Correspondence to “A novel lncRNA SNHG29 regulates EP300-related histone acetylation modification and inhibits FLT3-ITD AML development”

Abstract

We read the article “A novel lncRNA SNHG29 regulates EP300-related histone acetylation modification and inhibits FLT3-ITD AML development” by Liu Shan et al. with great interest [1]. The study identified the role of the novel lncRNA SNHG29 in FLT3-ITD acute myeloid leukemia (AML), demonstrating that it suppresses AML progression by binding to and regulating the histone acetyltransferase EP300, thereby influencing histone acetylation modifications and the expression of key AML-related genes. The research team has provided new potential therapeutic targets and research directions for AML treatment, and their findings hold significant implications for developing novel therapeutic strategies against AML.

The article makes an important contribution to the field of AML research, but we note a number of issues that may affect reader understanding and the reproducibility of experimental results. First, in the results section titled “SNHG29 is associated with proliferation and drug sensitivity of FLT3-ITD AML cells”, the authors report that “Overexpressed SNHG29 significantly inhibited proliferation and colony formation of MV4-11 and MOLM-13 cells, manifested by CCK-8 and clone formation (Fig. 3C) results.” However, the colony-forming assay lacks critical experimental parameters that may affect the reproducibility of the experiments. We recommend that the authors provide essential methodological details (e.g., agar concentration, culture conditions, and colony-counting criteria [2, 3]) and include representative colony images for both the OV-NC and OV-SNHG29 groups to enhance the rigor of the data [4, 5].