Membrane expression of TRAIL receptors DR4, DR5, DcR1 and DcR2 in the normal endometrium, atypical endometrial hyperplasia and endometrioid adenocarcinoma: a tissue microarray study

Gottwald, Leszek; Piekarski, Janusz; Kubiak, Robert; Szwalski, Jarosław; Pasz-Walczak, Grażyna; Sęk, Piotr; Spych, Michał; Suzin, Jacek; Tyliński, Wiesław; Jeziorski, Arkadiusz

doi:10.1007/s00404-013-2840-x

Cited by 11 publications

(9 citation statements)

References 33 publications

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“…(TRID, TRAIL-R3), DcR2 (TRUNDD, TRAIL-R4), and osteoprotegerin. (Gottwald et al, 2013;Wang & El-Deiry, 2003). Thus, exploring the agents which target the TRAIL-mediated apoptosis pathway has attracted obvious attention in the study field of cancer therapy (Koschny, Walczak, & Ganten, 2007).…”

Section: Ros Role In Crc Treatments Via Extrinsic Death Receptor Pathwaymentioning

confidence: 99%

Reactive oxygen species and colorectal cancer

Lin¹,

Li²,

Zamyatnin

et al. 2018

Journal Cellular Physiology

124

107

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Colorectal cancer (CRC) has become the fourth leading cause of cancer-related death in the worldwide. It is urgent to find more effective therapeutic strategies for it. Reactive oxygen species (ROS) play multiple roles in normal cellular physiology processes. Thus, a certain level of ROS is essential to keep normal cellular function. However, the accumulation of ROS shows dual roles for cells, which is mainly dependent on the concentration of ROS, the origin of the cancer cell and the activated signaling pathways during tumor progression. In general, moderate level of ROS leads to cell damage, DNA mutation and inflammation, which promotes the initiation and development of cancer. Excessive high level of ROS induces cancer cell death, showing an anti-cancer role. ROS are commonly higher in CRC cells than their normal counterpart cells. Therefore, it is possible that ROS induce cell death in cancer cells while not affecting the normal cells, demonstrating lower side effects. Besides, ROS also play a role in tumor microenvironment and drug resistance. These multiple roles of ROS make them a promising therapeutic target for cancer. To explore potential ROS-target therapies against CRC, it is worth to comprehensively understanding the role of ROS in CRC and therapy. In this review, we mainly discuss the strategies of ROS in CRC therapy, including direct CRC cell target and indirect tumor environment target. In addition, the influences of ROS in drug resistance will also been discussed.

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Section: Ros Role In Crc Treatments Via Extrinsic Death Receptor Pathwaymentioning

confidence: 99%

Reactive oxygen species and colorectal cancer

Lin¹,

Li²,

Zamyatnin

et al. 2018

Journal Cellular Physiology

124

107

View full text Add to dashboard Cite

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“…Overexpressed DCR2 is also seen in other human malignancies such as colon cancer and lung cancer [25, 26]. In contrast, Gottwald et al reported DCR2 protein is less common in endometrioid adenocarcinoma compared to normal endometrium [27]. Physiologically, DCR2 is frequently expressed in normal tissues, but often silenced by hypermethylation in a wide range tumour cells including breast cancer, cervical cancer, malignant mesothelioma, neuroblastoma and prostate cancer [28].…”

Section: Discussionmentioning

confidence: 99%

Differential expression of senescence tumour markers and its implications on survival outcomes of breast cancer patients

et al. 2019

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Breast cancer is a heterogeneous disease displaying different histopathological characteristics, molecular profiling and clinical behavior. This study describes the expression patterns of senescence markers P53, DEC1 and DCR2 and assesses their significance on patient survival as a single or combined marker with P16 or P14 using breast cancer progression series. One thousand and eighty (1080) patients with primary invasive ductal carcinoma, no special type, were recruited through an 11-year retrospective study period. We constructed tissue microarrays of normal, benign hyperplasia, ductal carcinoma in situ and invasive ductal carcinoma from each patient and performed immunohistochemical staining to study the protein expression. Statistical analysis includes Pearson chi-square, Kaplan-Meier log ran test and Cox proportional hazard regression were undertaken to determine the associations and predict the survival outcomes. P53, DEC1 and DCR2 expression correlated significantly with normal, benign, premalignant and malignant tissues with (p<0.05). The expression profile of these genes increases from normal to benign to premalignant and plateaued from premalignant to malignant phenotype. There is a significant association between P53 protein expression and age, grade, staging, lymphovascular invasion, estrogen receptor, progesterone receptor and HER2 whereas DCR2 protein expression significantly correlated with tumour grade, hormone receptors status and HER2 (p<0.05 respectively). P53 overexpression correlated with increased risk of relapse (p = 0.002) specifically in patients who did not receive hormone therapy (p = 0.005) or chemotherapy (p<0.0001). The combination of P53+/P16+ is significantly correlated with poor overall and disease-free survival, whereas a combination of P53+/P14+ is associated with worse outcome in disease-free survival (p<0.05 respectively). P53 overexpression appears to be a univariate predictor of poor disease-free survival. The expression profiles of DEC1 and DCR2 do not appear to correlate with patient survival outcomes. The combination of P53 with P16, rather P53 expression alone, appears to provide more useful clinical information on patient survival outcomes in breast cancer.

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“…Moreover, OPG exhibits strong binding affinity with Receptor activator of NK-kappa-B ligand (RANKL), and plays a prominent role in osteoclastogenesis [28,29]. Contrary to DR4 and DR5 [30,31,32,33], DcR1, DcR2, or OPG have been found to be expressed in normal tissues, but are rarely found in tumor cells [34,35,36].…”

Section: Apoptosis Induced By Trailmentioning

confidence: 99%

Antibodies and Derivatives Targeting DR4 and DR5 for Cancer Therapy

Dubuisson

Micheau

2017

Antibodies

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Developing therapeutics that induce apoptosis in cancer cells has become an increasingly attractive approach for the past 30 years. The discovery of tumor necrosis factor (TNF) superfamily members and more specifically TNF-related apoptosis-inducing ligand (TRAIL), the only cytokine of the family capable of eradicating selectively cancer cells, led to the development of numerous TRAIL derivatives targeting death receptor 4 (DR4) and death receptor 5 (DR5) for cancer therapy. With a few exceptions, preliminary attempts to use recombinant TRAIL, agonistic antibodies, or derivatives to target TRAIL agonist receptors in the clinic have been fairly disappointing. Nonetheless, a tremendous effort, worldwide, is being put into the development of novel strategic options to target TRAIL receptors. Antibodies and derivatives allow for the design of novel and efficient agonists. We summarize and discuss here the advantages and drawbacks of the soar of TRAIL therapeutics, from the first developments to the next generation of agonistic products, with a particular insight on new concepts.

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Membrane expression of TRAIL receptors DR4, DR5, DcR1 and DcR2 in the normal endometrium, atypical endometrial hyperplasia and endometrioid adenocarcinoma: a tissue microarray study

Cited by 11 publications

References 33 publications

Reactive oxygen species and colorectal cancer

Reactive oxygen species and colorectal cancer

Differential expression of senescence tumour markers and its implications on survival outcomes of breast cancer patients

Antibodies and Derivatives Targeting DR4 and DR5 for Cancer Therapy

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