Loss of 4.1B Drives PRMT3-Mediated Regulation of GBM Brain Tumour Stem Cell Growth
, Samir Assaf 1,2, Orsolya Cseh 1,2, Xiaoguang Hao 1,2, Rozina Hassam 1,2, Panagiotis Prinos 3, H. Artee Luchman 1,2,*,†and Samuel Weiss 1,2,*,†
Julio Sotelo
Round 1
Reviewer 1 Report
Comments and Suggestions for AuthorsThe subject of GBM therapy is currently limited and the results dismal, then a potential novel molecular approach is relevant, the text by Bahia, RK et. al. describes a tumoral protein gene that might be a target for furthers chemotherapy studies. The study was well designed and properly conducted; thus, I think that it should be published.
Only a minor suggestion, the description of the molecular characteristics of this axis makes obscure the interpretation of non-experts the contents of this publication, I think that the title should be simplified and clarified, the text describes adequately the molecular characteristics of the gene PRMT3 studied.
Author Response
Comment 1: Only a minor suggestion, the description of the molecular characteristics of this axis makes obscure the interpretation of non-experts the contents of this publication, I think that the title should be simplified and clarified, the text describes adequately the molecular characteristics of the gene PRMT3 studied.
Response 1: The title has been simplified in the revised manuscript as suggested by the reviewer #1.
Reviewer 2 Report
Comments and Suggestions for AuthorsIn the manuscript entitled "A 4.1B-PRMT3-UHRF1/DNMT1 Signaling Axis Promotes GBM Brain Tumour Stem Cell Growth" by Bahia R et al., the Authors reported that tumour suppressor protein 4.1B, a negative regulator of PRMT3 that is involved in cancer progression, predicts the response of GBM brain tumour stem cells (BTSCs) to the PRMT3 chemical probe. In addition, PRMT3 regulates the downstream effector UHRF1 that in turn, together with DNMT1, may suppress the expression of 4.1B through promoter methylation, promoting BTSCs growth. The Authors suggested that targeting PRMT3 or UHRF1/DNMT1, especially in tumours with low endogenous 4.1B protein, may represent a potential therapeutic strategy in GBM. The topic is very interesting and many experiments are shown to sustain Author's conclusions. However, there are some concerns that needs to be addressed by the Authors:
- Patients clinical information in Table 3 are too limited. Additional information about histological grading and diagnosis (according to the WHO 2021) as well as follow-ups data are very important.
- Fluorescence images that appear in Fig.2 and Fig.6 are not very clear (poor resolution due to pdf conversion?).
Author Response
Comment 1: Patients clinical information in Table 3 are too limited. Additional information about histological grading and diagnosis (according to the WHO 2021) as well as follow-ups data are very important.
Response 1: The patients diagnosis data have been provided in the table, and we have added additional details in the methods section on the GBM tissue grading by a board-certified neuropathologist according to the WHO 2021 recommendations.
Comment 2: Fluorescence images that appear in Fig.2 and Fig.6 are not very clear (poor resolution due to pdf conversion?).
Response 2: The poor resolution of Fluorescence images presented in Fig.2 and Fig.6 was due to pdf conversion. The images in Fig 2: top panel have been replaced with higher resolution images.
Round 2
Reviewer 2 Report
Comments and Suggestions for AuthorsNo further comments
