Increased expression of survivin in gastric cancer patients and in first degree relatives

Yu, Jun; Leung, Wai K.; Ebert, Matthias P.; Ng, Enders Kwok Wai; Go, Minnie Y.Y.; Wang, H B; Chung, Sai Ho; Malfertheiner, Peter; Sung, Joseph J.Y.

doi:10.1038/sj.bjc.6600421

Cited by 57 publications

(42 citation statements)

References 25 publications

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“…Survivin is highly expressed in various human cancers [45][46][47][48] and plays an important role in suppressing apoptosis by interacting with caspase-3, -7, and -9 to inhibit their proapoptotic effects. 49 Accordingly, we observed that overexpression of Survivin inhibited cell apoptosis and activation of caspase-3, -7, -8, and -9 triggered by overexpressing JUN in myeloma cell lines.…”

Section: Discussionmentioning

confidence: 99%

Identification of early growth response protein 1 (EGR-1) as a novel target for JUN-induced apoptosis in multiple myeloma

Chen

Wang

Zhou

et al. 2010

Blood

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Tumor–bone marrow microenvironment interactions in multiple myeloma (MM) are documented to play crucial roles in plasma-cell growth/survival. In vitro coculture of MM cells with osteoclasts supported cell survival and significantly down-regulated JUN expression. JUN expression in myeloma cells from late-stage and high-risk MM was significantly lower than in plasma cells from healthy donors, monoclonal gammopathy of undetermined significance, smoldering MM, and low-risk MM; patients with low-JUN–expressing MM cells had earlier disease-related deaths. JUN overexpression in MM cells induced cell death and growth inhibition and up-regulated expression of early growth response protein 1 (EGR-1), whose low expression also carried unfavorable clinical implications. EGR-1 knockdown in MM cells abrogated JUN overexpression-induced MM cell death and growth inhibition, indicating that EGR-1 acts directly downstream of JUN. JUN modulates myeloma cell apoptosis through interacting with EGR-1, which down-regulates Survivin and triggers caspase signaling. Importantly, high JUN or EGR-1 expression was associated with improved outcome in Total Therapy 3, in which bortezomib is given throughout therapy, versus Total Therapy 2, in which bortezomib is given only at relapse. Consistently, JUN or EGR-1 knockdown in cultured MM cells enhanced their resistance to bortezomib, demonstrating the crucial role of low JUN/EGR-1 expression in MM resistance to bortezomib.

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Section: Discussionmentioning

confidence: 99%

Identification of early growth response protein 1 (EGR-1) as a novel target for JUN-induced apoptosis in multiple myeloma

Chen

Wang

Zhou

et al. 2010

Blood

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“…[7] Survivin is switched off during fetal development and is not found in non-neoplastic adult tissues. However, it is prominently reexpressed by all the most common human cancers including cancers of the lung, genito-urinary, malignant melanoma, neuroblastoma, hepatocellular, pancreas, stomach, colon, breast cancers and soft tissue sarcomas [8,9]. The prognostic value of survivin in hemopoietic neoplasias has not been as widely studied as in solid tumors.…”

Section: Introductionmentioning

confidence: 99%

Prognostic Significance of Survivin in Pediatric Acute Lymphoblastic Leukemia

Esh

Atfy

Azizi

et al. 2011

Indian J Hematol Blood Transfus

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Impaired apoptosis is mediated by members of the inhibitor of apoptosis proteins (IAP) family such as survivin. Survivin was described in number of different tumors and found to correlate with poor prognosis in a variety of cancers including hematologic malignancies. The aim of this study was to determine survivin in pediatric ALL and compare it with clinical and hematological findings, response to therapy and outcome. Flowcytometry was used for detection of intracellular survivin and determine its mean fluorescence intensity (MFI) in bone marrow mononuclear cells. Patients were followed up for 28 months after induction therapy. Survivin was detected in 63.3% of the patients BM. In spite of no association of survivin levels with established risk factors (P [ 0.05) except with high WBC, there was significant higher level of survivin expression in high risk group patients when patients were stratified into high and standard risk groups. According to response to induction therapy, there was no significant difference, in survivin level between patients who achieved CR, RD and ED. However, patients suffering relapse of the disease, had a significant higher basal level of survivin than patients still in remission. Over expression of survivin is a candidate parameter to determine poor prognosis in ALL patients and it may serve to refine treatment stratification with intensification of therapy in those patients prone to relapse.

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“…Others and we have demonstrated the up-regulation of survivin and angiogenic factors induced by Helicobacter pylori in gastric cancer as well as in solid tumors and their surrounding areas, suggesting the importance of survivin for the inhibition of apoptosis in the pathogenesis of gastric cancer. 9,10 The intra-tumor plasmid gene therapy with survivin antagonists could block the expression of survivin and angiogenic factors could enhance the anti-tumor activity. 11 The expression of survivin in gastric cancer was associated with reduced apoptosis and COX-2 expression.…”

Section: Introductionmentioning

confidence: 99%

Microbial based therapy of cancer: A new twist to an age old practice

Punj

Saint‐Dic²,

Daghfal³

et al. 2004

Cancer Biology & Therapy

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The use of bacteria in the regression of tumors has long been known. Various approaches for using bacteria in cancer therapy include the use of bacteria as sensitizing agents for chemotherapy, as delivery agents for cancer drugs and as agents for gene therapy. The tumor regression stimulated by infecting microorganisms has been attributed to activation of the immune system of the host. However, recent studies indicate that when tumorharboring mice with defective immune systems are infected with certain microorganisms, the regression of the tumor is still observed, suggesting that there are other host factors contributing to the microbial associated regression of tumors. Since the use of live or attenuated bacteria for tumor regression has associated toxic effects, studies are in progress to identify a pure microbial metabolite or any component of the microbial cell that might have anti-cancer activity. It has now been demonstrated that a redox protein from Pseudomonas aeruginosa, a cupredoxin, can enter into human cancer cells and trigger the apoptotic cell death. In vivo, this cupredoxin can lead to the regression of tumor growth in immunodeficient mice harboring xenografted melanomas and breast cancer tumors without inducing significant toxic effects, suggesting that it has potential anti-cancer activity. This bacterial protein interacts with p53 and modulates mammalian cellular activity. Hence, it could potentially be used as an anti-cancer agent for solid tumors and has translational value in tumor-targeted or in combinational-biochemotherapy strategies for cancer treatments. Here, we focus on diverse approaches to cancer biotherapy, including bacteriolytic and bacterially-derived anti-cancer agents with an emphasis on their mechanism of action and therapeutic potential.

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Increased expression of survivin in gastric cancer patients and in first degree relatives

Cited by 57 publications

References 25 publications

Identification of early growth response protein 1 (EGR-1) as a novel target for JUN-induced apoptosis in multiple myeloma

Identification of early growth response protein 1 (EGR-1) as a novel target for JUN-induced apoptosis in multiple myeloma

Prognostic Significance of Survivin in Pediatric Acute Lymphoblastic Leukemia

Microbial based therapy of cancer: A new twist to an age old practice

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