ERK-CREB pathway is involved in HSPB8-mediated glioma cell growth and metastatic properties

Li, Xia; Sun, Chengyi; Chen, Jing; Ma, Ji-Fen; Pan, Yi-Heng

doi:10.1016/j.yexmp.2021.104653

Cited by 3 publications

(2 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Heat shock proteins are a large family of proteins that increase when exposed to environmental stresses. The HSPB family contains HSPB8, which participates in diverse pathological processes, such as neurological diseases [19,20], myocardial ischemia [21], cancers [22][23][24], and autoimmune diseases [25]. Overexpression of HSPB8 in RBE cells facilitated Vimentin expression and the LC3-II/LC3-I ratio and inhibited E-cadherin and p62 expression, hence promoting intrahepatic cholangiocarcinoma progression by accelerating EMT and autophagy [26].…”

Section: Discussionmentioning

confidence: 99%

HSPB8 Facilitates the Oncogenesis and Advancement of Bladder Cancer via Activation of HSP27

Du,

Guo,

Wang

et al. 2024

J. Cancer

View full text Add to dashboard Cite

Bladder cancer (BCa) stands as a significant malignancy within the genitourinary system. Notably, heat shock proteins (HSPs) exhibit elevated expression in cells subjected to environmental stresses and have been linked to the progression of many human malignancies. Among these, the functional implications and specific mechanism of HSPB8 in BCa have yet to be fully explored. In this study, we measured HSPB8 expression in both BCa tissues and various cell lines, further delving into its influence on cellular behaviors. Our observations pinpoint an upregulation of HSPB8 in BCa, a trend strongly associated with more advanced clinical manifestations. Suppressing HSPB8 exhibited marked reductions in cell proliferation and migration capabilities, while simultaneously amplifying apoptosis and inducing cell cycle arrest. Reinforcing these findings, our in vivo analyses using mouse models showed similar trends. Notably, upon HSPB8 knockdown, levels of specific proteins including eNOS (S1177), Hsp27 (S78/S82), PRAS40(T246), RSK1/2(S221/S227), and STAT3 (S727) decreased, with Hsp27 (S78/S82) and PRAS40(T246) experiencing the most profound drops. Furthermore, the application of an HSP27 inhibitor effectively reversed the phenotypes caused by increased HSPB8 expression. Collectively, our results suggest that elevated HSPB8 expression could act as a potential prognostic marker for BCa, and targeting HSPB8 might open new therapeutic avenues for treating this malignancy.

show abstract

Section: Discussionmentioning

confidence: 99%

HSPB8 Facilitates the Oncogenesis and Advancement of Bladder Cancer via Activation of HSP27

Du,

Guo,

Wang

et al. 2024

J. Cancer

View full text Add to dashboard Cite

show abstract

“…Heat shock protein B8 (HSPB8), a ubiquitous member of small heat shock proteins family, has been demonstrated to be involved in the regulation of multiple cellular functions, such as growth, aging, oxidative stress, migration and apoptosis (18)(19)(20). As a stress-related protein, HSPB8 accelerates the migration and invasion of hepatocellular carcinoma, breast cancer and cholangiocarcinoma (21)(22)(23).…”

Section: Introductionmentioning

confidence: 99%

HSPB8 binding to c-Myc alleviates hypoxia/reoxygenation-induced trophoblast cell dysfunction

Chen,

Wu,

Zhou

2024

Exp Ther Med

View full text Add to dashboard Cite

Preeclampsia (PE) is a pregnancy-specific syndrome with complex pathogenesis. The present study aimed to explore the role of heat shock protein B8 (HSPB8) and c-Myc in trophoblast cell dysfunction using a hypoxia/reoxygenation (H/R)-treated HTR8/SVneo cell model. HSPB8 expression in tissues of patients with PE was analyzed using the Gene Expression Omnibus database. Following detection of HSPB8 expression in H/R-stimulated HTR8/SVneo cells, HSPB8 was overexpressed by transfection of the gene with a HSPB8-specific plasmid. Cell Counting Kit-8, wound healing and Transwell assays were used to evaluate the proliferation, migration and invasion of HTR8/SVneo cells exposed to H/R conditions. Reactive oxygen species (ROS) were determined by 2,7-dichlorodihydrofluorescein diacetate staining. 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolocarbo-cyanine iodide (JC-1) staining was applied to assess mitochondrial membrane potential. Malondialdehyde (MDA) and superoxide dismutase (SOD) levels were detected using the corresponding commercial kits. In addition, the induction of apoptosis was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. Moreover, the Biogrid database predicted that HSPB8 was bound to c-Myc, and a co-immunoprecipitation (Co-IP) assay was used to verify this interaction. Subsequently, c-Myc expression was silenced to conduct rescue experiments in HTR8/SVneo cells exposed to H/R conditions and upregulated HSPB8 expression. Notably, reduced HSPB8 expression was noted in PE tissues and H/R-stimulated HTR8/SVneo cells. HSPB8 enforced expression promoted the proliferation, migration and invasion of HTR8/SVneo cells. Moreover, H/R caused an increase in ROS and MDA levels as well as in TUNEL staining and a decrease in aggregated JC-1 fluorescence and SOD activity levels, which were restored following HSPB8 overexpression.Co-IP confirmed the interaction between HSPB8 and c-Myc. Moreover, knockdown of c-Myc expression compromised the effects of HSPB8 upregulation on trophoblast cell dysfunction following induction of H/R. Collectively, the data indicated that HSPB8 could improve mitochondrial oxidative stress by binding to c-Myc to alleviate trophoblast cell dysfunction. The findings may provide new insights into the pathogenesis of PE and highlight the role of HSPB8/c-Myc in the prevention and treatment of PE in the future.

show abstract

Epigenetic Alterations of Repeated Relapses in Patient-matched Childhood Ependymomas

Zhao

Zhang

et al. 2022

Nat Commun

View full text Add to dashboard Cite

Recurrence is frequent in pediatric ependymoma (EPN). Our longitudinal integrated analysis of 30 patient-matched repeated relapses (3.67 ± 1.76 times) over 13 years (5.8 ± 3.8) reveals stable molecular subtypes (RELA and PFA) and convergent DNA methylation reprogramming during serial relapses accompanied by increased orthotopic patient derived xenograft (PDX) (13/27) formation in the late recurrences. A set of differentially methylated CpGs (DMCs) and DNA methylation regions (DMRs) are found to persist in primary and relapse tumors (potential driver DMCs) and are acquired exclusively in the relapses (potential booster DMCs). Integrating with RNAseq reveals differentially expressed genes regulated by potential driver DMRs (CACNA1H, SLC12A7, RARA in RELA and HSPB8, GMPR, ITGB4 in PFA) and potential booster DMRs (PLEKHG1 in RELA and NOTCH, EPHA2, SUFU, FOXJ1 in PFA tumors). DMCs predicators of relapse are also identified in the primary tumors. This study provides a high-resolution epigenetic roadmap of serial EPN relapses and 13 orthotopic PDX models to facilitate biological and preclinical studies.

show abstract

ERK-CREB pathway is involved in HSPB8-mediated glioma cell growth and metastatic properties

Cited by 3 publications

References 36 publications

HSPB8 Facilitates the Oncogenesis and Advancement of Bladder Cancer via Activation of HSP27

HSPB8 Facilitates the Oncogenesis and Advancement of Bladder Cancer via Activation of HSP27

HSPB8 binding to c-Myc alleviates hypoxia/reoxygenation-induced trophoblast cell dysfunction

Epigenetic Alterations of Repeated Relapses in Patient-matched Childhood Ependymomas

Contact Info

Product

Resources

About