HMGB1 coordinates with Brahma-related gene 1 to promote epithelial-mesenchymal transition via the PI3K/Akt/mTOR pathway in BEAS-2B cells

Deng, Xuedan; Niu, Zhuoya; Hao, Changfu; Lin, Jisong; Yao, Wu

doi:10.1016/j.yexcr.2023.113522

Cited by 6 publications

(7 citation statements)

References 30 publications

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“…( 24 ) found HMGB1 participates in the tumorigenesis of colorectal cancer through the ERK1/2 pathway. Recent studies also found exogenous HMGB1 participated in the epithelial-mesenchymal transition via the PI3K/Akt/mTOR pathway in pulmonary fibrosis ( 44 ). Another study showed that HMGB1-RAGE through PI3K/AKT signaling promotes not only breast cancer cell invasion but also PD-L1 expression which leads to the destruction of the effector T cells ( 27 ).…”

Section: Discussionmentioning

confidence: 99%

USP50 regulates NLRP3 inflammasome activation in duodenogastric reflux-induced gastric tumorigenesis

Zhao,

Mu,

et al. 2024

Front. Immunol.

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Duodenogastric reflux (DGR) has been linked to the onset of gastric cancer (GC), although the precise mechanism is yet obscure. Herein, we aimed to investigate how refluxed bile acids (BAs) and macrophages are involved in gastric carcinogenesis. In both active human bile reflux gastritis and the murine DGR model, ubiquitin specific protease 50 (USP50) was dramatically raised, and macrophages were the principal leukocyte subset that upregulated USP50 expression. Enhancing USP50 expression amplified bile acid-induced NLR family pyrin domain containing 3 (NLRP3) inflammasome activation and subsequent high-mobility group box protein 1 (HMGB1) release, while USP50 deficiency resulted in the reversed alteration. Mechanistically, USP50 interacted with and deubiquitinated apoptosis-associated speck-like protein containing CARD (ASC) to activate NLRP3 inflammasome. The release of HMGB1 contributes to gastric tumorigenesis by PI3K/AKT and MAPK/ERK pathways. These results may provide new insights into bile reflux-related gastric carcinogenesis and options for the prevention of DGR-associated GC.

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Section: Discussionmentioning

confidence: 99%

USP50 regulates NLRP3 inflammasome activation in duodenogastric reflux-induced gastric tumorigenesis

Zhao,

Mu,

et al. 2024

Front. Immunol.

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“…Taken together, our data indicated that NEP‐regulating tubular cell ferroptosis played an important role in kidney fibrosis. Theoretically, ferroptotic tubular epithelial cells secrete high mobility group box 1 (Figure S12), which may promote inflammation and transdifferentiation of RTECs into myofibroblasts, and lead to fibrosis 32,33 …”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…Theoretically, ferroptotic tubular epithelial cells secrete high mobility group box 1 (Figure S12), which may promote inflammation and transdifferentiation of RTECs into myofibroblasts, and lead to fibrosis. 32,33 However, the hyperfine interaction between NEP and ACSL4-mediated ferroptosis remains obscure. Functionally, NEP may indirectly lead to alteration of ACSL4 expression by affecting some peptides, and the specific mechanism warrants exploration in the future.…”

Section: F I G U R E 8 Neprilysin Aggravated Fibrosis By Acsl4-mediat...mentioning

confidence: 99%

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Novel aspect of neprilysin in kidney fibrosis via ACSL4‐mediated ferroptosis of tubular epithelial cells

Lai

Huang

Wang

et al. 2023

MedComm

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Although inhibition of neprilysin (NEP) might be a therapeutic strategy with the potential to improve the outcome of chronic kidney disease (CKD), the versatile function of NEP with its mechanism remains obscure in kidney fibrosis. In the study, we found that NEP was abnormally increased in tubular epithelial cells of CKD patients, as well as unilateral ureteral obstruction and adenine diet‐induced mice. Treatment with a United States Food and Drug Administration‐approved NEP inhibitor Sacubitrilat (LBQ657) could alleviate ferroptosis, tubular injury, and delay the progression of kidney fibrosis in experimental mice. Similarly, genetic knockdown of NEP also inhibited tubular injury and fibrosis in transforming growth factor (TGF)‐β1 ‐induced tubular cells. Mechanically, NEP overexpression aggravated the ferroptotic and fibrotic phenotype, which was restored by acyl‐CoA synthetase long‐chain family member 4 (ACSL4) knockdown. The NEP silencing attenuated TGF‐β1‐induced tubular cell ferroptosis and was exacerbated by ACSL4 overexpression. Collectively, for the first time, a novel aspect of NEP was explored in kidney fibrosis through ACSL4‐mediated tubular epithelial cell ferroptosis. Our data further confirmed that NEP inhibition exerted a promising therapeutic against fibrotic kidney diseases.

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“…High plasma HMGB1 has been recognized as a biomarker for endometriosis [ 31 ] . Mechanistically, HMGB1 activated the PI3K/AKT/mTOR signaling pathway to increase cell proliferation and migration, promoting endothelial-mesenchymal transition in pulmonary fibrosis [ 32 ] . In the present study, we showed that lactate mediated H3K18lac to promote the expression of HMGB1 in endometriosis, and HMGB1 knockdown significantly decreased the cell viability, migration, and invasion of the lactate-treated nESCs; besides, lactate induced the expression of HMGB1 and increased the phosphorylation of AKT and the expression of c-MYC and Cyclin D1, all of which could be blocked by HMGB1 silencing.…”

Section: Discussionmentioning

confidence: 99%

Histone lactylation promotes cell proliferation, migration and invasion through targeting HMGB1 in endometriosis

Chen¹,

Qin²,

Sun³

et al. 2023

J Biomed Res

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Endometriosis is defined as a condition with endometrium-like tissues migrating outside of the pelvic cavity. However, the mechanism of endometriosis is still unclear. Lactate can be covalently modified to lysine residues of histones and other proteins, which is called lactylation. The results showed that the higher level of lactate and lactate dehydrogenase A enhanced the histone H3 lysine 18 lactylation (H3K18lac) in ectopic endometrial tissues and ectopic endometrial stromal cells than that in normal endometrial tissues and normal endometrial stromal cells. Lactate promoted cell proliferation, migration, and invasion in endometriosis. Mechanistically, lactate induced H3K18lac to promote the expression of high-mobility group box 1 (HMGB1) in endometriosis, and HMGB1 knockdown significantly reduced the cell proliferation, migration, and invasion of the lactate-treated cells through the phosphorylation of AKT. In conclusion, lactate could induce histone lactylation to promote endometriosis progression by upregulating the expression of HMGB1, which may provide a novel target for the prevention and treatment of endometriosis.

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HMGB1 coordinates with Brahma-related gene 1 to promote epithelial-mesenchymal transition via the PI3K/Akt/mTOR pathway in BEAS-2B cells

Cited by 6 publications

References 30 publications

USP50 regulates NLRP3 inflammasome activation in duodenogastric reflux-induced gastric tumorigenesis

USP50 regulates NLRP3 inflammasome activation in duodenogastric reflux-induced gastric tumorigenesis

Novel aspect of neprilysin in kidney fibrosis via ACSL4‐mediated ferroptosis of tubular epithelial cells

Histone lactylation promotes cell proliferation, migration and invasion through targeting HMGB1 in endometriosis

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