Y-box-binding protein-1 (YB-1) promotes cell proliferation, adhesion and drug resistance in diffuse large B-cell lymphoma

Miao, Xiaobing; Wu, Yong; Wang, Yuchan; Zhu, Xinghua; Yin, Haibing; He, Yunhua; Li, Chunsun; Liu, Yushan; Lu, Xiaoyun; Chen, Yali; Shen, Rong; Xu, Xiaohong; He, Song

doi:10.1016/j.yexcr.2016.07.003

Cited by 37 publications

(22 citation statements)

References 28 publications

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“…Cell growth is strictly regulated and controlled by a careful balance of regulatory systems. Abnormal cell growth is the critical feature of malignant tumors . In this study, we observed a significant suppression of cell proliferation of chordoma cell lines after YBX1 knockdown, consistent with previous studies.…”

Section: Discussionsupporting

confidence: 92%

“…Okada et al report that specific small interfering RNA to YBX1 induced G1/S arrest. Miao et al suggest that YBX1 could promote cell proliferation by accelerating the G1/S transition in diffuse large B‐cell lymphoma. Similarly, cell cycle analysis showed that there was delayed G1/S transition with YBX1 knockdown and accelerated G1/S transition with YBX1 overexpression in chordoma.…”

Section: Discussionmentioning

confidence: 99%

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Y‐box binding protein‐1 promotes tumorigenesis and progression via the epidermal growth factor receptor/AKT pathway in spinal chordoma

Chen

Lei

et al. 2018

Cancer Science

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Chordomas are rare bone tumors with a poor prognosis and no approved targeted therapy. Y‐box binding protein‐1 (YBX1) promotes tumor growth, invasion and drug resistance. However, the role of YBX1 in chordoma is unclear. In this study, we examined the expression of YBX1 using immunohistochemistry and found that YBX1 was significantly upregulated in 32 chordoma tissues compared to distant normal tissues. In addition, YBX1 upregulation was associated with surrounding tissue invasion, recurrence and poor prognosis. Biological function studies demonstrated that YBX1 promoted cell proliferation and invasion, accelerated G1/S phase transition, and inhibited apoptosis. Further investigation revealed that YBX1 enhanced epidermal growth factor receptor (EGFR) transcription by directly binding to its promoter in chordoma cells. YBX1 regulated protein expression of p‐EGFR, p‐AKT and its downstream target genes that influenced cell apoptosis, cell cycle transition and cell invasion. YBX1 activated the EGFR/AKT pathway in chordoma and YBX1‐induced elevated expression of key molecules in the EGFR/AKT pathway were downregulated by EGFR and AKT pathway inhibitors. These in vitro results were further confirmed by in vivo data. These data showed that YBX1 promoted tumorigenesis and progression in spinal chordoma via the EGFR/AKT pathway. YBX1 might serve as a prognostic and predictive biomarker, as well as a rational therapeutic target, for chordoma.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Y‐box binding protein‐1 promotes tumorigenesis and progression via the epidermal growth factor receptor/AKT pathway in spinal chordoma

Chen

Lei

et al. 2018

Cancer Science

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“…17,18 The pathogenesis of DLBCL is complicated, being involved in different genetic and epigenetic changes. 19,20 Recently, miRNAs were reported to be associated with the formation and development of DLBCL. 6,7 miR-101 is reported to be associated with tumor formation and plays key roles in cell apoptosis, proliferation, migration and invasion.…”

Section: Discussionmentioning

confidence: 99%

<p>miR-101 regulates cell proliferation and apoptosis by targeting KDM1A in diffuse large B cell lymphoma</p>

Huang¹,

Zou²,

Lin³

et al. 2019

CMAR

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Background miR-101 is reported to be associated with cell proliferation and apoptosis. However, it is unknown whether miR-101 expression affects cell proliferation and apoptosis in diffuse large B cell lymphoma (DLBCL). The aim of the present study was to investigate the expression of miR-101 and its effect on cell proliferation and apoptosis in DLBCL. Methods miR-101 expression was detected in 30 cases of patients with DLBCL and normal lymph node by qRT-PCR. Then, miR-101 expression was up-regulated and down-regulated in Originated Cell Line-Large Lymphoma 8 (OCL-LY8) cell line, respectively. MTT and flow cytometry assay were used to evaluate the effect of miR-101 on cell proliferation and apoptosis, respectively. As KDM1A was confirmed to be as a specific target of miR-101 by TargetScanHuman, the relationship between MiR-101 and KDM1A was further investigated. Results miR-101 expression in patients with DLBCL was significantly reduced compared those in normal lymph node (P<0.05). miR-101 expression was significantly associated with tumor size, clinical stage and International Prognostic Index (IPI) scores (P<0.05). In OCL-LY8 cell line, miR-101 down-regulation significantly promoted cell proliferation and suppressed cell apoptosis. Meanwhile, miR-101 up-regulation reversed this effect. In addition, miR-101 negatively regulated the expression of KDM1A. KDM1A down-regulation was oberved in normal tissues compared with those in DLBCL tissues, which inhibited cell proliferation and promoted cell apoptosis. Conclusion These data indicate that miR-101 regulates cell proliferation and apoptosis by targeting KDM1A, which provides a potential therapeutic for DLBCL patients.

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“…and cyclin E 19 . In contrast, a role for an N-terminal 77 amino acid domain of YB-1 has been implicated in regulating progression of the G2/M phases of the cell cycle 20 and other studies have demonstrated that inhibiting YB-1 caused an arrest at G2/M 21,22 .…”

Section: Introductionmentioning

confidence: 97%

Critical role for cold shock protein YB-1 in cytokinesis

Mehta

Algie

Al-Jabri

et al. 2020

Preprint

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Y-box-binding protein-1, YB-1, is essential for cell division, but it is not clear how it functions. Using live imaging and confocal microscopy we show that YB-1 functions only in the last step of division, specifically being required to initiate cytokinesis. ABSTRACTHigh levels of the cold shock protein Y-box-binding protein-1, YB-1, are tightly correlated with increased cell proliferation and cancer progression. However, the precise mechanism by which YB-1 regulates proliferation is unknown. Here, we found that YB-1 depletion in several cell lines resulted in cytokinesis failure, multinucleation and an increase in G1 transit time. Rescue experiments indicated that YB-1 was required for completion of cytokinesis. Using confocal imaging of cells undergoing cytokinesis both in vitro and in zebrafish embryos, we found that YB-1 was critical for microtubule organization during cytokinesis. Using mass spectrometry we identified multiple novel phosphorylation sites on YB-1. We show that phosphorylation of YB-1 at multiple serine residues was essential for its function during cytokinesis. Using atomistic modelling we show how multiple phosphorylations alter YB-1 conformation, allowing it to interact with protein partners. Our results establish phosphorylated YB-1 as a critical regulator of cytokinesis, defining for the first time precisely how YB-1 regulates cell division.Word Count 157 / 160 words

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Y-box-binding protein-1 (YB-1) promotes cell proliferation, adhesion and drug resistance in diffuse large B-cell lymphoma

Cited by 37 publications

References 28 publications

Y‐box binding protein‐1 promotes tumorigenesis and progression via the epidermal growth factor receptor/AKT pathway in spinal chordoma

Y‐box binding protein‐1 promotes tumorigenesis and progression via the epidermal growth factor receptor/AKT pathway in spinal chordoma

<p>miR-101 regulates cell proliferation and apoptosis by targeting KDM1A in diffuse large B cell lymphoma</p>

Critical role for cold shock protein YB-1 in cytokinesis

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