miR‐129 targets CDK1 and iASPP to modulate Burkitt lymphoma cell proliferation in a TAp63‐dependent manner

Zou, Hui; Zou, Run-Ying; Chen, Keke; Zhu, Chengguang; Tian, Xin; You, Yalan; He, Xinguang

doi:10.1002/jcb.27189

Cited by 3 publications

(6 citation statements)

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“…Since TAp63α is expressed in some Burkitt lymphomas and diffuse large B cell lymphomas [ 79 , 80 ] and TAp63α over-expression inhibits lytic reactivation in NOKs-Akata cells, we asked whether TAp63α helps maintain EBV latency in a lymphoma cell line that expresses TAp63α. The level of TAp63α protein expression in various EBV-infected lymphoma cell lines or lymphoblastoid cell lines (including the ILB1 DLBCL line, the Akata BL cell line, an Akata EBV strain virus transformed lymphoblastoid cell line (LCL), and an AG876 EBV strain virus transformed LCL) was examined by immunoblot analysis.…”

Section: Resultsmentioning

confidence: 99%

“…The ΔNp63α isoform is the primary isoform expressed in epithelial cells. Interestingly, TAp63α is expressed in some B-cell lymphomas, including Burkitt lymphoma and diffuse large B cell lymphomas (DLBCL), and is a potential marker for poor patient prognosis [42,55,[78][79][80][81]. ΔNp63α does not bind directly to the EBV immediate-early gene promoters or prevent R binding to the EBV genome.…”

Section: The C-terminal Domain Of Tap63 and δNp63 Inhibits R-induced Lytic Reactivationmentioning

confidence: 99%

“…Since TAp63α is expressed in some Burkitt lymphomas and diffuse large B cell lymphomas [79,80] and TAp63α over-expression inhibits lytic reactivation in NOKs-Akata cells, we asked…”

Section: Tap63α Acts As a Repressor Of Ebv Lytic Reactivation In The Akata Burkitt Lymphoma Cell Linementioning

confidence: 99%

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ΔNp63α promotes Epstein-Barr virus latency in undifferentiated epithelial cells

et al. 2021

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Epstein-Barr virus (EBV) is a human herpesvirus that causes infectious mononucleosis and contributes to both B-cell and epithelial-cell malignancies. EBV-infected epithelial cell tumors, including nasopharyngeal carcinoma (NPC), are largely composed of latently infected cells, but the mechanism(s) maintaining viral latency are poorly understood. Expression of the EBV BZLF1 (Z) and BRLF1 (R) encoded immediate-early (IE) proteins induces lytic infection, and these IE proteins activate each other’s promoters. ΔNp63α (a p53 family member) is required for proliferation and survival of basal epithelial cells and is over-expressed in NPC tumors. Here we show that ΔNp63α promotes EBV latency by inhibiting activation of the BZLF1 IE promoter (Zp). Furthermore, we find that another p63 gene splice variant, TAp63α, which is expressed in some Burkitt and diffuse large B cell lymphomas, also represses EBV lytic reactivation. We demonstrate that ΔNp63α inhibits the Z promoter indirectly by preventing the ability of other transcription factors, including the viral IE R protein and the cellular KLF4 protein, to activate Zp. Mechanistically, we show that ΔNp63α promotes viral latency in undifferentiated epithelial cells both by enhancing expression of a known Zp repressor protein, c-myc, and by decreasing cellular p38 kinase activity. Furthermore, we find that the ability of cis-platinum chemotherapy to degrade ΔNp63α contributes to the lytic-inducing effect of this agent in EBV-infected epithelial cells. Together these findings demonstrate that the loss of ΔNp63α expression, in conjunction with enhanced expression of differentiation-dependent transcription factors such as BLIMP1 and KLF4, induces lytic EBV reactivation during normal epithelial cell differentiation. Conversely, expression of ΔNp63α in undifferentiated nasopharyngeal carcinoma cells and TAp63α in Burkitt lymphoma promotes EBV latency in these malignancies.

