Pillar 1 - FTO (new thread), page-1466

Hi @Mason14

First of all - I'd just like to express my appreciation as many others on this board have for your consistently thorough and insightful analysis and information.

I was wondering how much you had looked into the specific mechanics of the METTL3, METTL14 and WTAP methyltransferases on certain types of cancer.

I've been doing some research into how what downregulation of these methyltransferases have on the growth/proliferation of particular cancers and I came across the following article on the effect a m6a demethylation/methylation on hepatocellular carcinoma tissue:

https://molecular-cancer.biomedcentral.com/articles/10.1186/s12943-019-1053-8

From what I understand, high levels of WTAP were correlated with poor prognosis outcomes in HCC tumour tissue (let me know if I've misunderstood this paper as I'm very new in this field).

Do you know whether FTO inhibition (induced by Bisantrene or any other FTO inhibitors you've come across) result in higher levels of WTAP/METTL3/METTL14 or does it simply reduce the proportion of demethylation to methylation (simply by a lower amount of FTO vs the methylases)?

I guess I'm curious to understand how exactly Bisantrene/other FTO inhibitors could interact with cancers that don't just correlate to FTO expression (higher demethylase levels), but also exist/demonstrate higher levels of metastasis/aggression where methylases like WTAP/METTL3/METTL14 are low.

Thanks for any insight you can provide!