Document Detail


Programmed cell death 4 and microRNA 21 inverse expression is maintained in cells and exosomes from ovarian serous carcinoma effusions.
MedLine Citation:
PMID:  24888238     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
BACKGROUND: Ovarian serous carcinoma (OSC) is a fatal gynecologic malignancy usually presenting with bilateral localization and malignant peritoneal effusion. Programmed cell death 4 (PDCD4) is a tumor suppressor gene whose expression is directly controlled by microRNA-21 (miR-21). Exosomes are small cell-derived vesicles that participate in intercellular communication, delivering their cargo of molecules to specific cells. Exosomes are involved in several physiological and pathological processes including oncogenesis, immunomodulation, angiogenesis, and metastasis. The current study analyzed the expression of PDCD4 and miR-21 in resected OSC specimens and in cells and exosomes from OSC peritoneal effusions.
METHODS: PDCD4 was immunohistochemically examined in 14 normal ovaries, 14 serous cystadenoma (CA), and 14 OSC cases. Quantitative reverse transcriptase-polymerase chain reaction analysis of PDCD4 and miR-21 expression was performed in CA and OSC cases and in cells and exosomes obtained from 10 OSC and 10 nonneoplastic peritoneal effusions. miR-21 was also evaluated by in situ hybridization.
RESULTS: Immunohistochemistry demonstrated a gradual PDCD4 loss from normal ovaries to CA and OSC specimens. Quantitative reverse transcriptase-polymerase chain reaction displayed higher PDCD4 messenger RNA levels in CA specimens compared with OSC cases and highlighted miR-21 overexpression in OSC specimens. In situ hybridization detected miR-21 only in OSC cells. This PDCD4 and miR-21 inverse expression was also noted in cells and exosomes from OSC peritoneal effusions compared with nonneoplastic effusions.
CONCLUSIONS: PDCD4 and miR-21 are involved in OSC oncogenesis. The transfer of miR-21 by exosomes could promote oncogenic transformation in target cells distant from the primary tumor without direct colonization by cancer cells and could be used as a diagnostic tool. Cancer (Cancer Cytopathol) 2014. © 2014 American Cancer Society.
Authors:
Rocco Cappellesso; Andrea Tinazzi; Thomas Giurici; Francesca Simonato; Vincenza Guzzardo; Laura Ventura; Marika Crescenzi; Silvia Chiarelli; Ambrogio Fassina
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-5-28
Journal Detail:
Title:  Cancer cytopathology     Volume:  -     ISSN:  1934-6638     ISO Abbreviation:  Cancer Cytopathol     Publication Date:  2014 May 
Date Detail:
Created Date:  2014-6-3     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101499453     Medline TA:  Cancer Cytopathol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
© 2014 American Cancer Society.
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