Stabilization of β-catenin upon B-cell receptor signaling promotes NF-kB target genes transcription in mantle cell lymphoma

Lazarian, Grégory; Friedrich, Chloé; Quinquenel, Anne; Tran, Julie; Ouriemmi, Souhail; Dondi, Elisabetta; Martin, Antoine; Mihoub, Imane; Chiron, David; Bellanger, Céline; Fleury, Carole; Gélébart, Pascal; McCormack, Emmet; Ledoux, Dominique; Thiéblemont, Catherine; Marzec, Jacek; Gribben, John G.; Cymbalista, Florence; Varin‐Blank, Nadine; Gardano, Laura; Baran‐Marszak, Fanny

doi:10.1038/s41388-020-1183-x

Cited by 16 publications

(10 citation statements)

References 44 publications

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“…Similar β-catenin expression patterns were also found in initiating cells of mantle cell lymphoma (MCL) ( Mathur et al., 2015 ). There are several ways of cross talk between Wnt/β-catenin and NF-κB pathways during inflammation ( Aghajanpour-Mir et al., 2016 ) and MCL lymphomagenesis ( Lazarian et al., 2020 ). The NFKB1 gene encodes canonical NF-κB subunit p105, which is processed by the proteasome into p50 to form a p65/p50 heterodimer transcription factor, and is considered a regulator of innate immunity.…”

Section: Discussionmentioning

confidence: 99%

“…The NFKB1 gene encodes canonical NF-κB subunit p105, which is processed by the proteasome into p50 to form a p65/p50 heterodimer transcription factor, and is considered a regulator of innate immunity. Canonical NF-κB signals are connected to pathological pathways in low-grade Mucosa-associated lymphoid tissue (MALT) lymphoma ( Hamoudi et al., 2010 ; Nagel et al., 2014 ), high-grade MCL ( Aghajanpour-Mir et al., 2016 ; Lazarian et al., 2020 ), as well as DLBCL of ABC type ( Compagno et al., 2009 ; Davis et al., 2001 ; Nagel et al., 2014 ). AR (androgen receptor) interplay with NF-κB has been linked in prostate cancer ( Malinen et al., 2017 ; Zhang et al., 2009 ).…”

Section: Discussionmentioning

confidence: 99%

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Bisphenol A-induced DNA damages promote to lymphoma progression in human lymphoblastoid cells through aberrant CTNNB1 signaling pathway

et al. 2021

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Bisphenol A-induced DNA damages promote to lymphoma progression in human lymphoblastoid cells through aberrant CTNNB1 signaling pathway

et al. 2021

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“… 34 , 35 The dysregulation of the Wnt/β-catenin signaling pathway modulates crucial cancer biological processes, such as proliferation, metastasis, metabolism, and cancer cells’ stemness. 36 - 38 As is well known, Wnt/β-catenin signaling pathway is thought to act key influences on LUAD. 39 For instance, it has demonstrated that Wnt/β-catenin signaling pathway could regulate the LUAD cell proliferation, migration and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

LINC00942 Promotes Tumor Proliferation and Metastasis in Lung Adenocarcinoma via FZD1 Upregulation

Wang

Zhang

et al. 2021

Technol Cancer Res Treat

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Background: Long non-coding RNAs (lncRNAs) have been reported to play important roles in the progression of human cancers. Herein, bioinformatic analysis identified that LINC00942 was a highly overexpressed lncRNA in lung adenocarcinoma (LUAD). The present study aimed to explore the roles and possible molecular mechanisms of LINC00942 in LUAD. Methods: First, on the basis of TCGA database, the expression and prognosis of LINC00942 were analyzed in LUAD tissues. Then, si-LINC00942 was transfected into A549 and H1299 cells to knockdown the expression of LINC00942. Cell viability was detected by MTT assay. Flow cytometry was used to analyze cell apoptosis. The expressions of PCNA, Bax, Bcl-2, and wnt/β-catenin pathway proteins were detected by western blotting. Dual-luciferase reporter assay was used to evaluate the regulatory relationship between LINC00942 and miR-5006-5p, or miR-5006-5p and FZD1. Results: We discovered that LINC00942 was up-regulated in LUAD tissues compared with adjacent tissues. Besides, we found the increased LINC00942 expression was associated with poor survival. In addition, silencing of LINC00942 suppressed the proliferation, migration, invasion and facilitated the apoptosis of A549 and H1299 cells. Moreover, silencing of LINC00942 repressed the expression of PCNA, Bcl-2, and enhanced Bax expression in A549 and H1299 cells. Mechanically, LINC00942 exerted its effects via enhancing Wnt signaling. LINC00942 functioned as competing endogenous RNA (ceRNA) by binding to miR-5006-5p, upregulating the expression of FZD1, which was a direct target of miR-5006-5p. Conclusion: Our findings indicated that LINC00942/miR-5006-5p/FZD1 axis played important roles in LUAD growth through enhancing Wnt signaling. LINC00942/miR-5006-5p/FZD1 axis might serve as a potential biomarker and therapeutic target for LUAD treatment.

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“…29,30 There are several studies of this polymorphism in cancer and other diseases. [31][32][33] These studies found that NFκB-94 ins/del polymorphism may influence the risk of cancer in Asian population. The variant allele of NFκB-94 ins/del ATTG (rs28362491) polymorphism was shown to be associated with higher risk of sporadic CRC in Malaysian population, and functional NFκB-94 ins/del ATTG polymorphism is associated with CSCC.…”

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confidence: 91%

Genetic Polymorphisms in NLRP3 Inflammasome-Associated Genes in Patients with B-Cell Non-Hodgkin’s Lymphoma

Liu¹,

Zhang²,

Jing³

et al. 2021

JIR

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Stabilization of β-catenin upon B-cell receptor signaling promotes NF-kB target genes transcription in mantle cell lymphoma

Cited by 16 publications

References 44 publications

Bisphenol A-induced DNA damages promote to lymphoma progression in human lymphoblastoid cells through aberrant CTNNB1 signaling pathway

Bisphenol A-induced DNA damages promote to lymphoma progression in human lymphoblastoid cells through aberrant CTNNB1 signaling pathway

LINC00942 Promotes Tumor Proliferation and Metastasis in Lung Adenocarcinoma via FZD1 Upregulation

Genetic Polymorphisms in NLRP3 Inflammasome-Associated Genes in Patients with B-Cell Non-Hodgkin’s Lymphoma

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