High YBX1 expression indicates poor prognosis and promotes cell migration and invasion in nasopharyngeal carcinoma

Zhou, Leilei; Ni, Jie; Feng, Wei; Yao, Rong; Yue, Shun; Zhu, Yanxia; Tang, Haiyan; Lv, Lingyun; Feng, Jifeng; Zhu, Weiguo

doi:10.1016/j.yexcr.2017.10.009

Cited by 30 publications

(34 citation statements)

References 41 publications

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“…In lung adenocarcinoma cells, Ha et al demonstrated that YB1 could promote the EMT mediated by transforming growth factor beta 1 (TGF‐β1) and promote the invasion and metastasis of cancer cells . What's more, it was validated that YB1 expression was higher in NPC specimens, negatively related to membrane E‐cadherin levels, but positively related to vimentin expression and associated with T stage and metastasis . These results mentioned were consistent with our findings.…”

Section: Discussionsupporting

confidence: 91%

Elevated expression of G3BP1 associates with YB1 and p‐AKT and predicts poor prognosis in nonsmall cell lung cancer patients after surgical resection

et al. 2019

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Purpose G3BP1 is an RNA‐binding protein and plays roles in regulating signaling pathway. YB‐1 is a DNA/RNA binding protein encoded by YBX1 gene. Phosphorylated AKT (p‐AKT) acts as a pivotal molecule in PI3K/AKT pathway. YB‐1 drives stress granules (SGs) formation by activating G3BP1 translation under diverse conditions. SGs are involved in many different metabolic and signaling pathways which may include PI3K/AKT/mTOR. So far, there has been no report on the relationship between expression of G3BP1, p‐AKT, and YB1 and clinicopathological features/prognosis in surgically resected nonsmall cell lung cancer (NSCLC) patients. Methods In this study, data from TCGA (The Cancer Genome Atlas) were downloaded to investigate the mRNA expression of G3BP1 and YB1 (YBX1) and their correlation in NSCLC. Also, expression of G3BP1, YB1, and p‐AKT proteins was studied using immunohistochemistry in tissue microarrays of NSCLC and in noncancerous lung tissues. Results We found that the mRNA expression of G3BP1 and YB1 was higher in NSCLC tissues (both P < .05), and G3BP1 was positively correlated with YB1 in mRNA level (r = .399, P < .001). Also, expression of G3BP1, YB1, and p‐AKT proteins was higher in NSCLC tissues (all P < .05). And higher expression of G3BP1 and YB1 proteins was seen in patients with clinical stage II and III compared with stage I (both P < .05). Besides, expression of G3BP1 protein had a positive correlation with YB1 and p‐AKT (both P < .05). Moreover, overall survival was shorter in patients with overexpression of G3BP1, YB1, and p‐AKT proteins (all P < .05). Multivariate analysis confirmed that overexpression of G3BP1 protein was an independent poorer prognostic factor for NSCLC patients (P = .039). Conclusion G3BP1 may play a crucial role in activating PI3K/AKT/mTOR pathway. G3BP1 might be served as a novel prognostic biomarker for surgically resected NSCLC patients, which afforded new insights into the study on the mechanism and therapy of NSCLC.

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Section: Discussionsupporting

confidence: 91%

Elevated expression of G3BP1 associates with YB1 and p‐AKT and predicts poor prognosis in nonsmall cell lung cancer patients after surgical resection

et al. 2019

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“…Accordingly, TGF-β signalling-associated induction of EMT is considered an important step in the progression of tumour metastasis. Alterations in EMT markers (increased Vimentin and decreased E-cadherin) were detected in clinical NPC samples [ 153 , 154 ], indicating that NPC cells undergo EMT in vivo. Although EBNA1 has been shown to suppress TGF-β-mediated transcription in AdAH and HL cells [ 95 , 100 ], in NPC cells, EBNA1 appeared to up-regulate the expression of TGF-β1 protein leading to a reduction in expression of miR-200a and miR-200b which in turn, up-regulated their target genes ZEB1 and ZEB2, well known mediators of EMT [ 149 ].…”

