Expression, correlation, and prognostic value of TRAF2 and TRAF4 expression in malignant plural effusion cells in human breast cancer

Zhao, Zhe; Ren, Bin; Yang, Bowen; Wang, Jian; Wu, Guang-Ping; Mi, Xiaoyi

doi:10.1002/dc.23330

Cited by 21 publications

(20 citation statements)

References 30 publications

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“…TRAF2 overexpression has been documented in tumor samples from certain types of cancer such as human pancreatic cancer, breast cancer and gastric cancer, and is associated with cancer progression, metastasis, and shorter patient survival [23, 25, 26]. The current study continues our previous exploration of the critical role of TRAF2-dependent enhancement of cancer cell invasion and metastasis induced by DR5 suppression [11] to further understand the mechanism by which TRAF2 is activated during DR5 suppression-induced promotion of cancer cell invasion.…”

Section: Discussionmentioning

confidence: 99%

DR5 suppression induces sphingosine-1-phosphate-dependent TRAF2 polyubiquitination, leading to activation of JNK/AP-1 and promotion of cancer cell invasion

Yue

Sun

2017

Cell Commun Signal

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BackgroundDeath receptor (DR5), a well-characterized death domain-containing cell surface pro-apoptotic protein, has been suggested to suppress cancer cell invasion and metastasis. However, the underlying mechanisms have not been fully elucidated. Our recent work demonstrates that DR5 suppression promotes cancer cell invasion and metastasis through caspase-8/TRAF2-mediated activation of ERK and JNK signaling and MMP1 elevation. The current study aimed at addressing the mechanism through which TRAF2 is activated in a caspase-8 dependent manner.ResultsDR5 knockdown increased TRAF2 polyubiquitination, a critical event for TRAF2-mediated JNK/AP-1 activation. Suppression of sphingosine-1-phosphate (S1P) generation or depletion of casapse-8 inhibited not only enhancement of cell invasion, but also elevation and polyubiquitination of TRAF2, activation of JNK/AP-1 activation and increased expression of MMP1 induced by DR5 knockdown.ConclusionsBoth S1P and caspase-8 are critical for TRAF2 stabilization, polyubiquitination, subsequent activation of JNK/AP1 signaling and MMP1 expression and final promotion of cell invasion.

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Section: Discussionmentioning

confidence: 99%

DR5 suppression induces sphingosine-1-phosphate-dependent TRAF2 polyubiquitination, leading to activation of JNK/AP-1 and promotion of cancer cell invasion

Yue

Sun

2017

Cell Commun Signal

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“…It was documented TRAF2 plays vital roles in regulating immunity response, embryonic development, and stress response. TRAF2 expression has been reported to be upregulated in breast cancer [ 25 ]. Zhao et al [ 25 ] found that TRAF2 expression was upregulated in primary tumor and metastatic lymph nodes compared with normal breast tissues.…”

Section: Discussionmentioning

confidence: 99%

“…TRAF2 expression has been reported to be upregulated in breast cancer [ 25 ]. Zhao et al [ 25 ] found that TRAF2 expression was upregulated in primary tumor and metastatic lymph nodes compared with normal breast tissues. Different biomarkers of prostate cancer have recently been identified [ 35 – 38 ].…”

Section: Discussionmentioning

confidence: 99%

“…Zhang et al [ 24 ] found that TRAF2 expression was significantly increased in gastric cancer patients, which might be an independent diagnostic and prognostic indicator in gastric cancer patients. In addition, TRAF2 expression was upregulated in malignant pleural effusion cells compared with normal breast tissues [ 25 ]. TRAF2 in malignant pleural effusion cells might be a potential prognostic factor and biomarker for predicting invasion and metastasis of breast cancer [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

“…In addition, TRAF2 expression was upregulated in malignant pleural effusion cells compared with normal breast tissues [ 25 ]. TRAF2 in malignant pleural effusion cells might be a potential prognostic factor and biomarker for predicting invasion and metastasis of breast cancer [ 25 ]. Currently, TRAF2 expression in prostate cancer and mechanisms governing the development and progression of prostate cancer are still unknown.…”

Section: Introductionmentioning

confidence: 99%

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TRAF2 is a Valuable Prognostic Biomarker in Patients with Prostate Cancer

