Dihydrolipoamide S-acetyltrans-ferase (DLAT), a mitochondrial protein involved in glucose metabolism, has been identified as a key gene associated with cuproptosis recently. However, studies on DLAT in pan-cancer have not been found. Aim of this study is to explore the expression profiles and clinical value of DLAT in pan-cancer. DLAT expression profiles were obtained from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), UALCAN and the Human Protein Atlas (HPA) websites. The prognostic and diagnostic values of DLAT and its relationship with immune cell infiltration were analyzed based on TCGA data. cBioPortal and UALCAN websites were used to search gene alteration and methylation status of DLAT in tumors, respectively. CancerSEA database was used to investigate the biological functions of DLAT at the single-cell level. Finally, STRING, GAPIA2.0 and TIMER databases were used to construct protein-protein interaction (PPI) networks and functional enrichment analyses. High DLAT expression was found in most cancers and predicted poor prognosis in patients with several tumors, such as breast cancer, esophageal cancer, head and neck squamous cell carcinoma. DLAT showed early diagnostic value in 17 tumors, especially in acute myeloid leukemia (LAML). Abnormal gene alterations and DNA methylation of DLAT were verified in pan-cancer. Single cell RNA sequencing (scRNAseq) analysis reflected that DLAT could regulate various biological functions of cancer cells. Abnormal expression of DLAT regulated infiltration of multiple immune cells in a variety of tumors. Gene enrichment analysis showed that DLAT was involved in mitochondrial matrix, coated vesicle and ribonucleoprotein granule. DLAT can be used as an important indicator of early diagnosis, prognosis and immunotherapy for a variety of tumors.
Background. 4-Methoxydalbergione (4MOD) is a flavonoid isolated from the heartwood of Dalbergia. Studies have demonstrated that 4MOD exerts anticancer activities on bladder cancer and astrocytoma. However, the anticancer activity of 4MOD in hepatocellular carcinoma (HCC) remains unknown. This study aims to examine its anticancer activities and mechanisms in human liver cancer cells. Methods. CCK-8, colony forming, wound healing, transwell migration, and AnnexinV/PI assays were used to assess the anticancer effects of 4MOD in HCC cells. RNA sequencing (RNA-Seq) was selected to explore the possible mechanisms underlying the anti-HCC activity of 4MOD. The mRNA expression levels of target genes were verified through quantitative real-time PCR (qRT-PCR). A lentiviral shRNA interference technique was used to silence GADD45G expression. GADD45G knockdown was employed to confirm the crucial role of GADD45G in the 4MOD-mediatedanti-HCC effects. Results. 4MOD inhibited HCC cells’ proliferation and migration and promoted tumor cell apoptosis. RNA-Seq and qRT-PCR analyses revealed that 4MOD treatment increased GADD45G expression. Silencing GADD45G reversed 4MOD-mediated inhibition of proliferation, migration, and promotion of apoptosis. Conclusions. Our findings show that 4MOD elicits anti-HCC effects by upregulating GADD45G expression and could be a valuable anticancer agent for liver cancer.
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