,

Bonifacio

Bonito

et al. 2008

Intervirology

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Objective: Oncogenic human papillomaviruses (HPVs) are the etiological agents of cervical cancer. Different cofactors might be needed for malignant transformation, but they still remain elusive. Methods: To delineate the role of Chlamydia trachomatis (CT) and herpes simplex virus type 2 (HSV2) in HPV-positive cervical intraepithelial neoplasia (CIN) lesions and cervical carcinoma a series of 149 cervical cancer and CIN biopsies were analyzed for CT and HSV2 DNA by PCR, and HPV genotyped by InnoLipa. Monitoring of aberrations in key intracellular pathways due to CT/HSV2 and HPV co-expression were analyzed with 13 biomarkers. Results: Of the 149 samples tested, 136 were HPV DNA positive; 32/136 contained also CT DNA and 29 HSV2 DNA. Detection of CT was significantly (p = 0.0001) related to multiple-type HPV infections, while HSV2 was of borderline significance (p = 0.053). Of the 13 biomarkers tested, cytoplasmic and nuclear NF-ĸB and VEGF-C were significantly increased in CT+/HPV+ lesions; p = 0.023, p = 0.045, and p = 0.020 as well as survivin, p = 0.026. Survivin was the only marker that was overexpressed also in HSV2+/HPV+ lesions, p = 0.027. Conclusions: CT infection favors the entry and persistence of multiple HR-HPV types, which leads to viral integration, inhibition of apoptosis, overexpression of E6/E7 oncogenes and cell transformation.

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Chlamydia trachomatis modulates expression of tumor suppressor gene caveolin-1 and oncogene C-myc in the transformation zone of non-neoplastic cervical tissue

Cited by 20 publications

References 54 publications

Role of Bacteria in Oncogenesis

Role of Bacteria in Oncogenesis

Caveolin-1: a critical regulator of lung injury

Co-Expression of HSV2 and <i>Chlamydia trachomatis</i> in HPV-Positive Cervical Cancer and Cervical Intraepithelial Neoplasia Lesions Is Associated with Aberrations in Key Intracellular Pathways

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