A pan-cancer analysis of the oncogenic function of HMGB1 in human tumors.

Background: Although high mobility group box protein 1 () has been researched in relation to cancer in many investigations, a thorough investigation of its role in pan-cancer has yet to be conducted. With the objective of bridging this gap, we delved into the functions of in various tumors.

Methods: This investigation employed The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases to examine gene expression differences and correlation with survival across various human tumors.

A natural mutation in the promoter of the aconitase gene influences fruit citric acid content in jujube.

Jujube ( Mill.) is the most economically important fruit tree of the Rhamnaceae and was domesticated from wild or sour jujube ( Mill. var.

Roscovitine attenuates renal interstitial fibrosis in diabetic mice through the TGF-β1/p38 MAPK pathway.

Tubulointerstitial fibrosis is the hallmark of diabetic nephropathy, which is the leading cause of end-stage renal disease worldwide. Roscovitine, an inhibitor of Cdks, exhibits anti-fibrosis effects. The present study was aimed to explore the protected role of roscovitine from renal fibrosis of diabetic nephropathy.

Acetylation targets HSD17B4 for degradation via the CMA pathway in response to estrone.

Dysregulation of hormone metabolism is implicated in human breast cancer. 17β-hydroxysteroid dehydrogenase type 4 (HSD17B4) catalyzes the conversion of estradiol (E2) to estrone (E1), and is associated with the pathogenesis and development of various cancers. Here we show that E1 upregulates HSD17B4 acetylation at lysine 669 (K669) and thereby promotes HSD17B4 degradation via chaperone-mediated autophagy (CMA), while a single mutation at K669 reverses the degradation and confers migratory and invasive properties to MCF7 cells upon E1 treatment.

Cullin 3 targets methionine adenosyltransferase IIα for ubiquitylation-mediated degradation and regulates colorectal cancer cell proliferation.

Cullin 3 (CUL3) serves as a scaffold protein and assembles a large number of ubiquitin ligase complexes. It is involved in multiple cellular processes and plays a potential role in tumor development and progression. In this study, we demonstrate that CUL3 targets methionine adenosyltransferase IIα (MAT IIα) and promotes its proteasomal degradation through the ubiquitylation-mediated pathway.

Acetylation of MAT IIα represses tumour cell growth and is decreased in human hepatocellular cancer.

Metabolic alteration is a hallmark of cancer. Dysregulation of methionine metabolism is implicated in human liver cancer. Methionine adenosyltransferase IIα (MAT IIα) is a key enzyme in the methionine cycle, catalysing the production of S-adenosylmethionine (SAM), a key methyl donor in cellular processes, and is associated with uncontrolled cell proliferation in cancer.