Expression of Survivin and Cell Apoptosis in Endometrial Cancer and Hyperplastic Endometrium

Tarkowski, Rafał; Jurczak-Jamroz˙, Wioletta; Kotarski, J

doi:10.1136/ijgc-00009577-200303001-00263

Cited by 3 publications

(3 citation statements)

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“…Survivin expression in hyperplastic endometrium is not known. We found only one small report in Polish covering six patients (20) . In our study, we studied its expression in 38 hyperplastic endometrium cases and found survivin protein expression to be increased in a spectrum from proliferative endometrium to hyperplasic to carcinomatous endometrium, supporting in part the findings of Takai et al; however, survivin had no correlation with clinicopathologic prognostic factors and survival.…”

Section: Discussionmentioning

confidence: 96%

Expression of survivin, PTEN and p27 in normal, hyperplastic, and carcinomatous endometrium

Erkanli

Kayaselçuk

Kuşçu

et al. 2006

Int J Gynecol Cancer

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We aimed to investigate if expressions of survivin and p27 proteins are involved in the development of endometrioid carcinoma, along with whether there are any correlations between these proteins and loss of wild-type PTEN that is found in up to 80% of endometrial carcinomas. We also studied their correlations with classical prognostic factors and survival in endometrial carcinoma. To our knowledge, this is the first time survivin expression is investigated in endometrial hyperplasia along with endometrioid adenocarcinoma. For immunohistochemical analysis, 29 endometrioid adenocarcinoma, 38 endometrial hyperplasia, and 10 proliferative endometrium tissue samples were selected in the pathology archives. Staining of cells was scored as +2 if >50%, +1 if <50%, and negative if none were stained positive. Survivin expression increased from proliferative to hyperplasia to carcinoma cases. PTEN and p27 expressions decreased in hyperplasia and carcinoma cases with respect to proliferative endometrium. All these differences were statistically significant (P < 0.05). PTEN positively correlated to p27 (P < 0.05); however, neither was correlated with survivin. None of these genes were correlated with classical prognostic factors such as grade and myometrial invasion in endometrioid adenocarcinoma. However, mean survival was statistically significantly higher in PTEN-positive cases (46.6 vs 16.4 months) (P < 0.05). Survivin overexpression might be one of the important mechanisms in the development of endometrioid adenocarcinoma along with lost or decreased activity of PTEN and p27. However, survivin seems to exert its role in ways different from those of PTEN or p27 in the development of endometrioid adenocarcinoma. These findings on the role of survivin in endometrioid adenocarcinoma should be confirmed and the pathways through which survivin acts in endometrioid adenocarcinoma studied further with a larger sample size.

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Section: Discussionmentioning

confidence: 96%

Expression of survivin, PTEN and p27 in normal, hyperplastic, and carcinomatous endometrium

Erkanli

Kayaselçuk

Kuşçu

et al. 2006

Int J Gynecol Cancer

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“…The studies on the existence of survivin (BIRC5), the smallest member of apoptosis inhibitor protein (IAP) family in female genital system, are usually focused on uterus (Saitoh et al, 1999) and cervix cancers (Kim et al, 2002;Lee et al, 2005). Furthermore, previous reports on survivin gene expression in the cycling human endometrium have been conflicting (Konno et al, 2000;Lehner et al, 2002;Nabilsi and Loose, 2010;Tarkowski et al, 2000). Konno et al (2000) reported that survivin transcript and protein are increased in the secretory phase rather than the proliferative phase of cycling human endometrium (Konno et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Involution dependent changes in distribution and localization of bax, survivin, caspase‐3, and calpain‐1 in the rat endometrium

