HCG up-regulates survivin mRNA in human granulosa cells

Kumazawa, Yukiyo; Kawamura, Kazuhiro; Sato, Tutomu; Sato, Naoki; Konishi, Yoshitomo; Shimizu, Yosushi; Fukuda, Jun; Kodoma, Hideya; Tanaka, Toshinobu

doi:10.1093/molehr/gah146

Cited by 23 publications

(14 citation statements)

References 25 publications

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“…Survivin expression has also been reported in melanocytes (82), keratinocytes (83), testes (84), and ovary (85) in humans. Stem cell factor and human chorionic gonadotropin also induce survivin expression in testes (84) and in ovarian granulosa cells (85), suggesting that survivin may have a role in the regulation of spermatogenesis and oogenesis.…”

Section: Survivin In Other Adult Tissuesmentioning

confidence: 99%

Survivin, a cancer target with an emerging role in normal adult tissues

Fukuda

Pelus

2006

Molecular Cancer Therapeutics

429

360

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Survivin, an inhibitor of apoptosis protein, is highly expressed in most cancers and associated with chemotherapy resistance, increased tumor recurrence, and shorter patient survival, making antisurvivin therapy an attractive cancer treatment strategy. However, growing evidence indicates that survivin is expressed in normal adult cells, particularly primitive hematopoietic cells, T lymphocytes, polymorphonuclear neutrophils, and vascular endothelial cells, and may regulate their proliferation or survival. In preclinical animal models, targeted antisurvivin therapies show efficacy without overt toxicity. However, consequences of prolonged survivin disruption in normal cells, particularly those associated with continuous renewal, have not been clearly determined. Understanding the role of survivin in normal versus malignant cells will be important in identifying strategies that maximally disrupt survivin in cancer cells with minimal effect on normal tissues. In this review, we summarize the prognostic relevance of survivin in cancer that justifies the pursuit of antisurvivin therapies and discuss differences in survivin expression between normal and cancer cells. We subsequently review expression of survivin in normal adult tissues and evaluate preclinical antisurvivin therapies reported to date in light of emerging roles for survivin in normal physiology, particularly hematopoiesis, angiogenesis, and immune function. [Mol Cancer Ther 2006;5(5):1087 -98]

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Section: Survivin In Other Adult Tissuesmentioning

confidence: 99%

Survivin, a cancer target with an emerging role in normal adult tissues

Fukuda

Pelus

2006

Molecular Cancer Therapeutics

429

360

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“…In fact, HCG increases Bcl-2 expression and decreases Bax expression in the corpus luteum in vitro [49,65]. In addition, there is a report indicating that HCG upregulates survivin in human granulosa cells, which is an inhibitor of apoptosis protein that directly interacts with several caspases to inhibit apoptosis [64].…”

Section: Anti-apoptotic Effects Of Hcgmentioning

confidence: 99%

“…Extracellular adenosine triphosphate (ATP) induces apoptosis via mitochondrial depolarization in human granulosa cells in vitro, and HCG inhibits ATP-induced apoptosis [63]. Matsubara et al [60] also reported that suppression of apoptosis by HCG is mediated not only by inhibition of the Fas pathway but also by the Bcl-2 and Bax system in luteinized granulosa cells [64]. In fact, HCG increases Bcl-2 expression and decreases Bax expression in the corpus luteum in vitro [49,65].…”

Section: Anti-apoptotic Effects Of Hcgmentioning

confidence: 99%

Species-Related Differences in the Mechanism of Apoptosis During Structural Luteolysis

Sugino

Okuda

2007

J. Reprod. Dev.

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Abstract. Luteolysis is defined as the loss of function and subsequent involution of the luteal structure. The luteolytic process is usually subdivided, whereby the decline in progesterone is described as functional luteolysis and the structural involution is described as structural luteolysis. After the corpus luteum ceases to produce progesterone, it decreases in size, experiences a loss of cellular integrity, and then disappears from the ovary as a result of apoptosis of luteal cells. However, the control mechanisms responsible for initiating and mediating apoptosis during structural luteolysis seem more complex than originally envisioned. Furthermore, efforts to elucidate the apoptotic mechanisms have been complicated by the fact that different mammalian species have different mechanisms for controlling luteal function. Therefore, it is of interest to know whether different mammalian species have different apoptotic mechanisms. The goal of this review was to focus on species-related differences in the mechanism of apoptosis during structural luteolysis in rodents, cattle and humans, the species that are used most for luteolysis research.

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“…Such DcRs lack an intracellular DD and are proposed to sequester and prevent TRAIL binding to DR4 or DR5 and/or interfere with receptor trimerization (Degli-Esposti et al 1997a, 1997b, Emery et al 1998. In mammalian granulosa cells, the expression of a variety of intracellular proteins, such as Fas-associated death domain-like interleukin-1b-converting enzyme (FLICE)-inhibiting protein (FLIP L ; Xiao et al 2002), anti-apoptotic Bcl-2 family members (e.g., Bcl-2 and Bcl-x; Tilly et al 1995, Hsu et al 1996, inhibitor of apoptosis proteins (IAPs; Xiao et al 2001), and survivin (Kumazawa et al 2005), can attenuate caspase activity and/or are associated with a reduced incidence of apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Tumor necrosis factor-related apoptosis inducing ligand expression and activity in hen granulosa cells

et al. 2007

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Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) represents one of several cytokine members of the tumor necrosis factor superfamily reported to initiate apoptosis in a wide range of transformed, but not most normal, cell types. The present studies were conducted to evaluate the potential for TRAIL to promote apoptotic cell death in differentiated granulosa cells collected from hen preovulatory follicles. While mRNA encoding critical components (including TRAIL) required for a functional extrinsic cell death pathway are expressed in granulosa cells, TRAIL treatment by itself fails to induce either caspase-3 activity or a decrease in cell viability. On the other hand, preculture of cells with the conventional chemotherapeutic, cisplatin, or the 20S proteosome inhibitor, Z-LLF-CHO, sensitizes granulosa cells to TRAIL as evidenced by enhanced caspase-3 activity after 4 h of culture and loss of cell viability after 24 h when compared with either cisplatin or Z-LLF-CHO treatment alone. Moreover, the sensitizing effect of Z-LLF-CHO on TRAIL-induced loss of cell viability is prevented by the selective caspase-8 inhibitor, Z-IETD-FMK. Interestingly, TRAIL mRNA expression is elevated both in prehierarchal follicles undergoing spontaneous atresia and in prehierarchal follicles induced to undergo atresia for 6 h in vitro. In summary, the data demonstrate the presence of a functional TRAIL signaling pathway in hen granulosa cells, and are consistent with the possibility that TRAIL signaling may directly or indirectly participate in the process of follicle atresia in vivo.

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HCG up-regulates survivin mRNA in human granulosa cells

Cited by 23 publications

References 25 publications

Survivin, a cancer target with an emerging role in normal adult tissues

Survivin, a cancer target with an emerging role in normal adult tissues

Species-Related Differences in the Mechanism of Apoptosis During Structural Luteolysis

Tumor necrosis factor-related apoptosis inducing ligand expression and activity in hen granulosa cells

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