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Section: Resultsmentioning

confidence: 99%

Section: The C-terminal Domain Of Tap63 and δNp63 Inhibits R-induced Lytic Reactivationmentioning

confidence: 99%

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ΔNp63α promotes Epstein-Barr virus latency in undifferentiated epithelial cells

et al. 2021

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“…These findings suggested that miR-129 can be developed into an effective therapeutic target for these types of cancer. In addition, multiple targets of miR-129 have been validated, including CDK1 and iASPP in Burkitt lymphoma,32 PAK5 in hepatocellular carcinoma,33 and MAL2 in papillary thyroid carcinoma 34. These studies suggested that miR-129 exhibited tissue-specific functions.…”

Section: Discussionmentioning

confidence: 97%

<p>Targeting ZEB2 By microRNA-129 In Non-Small Cell Lung Cancer Suppresses Cell Proliferation, Invasion And Migration Via Regulating Wnt/β-Catenin Signaling Pathway And Epithelial–Mesenchymal Transition</p>

Li¹,

Bi³

et al. 2019

OTT

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IntroductionNon-small cell lung cancer (NSCLC) is a common cause of deaths all over the world. Emerging evidence has indicated that microRNA (miR) play key roles in NSCLC progression. We aimed to determine the functions of miR-129 in NSCLC. miR-129 was dramatically downregulated in NSCLC tissue samples and cells. The decreased miR-129 was found to be associated with poorer prognosis and malefic phenotype of NSCLC patients. We demonstrated that miR-129 upregulation could inhibit NSCLC cell growth. Furthermore, we also sought the molecular mechanism by which miR-129 repressed NSCLC development.MethodsQRT-PCR was applied to detect the expressions of miR-129 in 51 pairs of NSCLC tissue samples. We further performed the Kaplan–Meier analysis to determine the association between miR-129 expressions and the survival rate of NSCLC patients. We then measured the expression levels of miR-129 in NSCLC cell lines. After that, MTT assays were performed to determine the influence of miR-129 on A549 cell proliferation. Transwell assay was then conducted to explore the biological functions of miR-129 in invasion and migration of NSCLC cells.ResultsResults showed that ZEB2 was directly targeted by miR-129 in NSCLC cell lines. Moreover, miR-129 restoration could inhibit EMT and Wnt/β-catenin in NSCLC cell lines.ConclusionIn short, all these results indicated that miR-129/ZEB2 axis maybe a useful diagnostic and prognostic biomarker for NSCLC treatment.

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“…Most notably, the tumor suppressor miR-129 has been shown to suppress expression of CDK1 and iASPP through binding with their transcripts. Moreover, CDK1 targeting by miR-129 can lead to inhibition of iASPP phosphorylation, therefore deterring nuclear localization of iASPP and its suppressive impact on p53 and TAp63 [ 13 ].…”

Section: Cyclin-dependent Kinase 1 (Cdk1)mentioning

confidence: 99%

A review on the role of cyclin dependent kinases in cancers

et al. 2022

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The Cyclin-dependent kinase (CDK) class of serine/threonine kinases has crucial roles in the regulation of cell cycle transition and is mainly involved in the pathogenesis of cancers. The expression of CDKs is controlled by a complex regulatory network comprised of genetic and epigenetic mechanisms, which are dysregulated during the progression of cancer. The abnormal activation of CDKs results in uncontrolled cancer cell proliferation and the induction of cancer stem cell characteristics. The levels of CDKs can be utilized to predict the prognosis and treatment response of cancer patients, and further understanding of the function and underlying mechanisms of CDKs in human tumors would pave the way for future cancer therapies that effectively target CDKs. Defects in the regulation of cell cycle and mutations in the genes coding cell-cycle regulatory proteins lead to unrestrained proliferation of cells leading to formation of tumors. A number of treatment modalities have been designed to combat dysregulation of cell cycle through affecting expression or activity of CDKs. However, effective application of these methods in the clinical settings requires recognition of the role of CDKs in the progression of each type of cancer, their partners, their interactions with signaling pathways and the effects of suppression of these kinases on malignant features. Thus, we designed this literature search to summarize these findings at cellular level, as well as in vivo and clinical levels.

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miR‐129 targets CDK1 and iASPP to modulate Burkitt lymphoma cell proliferation in a TAp63‐dependent manner

Cited by 3 publications

References 47 publications

ΔNp63α promotes Epstein-Barr virus latency in undifferentiated epithelial cells

ΔNp63α promotes Epstein-Barr virus latency in undifferentiated epithelial cells

<p>Targeting ZEB2 By microRNA-129 In Non-Small Cell Lung Cancer Suppresses Cell Proliferation, Invasion And Migration Via Regulating Wnt/β-Catenin Signaling Pathway And Epithelial–Mesenchymal Transition</p>

A review on the role of cyclin dependent kinases in cancers

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