Alan

Lïman

2016

Microscopy Res & Technique

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The endometrial layer of the uterus is characterized by continuous cycle of cell growth and apoptosis in response to hormonal changes. Apoptosis is regulated by several apoptotic regulators, but their significance in involuting uterus has not been well understood. For that reason, aim of this study was to investigate possible role of apoptosis-related proteins (bax and survivin) and enzymes (caspase-3 and calpain-1) in the involuting uterus of the rat, using immunohistochemistry. Our results indicated cytoplasmic and nuclear immunostaining for bax, caspase-3, calpain-1 and survivin proteins were found in the endometrial epithelium and stromal cells such as fibroblasts, mast cells and macrophages, and blood vessels; however, calpain-1 immunoreactivity in the endometrial fibroblast was quite weak or absent. Supranuclear punctate bax immunolabelling was also observed in the endometrial fibroblasts and luminal and glandular epithelial cells from days 1st and 3rd following parturition, respectively. Although survivin was localized in the apical cytoplasm underneath the apical membrane of the luminal epithelium on the 1st and 3rd days, it was also localized in the apicolateral membrane and basal cytoplasm on the 10th and 15th days of involution. Immunostainigs demonstrated that expression patterns of all examined proteins varied with structural changes in the luminal epithelium, and number of immunopositive fibroblasts for bax, caspase-3 and survivin increased with advance of postpartum days and reached a maximum on postpartum days 10 and 15. These results suggest that the process of postpartum involution of endometrium may be regulated by apoptotic and non-apoptotic activity of bax, caspase-3, calpain-1, and survivin.

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“…Recently, it has been demonstrated that the survivin expression rate in endometrial carcinoma tissue is (100%) higher than that in longer endometrial hyperplasia (73%) [ 27 ], implying that survivin may be closely associated to malignant transformation of endometrium. More importantly, earlier work has pointed out that the survival protein survivin can strongly inhibit apoptosis stimulated by diverse factors [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

Apoptosis-Promoting Effects of Hematoporphyrin Monomethyl Ether-Sonodynamic Therapy (HMME-SDT) on Endometrial Cancer

Sun

Gào

et al. 2015

PLoS ONE

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ObjectiveThe aim of the present study was to examine the apoptosis-promoting effects and mechanisms of hematoporphyrin monomethyl ether (HMME)-sonodynamic therapy (SDT) on endometrial cancer cells in vitro.MethodsEndometrial cancer cell samples were divided into four groups: 1) untreated control group, 2) HMME group, 3) pure ultrasound group, and 4) HMME combined with ultrasound, i.e. SDT group. CCK-8 method was utilized to assess the inhibiting effect of SDT on the proliferation of endometrial cancer cells. Optical microscope and field emission transmission electron microscopy were used to characterize the morphology changes of the cancer cells induced by the treatments. Apoptosis rate, reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were examined by flow cytometer. Fluorescence intensity measured by laser scanning confocal microscopy was used to explore the variation of intracellular calcium ion (Ca2+) concentration. Apoptosis-related proteins involved in both intrinsic and extrinsic apoptosis signallings were analyzed by western blot.ResultsSDT can effectively induce the apoptosis of endometrial cancer cells. Compared with ultrasound which is known as an effective anti-tumor method, SDT leads to a significant improvement on suppression of cell viability and induction of apoptosis, together with more remarkable modifications on the morphology and substructure in both ultrasound sensitive and resistant endometrial cancer cells. Further studies reveals that SDT promotes ROS production, induces loss of MMP and increases intracellular Ca2+ concentration more efficiently than HMME or ultrasound alone. SDT groups also show a rather high expression of apoptosis-promoting proteins, including Bax, Fas and Fas-L, and a significant low expression of apoptosis-suspending proteins including Bcl-2 and Survivin. Meanwhile, both cleaved caspse-3 and caspase-8 are dramatically enhanced in SDT groups. Multiple pathways has been proposed in the process, including the intrinsic activation by excessive ROS and overloaded Ca2+, silencing survivin gene, and the extrinsic pathway mediated by the death receptor.ConclusionGiven its considerable effectivity in both ultrasound sensitive and resistant cells, SDT may therefore be a promising therapeutic method for treating endometrial cancers.

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Expression of Survivin and Cell Apoptosis in Endometrial Cancer and Hyperplastic Endometrium

Cited by 3 publications

References 0 publications

Expression of survivin, PTEN and p27 in normal, hyperplastic, and carcinomatous endometrium

Expression of survivin, PTEN and p27 in normal, hyperplastic, and carcinomatous endometrium

Involution dependent changes in distribution and localization of bax, survivin, caspase‐3, and calpain‐1 in the rat endometrium

Apoptosis-Promoting Effects of Hematoporphyrin Monomethyl Ether-Sonodynamic Therapy (HMME-SDT) on Endometrial Cancer

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