Mechanism of WASP and WAVE family proteins in the progression of prostate cancer

Mughees, Mohd; Bano, Faizia; Wajid, Saima

doi:10.1007/s00709-021-01608-2

Cited by 7 publications

(4 citation statements)

References 73 publications

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“…The WAS gene belongs to the Wiskott-Aldrich syndrome protein family, and N-WASP exhibits significantly downregulated expression in breast cancer, correlating with poor prognosis [40] . Similarly, WASP acts as a tumor suppressor in T cell lymphoma [41] , while in prostate cancer, it enhances cancer cell invasion and metastasis [42] . WASP and its family can also regulate actin polymerization in breast cancer, promoting cell invasion and migration, thus exhibiting oncogenic functions [43] .…”

Section: P R E P R I N T 10 4 Discussionmentioning

confidence: 99%

RNA-seq-based elucidation of lactylation in breast cancer

He,

Du,

Zhou

et al. 2024

Arch Med Sci

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IntroductionLactylation is the covalent modification of histones using lactate as a small molecule precursor, playing a role in epigenetic regulation. As a novel protein post-translational modification, it has demonstrated significant relevance in the field of cancer diagnosis and therapy. However, the interaction between lactylation and tumor cells in breast cancer has not been extensively investigated.Material and methodsWe acquired breast cancer-related data from the GEO and TCGA databases. Lactylation-related genes were identified from the differentially expressed genes. We utilized COX and LASSO regression to identify genes with significant prognostic value for constructing a prognostic model and assessing its predictive performance. This model was integrated with clinical parameters to create a nomogram. Finally, we conducted immune infiltration analysis, analyzed differences in biological functions, and assessed drug sensitivity.ResultsWe ultimately identified 3 lactylation-related genes significantly associated with prognosis. These genes were used to construct a prognostic model and calculate a risk score. Using the median score, patients were divided into high-risk and low-risk groups. Notably, the low-risk group patients exhibited better prognosis and higher levels of immune infiltration. GO/KEGG enrichment analysis revealed that PGK1, the gene with the highest HR among these genes, is widely involved in immune, metabolic, and proliferative signaling pathways. Its high expression also correlates with increased sensitivity to anti-tumor drugs.ConclusionsWe showcased the potential of lactylation-based molecular clustering and prognostic profiling for predicting survival, immune status, and treatment response in breast cancer patients. Additionally, we envision the utilization of PGK1 as a diagnostic marker and therapeutic target in the cancer.

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Section: P R E P R I N T 10 4 Discussionmentioning

confidence: 99%

RNA-seq-based elucidation of lactylation in breast cancer

He,

Du,

Zhou

et al. 2024

Arch Med Sci

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“…A recent study reported that Fraxetin inhibits proliferation and metastasis of glioma cells by inactivating JAK2/STAT3 signaling [ 6 ]. Tumor invasion and metastasis remain the major causes of deaths in prostate cancer patients [ 22 ]. Here, we showed that Fraxetin had no obvious effect on human normal prostatic epithelial cell RWPE-1, but significantly impaired cell viability of prostate cancer cell DU145 in a concentration-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

Fraxetin down-regulates polo-like kinase 4 (PLK4) to inhibit proliferation, migration and invasion of prostate cancer cells through the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway

Sun

Peng

2022

Bioengineered

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Fraxetin, a natural product isolated from herb Cortex Fraxini , has been demonstrated to exhibit anti-cancer effects on various cancers. The aim of this work is to investigate the anti-tumor effect of Fraxetin in prostate cancer and the potential mechanisms. In this study, the prostatic epithelial cell RWPE-1 and prostate cancer cell DU145 were exposed to Fraxetin (10, 20, 40, and 80 μM) to detect the changes in cell viability using cell counting kit-8 (CCK-8) assay. Fraxetin (10, 20, and 40 μM) was utilized to treat DU145 cell, then the changes in cell proliferation, apoptosis, migration, and invasion were assessed. Western blot assay was employed to detect the expression of proteins that participate in the above cellular processes as well as Polo-like kinase 4 (PLK4), phosphatidylinositol 3-kinase (PI3K). In addition to 40 μM Fraxetin treatment, DU145 cells were overexpressed with PLK4, and then the above experiments were repeated. Results revealed that Fraxetin markedly decreased DU145 cell viability, but didn’t affect the cell viability of RWPE-1. Fraxetin suppressed cell proliferation, migration, invasion, and induced apoptosis of DU145 cells in a concentration-dependent manner. Furthermore, the expression of PLK4 and phosphorylated PI3K and protein kinase B (Akt) were reduced upon Fraxetin treatment. Finally, PLK4 overexpression significantly reversed all the effects of Fraxetin on DU145 cells. Collectively, Fraxetin acted as a cancer suppressor in prostate cancer through inhibiting PLK4 expression thereby inactivating PI3K/Akt signaling.

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“…WAVE consists of three isoforms: WAVE1, WAVE2, and WAVE3. The activation of Arp2/3 by the WAVE family promotes actin polymerize, which is crucial for membrane protrusion events such as the formation of pseudopodia [ 110 ]. Research on WAVE and autophagy was limited.…”

Section: Npfs and Autophagymentioning

confidence: 99%

NPFs-mediated actin cytoskeleton: a new viewpoint on autophagy regulation

Dong,

Quan

2024

Cell Commun Signal

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Macroautophagy/autophagy is a lysosome-dependent catabolic process induced by various cellular stress conditions, maintaining the homeostasis of cells, tissues and organs. Autophagy is a series of membrane-related events involving multiple autophagy-related (ATG) proteins. Most studies to date have focused on various signaling pathways affecting ATG proteins to control autophagy. However, mounting evidence reveals that the actin cytoskeleton acts on autophagy-associated membranes to regulate different events of autophagy. The actin cytoskeleton assists in vesicle formation and provides the mechanical forces for cellular activities that involve membrane deformation. Although the interaction between the actin cytoskeleton and membrane makes the role of actin in autophagy recognized, how the actin cytoskeleton is recruited and assembles on membranes during autophagy needs to be detailed. Nucleation-promoting factors (NPFs) activate the Arp2/3 complex to produce actin cytoskeleton. In this review, we summarize the important roles of the actin cytoskeleton in autophagy regulation and focus on the effect of NPFs on actin cytoskeleton assembly during autophagy, providing new insights into the occurrence and regulatory mechanisms of autophagy.

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Mechanism of WASP and WAVE family proteins in the progression of prostate cancer

Cited by 7 publications

References 73 publications

RNA-seq-based elucidation of lactylation in breast cancer

RNA-seq-based elucidation of lactylation in breast cancer

Fraxetin down-regulates polo-like kinase 4 (PLK4) to inhibit proliferation, migration and invasion of prostate cancer cells through the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway

NPFs-mediated actin cytoskeleton: a new viewpoint on autophagy regulation

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