Livin and caspase-3 expression are negatively correlated in cervical squamous cell cancer

Overexpression in cancer cells of inhibitor of apoptosis proteins like livin appears to promote tumorigenesis by regulating expression of proteins involved in apoptosis signaling. Here, the authors investigated expression of livin and an apoptosis protein that is known to inhibit, caspase-3, in cerv...

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Veröffentlicht in:European journal of gynaecological oncology 2013, Vol.34 (2), p.152-155
Hauptverfasser: Xu, M, Xia, L P, Fan, L J, Xue, J L, Shao, W W, Xu, D
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Sprache:eng
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Zusammenfassung:Overexpression in cancer cells of inhibitor of apoptosis proteins like livin appears to promote tumorigenesis by regulating expression of proteins involved in apoptosis signaling. Here, the authors investigated expression of livin and an apoptosis protein that is known to inhibit, caspase-3, in cervical squamous cell carcinoma. Their expression was assessed for correlation with tumor invasiveness. Immunohistochemistry for livin and caspase-3 was used in 36 normal cervical tissues and in 98 samples of cervical squamous cell carcinoma. The percentage of cells expressing these proteins was compared between normal and cancer samples. Their expression rates in cancer samples were subsequently compared with one another and with the clinical and pathological characteristics of the samples. Livin was more commonly expressed in tumor samples than in normal tissues, while the opposite pattern was observed for caspase-3. Expression of livin was significantly associated with advanced clinical stage, higher pathological grade, and lymph node metastasis (p < 0.05). Expression of caspase-3 was significantly associated with lower clinical stage, lower pathological grade, and lack of lymph node metastasis (p < 0.05). Finally, expression of livin was negatively correlated to caspase-3 expression in cervical squamous cell carcinoma tissue (r = -0.57, p < 0.05). Livin may inhibit apoptosis in cervical squamous cell carcinoma by downregulating caspase-3, thereby promoting disease progression.
ISSN:0392-2936