Wei

Liang

et al. 2017

Med Sci Monit

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BackgroundTRAF2 exerts important functions in regulating the development and progression of cancer. The aim of this study is to investigate whether TRAF2 is a valuable prognostic biomarker and to determine if it regulates TRAIL-induced apoptosis in prostate cancer.Material/MethodsMicroarray gene expression data from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were used to determine TRAF2 expression in prostate cancer. TRAF2 expression in prostate cancer was further investigated by immunohistochemistry assay. Kaplan–Meier curves and log-rank test were used to assess the recurrence-free rate. Cox regression was used to analyze prognostic factors. Effects of TRAF2 on regulating TRAIL-induced apoptosis in DU-145 cells were further investigated.ResultsWe found that TRAF2 was significantly upregulated in prostate cancer compared with normal prostate samples (P<0.001). In addition, compared with primary prostate cancer, TRAF2 was upregulated in metastatic prostate cancer (P=0.006). Furthermore, our results showed that high expression of TRAF2 was significantly associated with tumor stage of prostate cancer (P=0.035). TRAF2 high expression was associated with poorer recurrence-free survival in prostate cancer patients (P=0.013). TRAF2 was found to be a valuable independent prognostic factor for predicting recurrence-free survival (P=0.026). In addition, the present results indicate that TRAF2 affects TRAIL-induced apoptosis in prostate cancer DU-145 cells via regulating cleaved Caspase-8 and c-Flip expression.ConclusionsTRAF2 could be a novel prognostic biomarker for predicting recurrence-free survival in patients with prostate cancer, which might be associated with the effects of TRAF2 in regulating TRAIL-induced apoptosis in prostate cancer cells via c-Flip/Caspase-8 signalling.

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Death receptor 6 promotes ovarian cancer cell migration through KIF11

et al. 2018

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The expression of death receptor 6 ( DR 6) is abnormal in some cancer types, but the function and underlying molecular mechanisms of DR 6 in tumor progression are not yet clear. In the present study, our analysis of ovarian cancer RNA sequencing data from The Cancer Genome Atlas revealed that DR 6 is upregulated in human ovarian cancer. We confirmed that the expression level of DR 6 is upregulated in ovarian cancer tissues when compared with matched adjacent normal tissues. In addition, DR 6 enhanced ovarian carcinoma cell migration ability, and decreased expression of DR 6 inhibited the expression of matrix metalloprotease ( MMP ) 2 and MMP 9, and increased the expression of E‐cadherin. Additionally, DR 6 sh RNA caused a significant decrease in phosphoinositide‐3‐kinase ( PI 3K), phospho (p) ‐ AKT , p‐extracellular signal‐regulated kinase ( ERK ), and p‐mitogen‐activated protein kinase kinase expression in SKOV 3 cells. These results suggested that DR 6 can enhance ovarian carcinoma cell migration ability through the mitogen‐activated protein kinase/ ERK and PI 3K/ AKT pathways. Notably, mass spectrometric analysis indicated that DR 6 co‐purified with kinesin family member 11 ( KIF 11), and we verified the interaction between KIF 11 and DR 6 by co‐immunoprecipitation and glutathione S ‐transferase pull‐down. Furthermore, we demonstrated that DR 6 can bind tumor necrosis factor receptor‐associated factor 4 ( TRAF 4) with co‐immunoprecipitation. Overexpression of KIF 11 or TRAF 4 eliminated the suppression of carcinoma cell migration by DR 6 knockdown. We also found that TRAF 4 and KIF 11 were upregulated in ovarian carcinomas and that their level of expression was positively correlated with that of DR 6. The findings above suggest that DR 6 may play a notable oncogenic role in ovarian malignancy by interacting with TRAF 4 and KIF 11, and that DR 6 may be an effective therapeutic target in ovarian cancer.

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Expression, correlation, and prognostic value of TRAF2 and TRAF4 expression in malignant plural effusion cells in human breast cancer

Abstract: TRAF2 and nuclear TRAF4 expression in malignant pleural effusion cells may represent potential prognostic factors and biomarkers of invasion and metastasis in breast cancer.

Cited by 21 publications

References 30 publications

DR5 suppression induces sphingosine-1-phosphate-dependent TRAF2 polyubiquitination, leading to activation of JNK/AP-1 and promotion of cancer cell invasion

DR5 suppression induces sphingosine-1-phosphate-dependent TRAF2 polyubiquitination, leading to activation of JNK/AP-1 and promotion of cancer cell invasion

TRAF2 is a Valuable Prognostic Biomarker in Patients with Prostate Cancer

Death receptor 6 promotes ovarian cancer cell migration through KIF11

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