Section: Tumour Promoting Roles Of Tgf-βmentioning

confidence: 99%

The Dynamic Roles of TGF-β Signalling in EBV-Associated Cancers

Velapasamy

Dawson

et al. 2018

Cancers

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The transforming growth factor-β (TGF-β) signalling pathway plays a critical role in carcinogenesis. It has a biphasic action by initially suppressing tumorigenesis but promoting tumour progression in the later stages of disease. Consequently, the functional outcome of TGF-β signalling is strongly context-dependent and is influenced by various factors including cell, tissue and cancer type. Disruption of this pathway can be caused by various means, including genetic and environmental factors. A number of human viruses have been shown to modulate TGF-β signalling during tumorigenesis. In this review, we describe how this pathway is perturbed in Epstein-Barr virus (EBV)-associated cancers and how EBV interferes with TGF-β signal transduction. The role of TGF-β in regulating the EBV life cycle in tumour cells is also discussed.

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“…The scoring system used has been previously described. 21 Briefly, the staining intensity of TIM-3 was scored using a 0-3 scale (0, no staining; 1, weak staining; 2, moderate staining; 3, strong staining). Scores 0-1 and 2-3 were considered low and high, respectively.…”

Section: Immunochemical Stainingmentioning

confidence: 99%

<p>TIM-3 Participates in the Invasion and Metastasis of Nasopharyngeal Carcinoma via SMAD7/SMAD2/SNAIL1 Axis-Mediated Epithelial-Mesenchymal Transition</p>

Qing

Chen

et al. 2020

OTT

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Background: T-cell immunoglobulin and mucin domain-containing molecule-3 (TIM-3) was originally found to negatively regulate immune response and mediate immune escape in tumors. Subsequently, an increasing body of evidence has shown that TIM-3 exerts positive functions in the development and progression of several tumors. However, the role of TIM-3 in nasopharyngeal carcinoma (NPC) remains unknown. Methods: Data from the Cancer Genome Atlas-head and neck squamous cell carcinoma and immunohistochemistry were analyzed to compare the expression of TIM-3 in NPC and noncancerous nasopharyngitis tissues. Cell proliferation was evaluated using the Cell counting kit-8 in vitro and xenograft experiment in nude mice in vivo. Flow cytometry was used to evaluate the cell cycle. The migration and invasion of NPC cells were assessed through wound healing and Transwell assays. In addition, Western blotting was used to analyze the expression of specific proteins. Results: Higher expression of TIM-3 was detected in NPC tissues than normal nasopharyngeal tissues and positively correlated with the clinical stage and T classification; however, it was not correlated with gender, age, and N classification. Furthermore, overexpression of TIM-3 using lentiviral vectors increased the malignancy of 6-10B and CNE-2 cell lines that lowly express TIM-3, by promoting cell proliferation, migration, and invasion in vitro and in vivo. In addition, overexpression of TIM-3 was associated with upregulation of matrix metalloproteinase 9 (MMP9) and MMP2, and led to epithelial-mesenchymal transition (EMT) by increasing the levels of mesenchymal markers (ie, N-cadherin, Vimentin) and decreasing those of the epithelial marker E-cadherin. Further study showed that SMAD7 was downregulated in the TIM-3 overexpression group. Relatively, phosphorylated SMAD2 and downstream molecule SNAIL1 were also upregulated in this group. Conclusion: TIM-3 exerts a tumor-promoting function in NPC by mediating changes in the SMAD7/SMAD2/SNAIL1 axis. These findings provide a new idea for the study of invasion, metastasis, and treatment of NPC.

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High YBX1 expression indicates poor prognosis and promotes cell migration and invasion in nasopharyngeal carcinoma

Cited by 30 publications

References 41 publications

Elevated expression of G3BP1 associates with YB1 and p‐AKT and predicts poor prognosis in nonsmall cell lung cancer patients after surgical resection

Elevated expression of G3BP1 associates with YB1 and p‐AKT and predicts poor prognosis in nonsmall cell lung cancer patients after surgical resection

The Dynamic Roles of TGF-β Signalling in EBV-Associated Cancers

<p>TIM-3 Participates in the Invasion and Metastasis of Nasopharyngeal Carcinoma via SMAD7/SMAD2/SNAIL1 Axis-Mediated Epithelial-Mesenchymal Transition</p>

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