Acetylation-mediated degradation of HSD17B4 regulates the progression of prostate cancer

Huang, Huichao; Liu, Ruijie; Huang, Ya‐Hui; Feng, Yuhua; Fu, Ying; Chen, Lin; Chen, Zhuchu; Cai, Yi; Zhang, Ye; Chen, Yongheng

doi:10.18632/aging.103530

Cited by 19 publications

(12 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several studies have demonstrated that phosphatidylserine (PS) can bind to D-bifunctional protein (D-BP) and localize to peroxisomes, implying that PS can also affect the β-oxidation process [123]. It is worth noting that some studies have pointed out that acetylation is important for the normal functioning of D-BP [124,125], but related studies are not common; thus, we do not know which factors affect its acetylation process. Another key regulatory enzyme of peroxisomal β-oxidation, Acetyl-CoA acyltransferase 1 (ACAA1), has been extensively studied.…”

Section: Othersmentioning

confidence: 99%

The Overlooked Transformation Mechanisms of VLCFAs: Peroxisomal β-Oxidation

Zong

Zhang

et al. 2022

Agriculture

View full text Add to dashboard Cite

Beta-oxidation(β-oxidation) is an important metabolic process involving multiple steps by which fatty acid molecules are broken down to produce energy. The very long-chain fatty acids (VLCFAs), a type of fatty acid (FA), are usually highly toxic when free in vivo, and their oxidative metabolism depends on the peroxisomal β-oxidation. For a long time, although β-oxidation takes place in both mitochondria and peroxisomes, most studies have been keen to explore the mechanism of β-oxidation in mitochondria while ignoring the importance of peroxisomal β-oxidation. However, current studies indicate that it is hard to provide effective treatment for diseases caused by the disorder of peroxisomal β-oxidation, such as X-ALD, SCOX deficiency, and D-BP deficiency; thus, actions should be taken to solve this problem. Based on existing research results, this review will summarize the importance of peroxisomal β-oxidation and help further learning.

show abstract

Section: Othersmentioning

confidence: 99%

The Overlooked Transformation Mechanisms of VLCFAs: Peroxisomal β-Oxidation

Zong

Zhang

et al. 2022

Agriculture

View full text Add to dashboard Cite

show abstract

“…37 Hsd17b4 is involved in the catabolism of fatty acids and steroid hormones, and various studies have revealed Hsdl7b4 to be implicated in the development of prostate and breast cancer. 38 , 39 Hsd17b4 is linked to the peroxisome, which catalyzes many critical metabolic activities, primarily related to lipid metabolism. Obesity alters peroxisome function, resulting in aberrant lipid metabolism.…”

Section: Discussionmentioning

confidence: 99%

Effects of Semaglutide on Cardiac Protein Expression and Cardiac Function of Obese Mice

Pan¹,

Yue²,

Ban³

et al. 2022

JIR

View full text Add to dashboard Cite

Using proteomics to study the effect of semaglutide on cardiac protein expression in obese mice. Assessment of the effect of semaglutide on cardiac function in obese mice. Materials and Methods:The mice were randomly divided into three groups: the control group (WC), the high-fat group (WF), and the high-fat diet with semaglutide intervention group (WS). Serum samples were collected, and lipids, blood glucose, inflammatory and oxidative stress markers, and cardiac ultrasound, were examined. The cardiac weight of each group of mice was measured, and pathological alterations were examined. Inflammation and oxidative stress levels in heart tissue were evaluated. The labeling coupled with liquid chromatography-tandem mass spectrometry (LC-MS/MS) platform was used to find differentially expressed proteins (DEPs) and screen for related pathways and key proteins in a proteomics study. Results: Semaglutide greatly alleviated obesity-induced lipid metabolism abnormalities, improved cardiac ventricular wall thickening, and significantly reduced myocardial collagen content in obese mice. Semaglutide significantly reduces obesity-induced inflammation and oxidative stress. There were 64 DEPs in the WF/WC group, with 39 upregulated proteins and 25 downregulated proteins. The WS/ WC group, on the other hand, had 83 DEPs, including 57 upregulated and 26 downregulated proteins. Following functional analysis, DEPs were shown to be largely associated with lipid metabolism and peroxisomes. Apolipoprotein A-II, catalase, diazepam-binding inhibitor, paraoxonase-1, and hydroxysteroid 17-dehydrogenase-4 were all upregulated in the WF group but significantly downregulated in the WS group. A high-fat diet increases the expression of lipid synthesis and transport proteins while increasing inflammation and oxidative stress damage. Conclusion: Semaglutide decreases lipid synthesis alleviates inflammation and oxidative stress and prevents lipid peroxidation and cardiac impairment.

show abstract

“…For instance, it was reported that HSD17B4 (hydroxysteroid 17-beta dehydrogenase 4) overexpression promotes proliferation and malignancy of prostate cancer cells. Acetylation of HSD17B4 promotes its degradation by CMA and leads to a subsequent decrease in prostate cancer progression [ 98 ]. In this case, autophagy does not participate in cell death, but leads to degradation of a factor that enhances prostate cancer progression.…”

Section: Autophagy and Prostate Cancermentioning

confidence: 99%

Targeting autophagy in prostate cancer: preclinical and clinical evidence for therapeutic response

Ashrafizadeh

Paskeh

Mirzaei

et al. 2022

J Exp Clin Cancer Res

View full text Add to dashboard Cite

Prostate cancer is a leading cause of death worldwide and new estimates revealed prostate cancer as the leading cause of death in men in 2021. Therefore, new strategies are pertinent in the treatment of this malignant disease. Macroautophagy/autophagy is a “self-degradation” mechanism capable of facilitating the turnover of long-lived and toxic macromolecules and organelles. Recently, attention has been drawn towards the role of autophagy in cancer and how its modulation provides effective cancer therapy. In the present review, we provide a mechanistic discussion of autophagy in prostate cancer. Autophagy can promote/inhibit proliferation and survival of prostate cancer cells. Besides, metastasis of prostate cancer cells is affected (via induction and inhibition) by autophagy. Autophagy can affect the response of prostate cancer cells to therapy such as chemotherapy and radiotherapy, given the close association between autophagy and apoptosis. Increasing evidence has demonstrated that upstream mediators such as AMPK, non-coding RNAs, KLF5, MTOR and others regulate autophagy in prostate cancer. Anti-tumor compounds, for instance phytochemicals, dually inhibit or induce autophagy in prostate cancer therapy. For improving prostate cancer therapy, nanotherapeutics such as chitosan nanoparticles have been developed. With respect to the context-dependent role of autophagy in prostate cancer, genetic tools such as siRNA and CRISPR-Cas9 can be utilized for targeting autophagic genes. Finally, these findings can be translated into preclinical and clinical studies to improve survival and prognosis of prostate cancer patients. Graphical abstract

show abstract

Acetylation-mediated degradation of HSD17B4 regulates the progression of prostate cancer

Cited by 19 publications

References 49 publications

The Overlooked Transformation Mechanisms of VLCFAs: Peroxisomal β-Oxidation

The Overlooked Transformation Mechanisms of VLCFAs: Peroxisomal β-Oxidation

Effects of Semaglutide on Cardiac Protein Expression and Cardiac Function of Obese Mice

Targeting autophagy in prostate cancer: preclinical and clinical evidence for therapeutic response

Contact Info

Product

Resources

About