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. 2022 Mar 11;13:795820. doi: 10.3389/fgene.2022.795820

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Copyright © 2022 Hu, Zhang, Yang, He and Zhao.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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(A) Expression of LYPD3 in cancer lines (the expression of LYPD3 is the highest in HL-60 cells); (B) LYPD3 gene knockdown mediated by siRNA-induced apoptosis in AML cells (HL-60 cells); (C) LYPD3 gene knockdown mediated by siRNA-suppressed proliferation in AML cells (HL-60 cells); (D) significantly enriched pathways in AML samples with high LYPD3 expression; (E) significantly enriched pathways (the P53 signaling pathways); (F) significantly enriched pathways (PI3K_AKT signaling pathway); (G) relationship between LYPD3 and the molecules Akt and P53 (the expression of the LYPD3 gene knockdown-mediated SiRNA group was obviously increased in p53 and PI3K_AKT signaling).