DLBCL developed into fatal liver failure during rituximab-containing                    chemotherapy

Shimazu, Yutaka; Nohgawa, Masaharu

doi:10.3960/jslrt.19004

Cited by 2 publications

(1 citation statement)

References 10 publications

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“…Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of lymphoma, representing 30-40% of all cases with adult non-Hodgkin lymphoma (Cheson, 2020). While approximately 10% of patients with DLBCL can be cured by the first-line treatment regimen currently used in clinics (Shimazu and Nohgawa, 2019;Morin and Scott, 2020), combined autologous hematopoietic stem cells with the present rescue chemotherapy regimen can only cure around 10% of all cases with relapsed and refractory DLBCL (Miao et al, 2019). It has become a major challenge for the present DLBCL treatment to enhance the therapeutic effects of the remaining 30% patients.…”

Section: Introductionmentioning

confidence: 99%

The m6A Methyltransferase METTL3 Is Functionally Implicated in DLBCL Development by Regulating m6A Modification in PEDF

Cheng

Wang

et al. 2020

Front. Genet.

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Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of lymphoma, whose treatment still has a major challenge of achieving a satisfactory curative effect. The underlying mechanisms also have not been fully illustrated. N 6-Methyladenosine (m6A) has been identified as the most prevalent internal modification of mRNAs present in eukaryotes, which is involved in the pathogenesis of cancers. It remains unclear how m6A mRNA methylation is functionally linked to the pathogenesis of DLBCL. In this study, we sought to explore the roles of METTL3 on DLBCL development. The results showed that m6A level for RNA methylation and the expression level of METTL3 were upregulated in DLBCL tissues and cell lines. Functionally, downregulated METTL3 expression in DLBCL cells inhibited the cell proliferation ability. Further mechanism analysis indicated that METTL3 knockdown abates the m6A methylation and total mRNA level of pigment epithelium-derived factor (PEDF). However, Wnt/β-catenin signaling was not thus activated. Overexpressed PEDF abrogates the inhibition of cell proliferation in DLBCL cells that is caused by METTL3 silence. In summary, the abovementioned results demonstrated that the METTL3 promotes DLBCL progression by regulating the m6A level of PEDF.

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