PSAT1 inhibits mTORC1 activation by preventing Rag heterodimer formation in lung adenocarcinoma.

The mechanistic target of rapamycin complex 1 (mTORC1) integrates environmental cues, especially amino acids, to regulate metabolism and ultimately cancer progression. Phosphoserine aminotransferase 1 (PSAT1) is a key enzyme in de novo serine synthesis and its overexpression has been reported to promote oncogenesis in various cancers. Knockdown of PSAT1 inhibits the proliferation and migration of cancer cells.

A clinical research: blood perfusion of artificial dermis detected by laser speckle contrast imaging influence the therapeutic effect on wound healing.

We aimed to assess blood flow perfusion in wounds using Laser Speckle Contrast Imaging (LSCI) technology and evaluate the influence of artificial dermis vascularization on wound healing. We retrospectively analyzed clinical data from 27 patients treated at the First Affiliated Hospital of Nanchang University between January 2022 and April 2024. Based on the distribution of speckle flow index (SFI) variation rate measured by LSCI in the wound area 1 day before skin grafting, patients were classified into three groups: low SFI variation rate group, medium SFI variation rate group and high SFI variation rate group, which were labeled as Group L (9 patients), Group M (10 patients), and Group H (8 patients).

Deacetylation of GLUD1 maintains the survival of lung adenocarcinoma cells under glucose starvation by inhibiting autophagic cell death.

Enhanced glutamine catabolism is one of the main metabolic features of cancer, providing energy and intermediate metabolites for cancer progression. However, the functions of glutamine catabolism in cancer under nutrient deprivation need to be further clarified. Here, we discovered that deacetylation of glutamate dehydrogenase 1 (GLUD1), one of the key enzymes in glutamine catabolism, maintains the survival of lung adenocarcinoma (LUAD) cells under glucose starvation by inhibiting autophagic cell death.

STUB1-mediated ubiquitination regulates the stability of GLUD1 in lung adenocarcinoma.

The dysregulation of glutamine metabolism provides survival advantages for tumors by supplementing tricarboxylic acid cycle. Glutamate dehydrogenase 1 (GLUD1) is one of the key enzymes in glutamine catabolism. Here, we found that enhanced protein stability was the key factor for the upregulation of GLUD1 in lung adenocarcinoma.

Amino acid metabolism regulated by lncRNAs: the propellant behind cancer metabolic reprogramming.

Metabolic reprogramming is one of the main characteristics of cancer cells and plays pivotal role in the proliferation and survival of cancer cells. Amino acid is one of the key nutrients for cancer cells and many studies have focused on the regulation of amino acid metabolism, including the genetic alteration, epigenetic modification, transcription, translation and post-translational modification of key enzymes in amino acid metabolism. Long non-coding RNAs (lncRNAs) are composed of a heterogeneous group of RNAs with transcripts of more than 200 nucleotides in length.

Remediation of -Linked Macrothrombocytopenia With Ezetimibe Therapy.

To investigate refractory hypercholesterolemia, a female patient and relatives were subjected to whole-genome sequencing. The proband was found to have compound heterozygous substitutions p. Arg446Gln and c.

The Risks of miRNA Therapeutics: In a Drug Target Perspective.

RNAi therapeutics have been growing. Patisiran and givosiran, two siRNA-based drugs, were approved by the Food and Drug Administration in 2018 and 2019, respectively. However, there is rare news on the advance of miRNA drugs (another therapeutic similar to siRNA drug).

FAIM-S functions as a negative regulator of NF-κB pathway and blocks cell cycle progression in NSCLC cells.

Tumorigenesis is closely related to the disorder of the cell cycle. The cell cycle progression includes the interphase (G0/G1, S, and G2 phase) and mitosis (M phase). CCND1 is a key protein that regulates the entry of the G0/G1 phase into the S phase.

BECN1 promotes the migration of NSCLC cells through regulating the ubiquitination of Vimentin.

BECN1/Beclin1 is one of the key proteins in autophagy regulation. However, the biological functions of BECN1 in non-small cell lung cancer (NSCLC) were obscure. Here, we found that neither BECN1 knockdown nor overexpression affected the proliferation of NSCLC cells.

Gene expression profile-based drug screen identifies SAHA as a novel treatment for NAFLD.

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide. Being part of the metabolic syndrome, NAFLD is characterized by the deposition of triglycerides (TGs) as lipid droplets in the cytoplasm of hepatic cells. Recently, the rapid development of high-throughput genome analysis technologies provided opportunities to screen for new drugs for NAFLD.

THZ1 suppresses human non-small-cell lung cancer cells in vitro through interference with cancer metabolism.

Cancer cells always require more nutrients, energy, and biosynthetic activity to sustain their rapid proliferation than normal cells. Previous studies have shown the impact of THZ1, a covalent inhibitor of cyclin-dependent kinase 7 (CDK7), on transcription regulation and cell-cycle arrest in numerous cancers, but its effects on cellular metabolism in cancer cells remain unknown. In this study we elucidated the anticancer mechanism of THZ1 in human non-small-cell lung cancer (NSCLC) cells.

Polymorphism of rs3737597 in DISC1 Gene on Chromosome 1q42.2 in sALS Patients: a Chinese Han Population Case-Control Study.

Although lots of genes have been revealed to relate to sporadic amyotrophic lateral sclerosis (sALS), its genetic mechanisms still need to be further explored. We aimed to search the novel genetic factors of sALS and assess their contribution. We constructed an integrative dataset based on the 3227 subsignificant genes (P value < 0.

[The progress of genetics of cholesterol metabolism disorder].

Cardiovascular disease (CVD) has become an increased risk to human health, and the abnormal cholesterol metabolism will increase the risk of developing CVD. Along with the development of high-throughput sequencing technology and population genomics, the scanning for genes or mutations related to complex traits (or diseases) has been greatly promoted. Also, it becomes possible to explore the genetic mechanism of cholesterol metabolism.