The immune system, apoptosis and apoptosis-related proteins in human ovarian tumors (A review)

Zusman, Itshak; Gurevich, Pavel; Gurevich, Eugeni; Ben‐Hur, Herzl

doi:10.3892/ijo.18.5.965

Cited by 22 publications

(20 citation statements)

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“…In the present study, immunized mice had severalfold-higher numbers of apoptotic fibroblasts in comparison to the shamimmunized controls. This may occur since mediators induced by the acquired response may act synergistically with those induced by the innate response to maximally induce apoptosis (33,47). In support of this, immunized mice had significantly higher levels of the proapoptotic factors TNF-␣, FasL, and caspase 3.…”

Section: Discussionmentioning

confidence: 58%

Immunization Enhances Inflammation and Tissue Destruction in Response toPorphyromonas gingivalis

et al. 2006

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It is well established that host-bacterium interactions play a critical role in the initiation and progression of periodontal diseases. By the use of inhibitors, it has been shown that mediators associated with the innate immune response significantly contribute to the disease process. Less is known regarding the role of the acquired immune response. To investigate mechanisms by which the acquired immune response to Porphyromonas gingivalis could affect connective tissue, we used a well-documented calvarial model to study hostbacterium interactions. Injection of P. gingivalis stimulated gamma interferon, interleukin 6, macrophage inflammatory protein 2, and monocyte chemoattractant protein 1 expression as determined by real-time PCR. Prior immunization against P. gingivalis significantly enhanced the mRNA levels of these cytokines and chemokines. Similarly, immunization significantly increased and prolonged the formation of a polymorphonuclear leukocyte and mononuclear cell infiltrate (P < 0.05). In addition, the area of connective tissue destruction, osteoclastogenesis, bone loss, mRNA expression of proapoptotic genes, and degree of fibroblast apoptosis were increased in immunized mice (P < 0.05). These results indicate that activation of the acquired immunity by P. gingivalis increases the inflammatory and destructive responses which occur in part through up-regulating the innate immune response and enhancing osteoclastogenesis and fibroblast apoptosis.

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Section: Discussionmentioning

confidence: 58%

Immunization Enhances Inflammation and Tissue Destruction in Response toPorphyromonas gingivalis

et al. 2006

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“…In addition, caspase-3 expression was decreased or undetectable in OC cells, and higher caspase-3 activity is expected to undergo apoptosis in response to anti-cancer therapy (Devarajan et al 2002). Many Bcl-2-positive cells are present in a subgroup of OC, and surprisingly, its absence was not correlated to induction of apoptosis (Zusman et al 2001). Importantly, the blockade of survivin expression contributes to the anti-tumor activity of chemotherapeutic agents in human OC (Jiang et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Apoptosis is triggered by melatonin in an in vivo model of ovarian carcinoma

Chuffa¹,

Alves²,

Martinez³

et al. 2015

Endocrine-Related Cancer

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Apoptosis plays an important role in the treatment of cancer, and targeting apoptosis-related molecules in ovarian cancer (OC) is of great therapeutic value. Melatonin (Mel) is an indoleamine displaying several anti-cancer properties and has been reported to modulate apoptosis signaling in multiple tumor subtypes. We investigated OC and the role of Mel therapy on the pro-apoptotic (p53, BAX, caspase-3, and cleaved caspase-3) and anti-apoptotic (Bcl-2 and survivin) proteins in an ethanol (EtOH)-preferring rat model. To induce OC, the left ovary was injected directly with a single dose of 100 mg 7,12-dimethylbenz(a)anthracene dissolved in 10 ml of sesame oil under the bursa. Right ovaries were used as sham-surgery controls. After developing OC, half of the animals received i.p. injections of Mel (200 mg/100 g BW per day) for 60 days. Body weight gain, EtOH consumption, and energy intake were unaffected by the treatments. Interestingly, absolute and relative OC masses showed a significant reduction after Mel therapy, regardless of EtOH consumption. To accomplish OC-related apoptosis, we first observed that p53, BAX, caspase-3, and cleaved caspase-3 were downregulated in OC tissue while Bcl-2 and survivin were overexpressed. Notably, Mel therapy and EtOH intake promoted apoptosis along with the upregulation of p53, BAX, and cleaved caspase-3. Fragmentation of DNA observed by TUNEL-positive nuclei was also enhanced following Mel treatment. In addition, Bcl-2 was downregulated by the EtOH intake and lower survivin levels were observed after Mel therapy. Taken together, these results suggest that Mel induce apoptosis in OC cells of EtOH-preferring animals.Key Words " ovarian cancer " melatonin " pro-apoptotic protein " anti-apoptotic protein

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“…The anti-proliferative action of VK2 has been reported in a variety of cancer cells including lung carcinomas (8), human ovarian cancer cells (6) and acute myeloid leukemia cells (4). In leukemia cells, VK2 induces autophagy and apoptosis simultaneously, indicating that the cell expression levels of BCL-2 appear to determine the phenotype of cell death (15).…”

Section: Discussionmentioning

confidence: 99%

“…Modulation of multiple antiapoptotic signaling pathways involving BCL-2, which are associated with growth factor-stimulated signal transduction in cell survival, is essential for enhancement of the cytotoxic effect of anticancer drugs (7). Several exceptions to the hypothesis that BCL-2 inhibits and p53 promotes apoptosis have been encountered (8). Furthermore, BCL-2 is an antagonist to Bax and inhibits mitochondrial membrane disruption, a mechanism that likely accounts for drug resistance in BCL-2-overexpressing tumors (9).…”

Section: Introductionmentioning

confidence: 99%

Enhanced therapeutic efficacy of vitamin K2 by silencing BCL-2 expression in SMMC-7721 hepatocellular carcinoma cells

et al. 2012

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Abstract. Vitamin K2 (VK2) exerts cell growth inhibitory effects in various human cancer cells such as SMMC-7721 hepatocellular carcinoma (HCC) cells. BCL-2 is an antiapoptotic protein that is frequently overexpressed in numerous tumors. Modulation of multiple antiapoptotic signaling pathways involving BCL-2, which are related to growth factor-stimulated signal transduction in cell survival, is essential for enhancement of the cytotoxic effect of anticancer drugs. In this study, we tested a new strategy of gene therapy by combining BCL-2 siRNA with VK2. In SMMC-7721 HCC cells, the combined treatment significantly enhanced cytotoxicity compared with treatment with either VK2 or siBCL-2 alone. We found that combined treatment induced a significantly different level of G2 stage inhibition. Furthermore, the p53 protein was overexpressed 24 h subsequent to combination treatment, and p21 was clearly increased at 36 h as a consequence of the increased p53 activity. In conclusion, these data suggest that the antitumor effect of VK2 may be improved by silencing BCL-2 expression in SMMC-7721 HCC cells and provides support for the combined use of VK2 and siBCL-2 as a promising approach in cancer gene therapy.

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The immune system, apoptosis and apoptosis-related proteins in human ovarian tumors (A review)

Cited by 22 publications

References 0 publications

Immunization Enhances Inflammation and Tissue Destruction in Response toPorphyromonas gingivalis

Immunization Enhances Inflammation and Tissue Destruction in Response toPorphyromonas gingivalis

Apoptosis is triggered by melatonin in an in vivo model of ovarian carcinoma

Enhanced therapeutic efficacy of vitamin K2 by silencing BCL-2 expression in SMMC-7721 hepatocellular carcinoma cells

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