LINC01128 (Long Intergenic Non-Protein Coding RNA 1128)

Rescue experiments revealed TRIM58 knockdown attenuated MLN4924's suppression of AKT phosphorylation and associated pro-apoptotic effects. In this study, we show that MLN4924 can upregulate LINC01128, which binds to and segregates DNMT1, thereby inhibiting methylation modification of the TRIM58 and ultimately suppressing AML.

Our results identified promising biomarkers that play a role in specific groups of prostate cancer patients. Detecting specific biomarkers may be an effective strategy for different groups of PC patients.

In PCa, high expression of LINC01128 may predict patients' unfavorable prognosis. LINC01128 promoted PCa cellular processes by negatively regulating miR-27b-3p.

In recent years, the importance of long non-coding RNA (lncRNA) in acute myeloid leukemia (AML) has attracted wide attention. Among them, lncRNAs that play a role in promoting cancer mainly include HOTAIR, UCA1, H19, ITGB2-AS1 and some genes of SNHG family, while in tumor suppression mainly include H22954, NEAT1, SNHG4, LINC01128 , etc. This article reviews the role of lncRNAs in the occurrence and development of AML, as well as those related to AML resistance and prognosis assessment, so as to provide a theoretical basis for the diagnosis and prognosis analysis of AML.

As an independent prognostic factor of CRC, upregulation of LINC01128 predicts poor prognosis and accelerates tumor deterioration through miR-363-3p.

Silencing LINC01128 inhibited the proliferation, migration, and invasion levels of glioma cells by targeting miR-27b-3p, thereby affecting the progression of gliomas.

In this perspective, using systems genomic approaches, we highlight the application of phenome-interactome networks in diabetes and provide deep insights. LINC01128, which we previously described as candidate for diabetes, is shown as an example to discuss the approach.