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Si-pgc-1 α LNP prevents bladder cancer metastasis by inhibiting mitochondrial biogenesis and energy metabolism in cancer cells

ABSTRACT: This study aims to explore the effect of PGC-1 α siRNA delivered by liposomal nanoparticles on cancer cells through transcriptome, proteome and metabolome technologies, so as to reveal its regulatory effect on cancer cell reprogramming and energy metabolism, so as to provide clues for the molecular mechanism of the treatment of metastatic bladder cancer.

ORGANISM(S): Mus Musculus

SUBMITTER: Hao Zhang

PROVIDER: PXD062155 | iProX | Sat Mar 22 00:00:00 GMT 2025

REPOSITORIES: iProX

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Nanoparticle-mediated targeting of PGC-1α reveals critical metabolic pathways in bladder cancer metastasis.

Liu Zhenghua Z Xin Peng P Wu Weiwei W Jin Mingyue M Du Yang Y Jiang Yuanjun Y Liu Tao T Zhang Hao H

Communications biology 20250523 1

Metastatic bladder cancer is characterized by its aggressive behavior and complex molecular mechanisms that remain largely undefined. This study explores the therapeutic potential of targeting peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) using liposomal nanoparticles to deliver PGC-1α siRNA to bladder cancer cells. We employed comprehensive transcriptomic, proteomic, and metabolomic analyses to investigate the impact of PGC-1α silencing. Our in vitro results demo ...[more]

PMID: 40404885

Similar Datasets

Targeting PGC-1α in Bladder Cancer: Unraveling Energy Metabolism Reprogramming for Therapeutic Intervention

Project description:Metastatic bladder cancer is a malignant tumor with high metastatic potential. The etiology and molecular mechanism are still not fully understood. This study aimed to investigate the effect of PGC-1 α siRNA delivered by liposomal nanoparticles on bladder cancer cells, in order to reveal its mechanism in tumor cell reprogramming and energy metabolism regulation. Through transcriptome, proteome and metabolomics, we found that PGC-1 α was significantly upregulated in bladder cancer metastasis, and constructed a nanoparticle delivery system for efficient delivery of PGC-1 α siRNA. In vitro results showed that PGC-1 α silencing inhibited mitochondrial biogenesis and energy metabolism in bladder cancer cells, and interfered with the extranuclear transport of mRNA. Metabolomic analysis further confirmed the changes in cellular metabolism, especially the effects of glycolysis and tricarboxylic acid cycle pathways. The in vivo model further verified that si-pgc-1 α LNP could significantly reduce the number of lung metastases of metastatic bladder cancer, showing anti metastatic potential. These findings reveal the important role of PGC-1 α in the regulation of energy metabolism and metastasis of bladder cancer cells, and provide a new strategic direction for the treatment of metastatic bladder cancer.

2025-03-22 | PXD062153 |

Pyruvate induces mitochondrial biogenesis by a PGC-1alpha independent mechanism

Project description:The present study examines the impact of altering energy provision on mitochondrial biogenesis in muscle cells. C2C12 myoblasts were chronically treated with supraphysiological levels of sodium pyruvate for 72 hr. Treated cells exhibited increased mitochondrial protein expression, basal respiratory rate and maximal oxidative capacity. The increase in mitochondrial biogenesis was independent of increases in PGC-1alpha and PGC-1alpha mRNA expression. To further assess whether PGC-1alpha expression was necessary for pyruvate action, cells were infected with adenovirus containing shRNA for PGC-1alpha prior to treatment with pyruvate. Despite a 70% reduction in PGC-1alpha mRNA the effect of pyruvate was preserved. Furthermore, pyruvate induced mitochondrial biogenesis in primary myoblasts from PGC-1alpha null mice. These data suggest that regulation of mitochondrial biogenesis by pyruvate in myoblasts is independent of PGC-1alpha, suggesting the existence of a novel energy-sensing pathway regulating oxidative capacity. Keywords: basal state versus treatment at one time point

2006-08-12 | GSE5497 | GEO

Expression data from a human lung metastatic cell line treated with siPGC1alpha or siControl

Project description:To understand global expression changes in a knockdown of PGC1alpha (siPGC1alpha) vs control (siControl) in a lung metastatic cell line (4175) Metabolic adaptations play a key role in fuelling tumour growth. However, less is known regarding the metabolic changes that promote cancer progression to metastatic disease. Herein, we reveal that PGC-1a expression and activity are differentially regulated depending on breast cancer metastatic sites. Breast cancer cells that preferentially metastasize to lung display striking upregulation of PGC-1a expression. PGC-1a promotes breast cancer cell migration and invasion in vitro and augments lung metastasis in vivo. MDA-MB-231 lung variant (4175) cells were treated with a short interfering RNA (siRNA) for human PGC-1a (PPARG1A) or control siRNA for 48hrs 24 hours post-plating cells.

2017-09-06 | GSE99554 | GEO

Genome-wide transcriptome analysis of PAK4 inhibition/knockdown in human bladder cancer cell line VMCUB1

Project description:Using multi-omic analyses, we identified PAK4 (P21 (RAC1) Activated Kinase 4) amplification and overexpression of Kinase PAK4 in a subset of bladder cancers. We confirmed the role of PAK4 in bladder cancer cell proliferation and invasion by in vitro experiments. Furthermore, our studies showed that PAK4 inhibitor is effective in curtailing bladder cancer cell growth. In order to understand the effect of PAK4 inhibition and knockdown on bladder cancer transcriptome, we performed RNA-sequencing of PAK4 siRNA transfected and PAK4 inhibitor (PF-3758309) treated bladder cancer cells (VM-CUB1). Analyses led to identification of direct targets of PAK4 in bladder cancer and associated pathways.

2020-04-20 | GSE130455 | GEO

Androgen deprivation therapy prevents bladder cancer recurrence.

Project description:Although accumulating preclinical evidence indicates the involvement of androgen receptor signals in bladder cancer (BC) development, its clinical relevance remains unclear. We aimed to evaluate the predictive role of androgen deprivation therapy (ADT) in BC recurrence in prostate cancer (PC) patients. We retrospectively reviewed 20,328 patients with PC diagnosed during 1991-2013 and identified 239 (1.2%) men having primary BC. After excluding ineligible patients, 162 patients made up a final cohort. With a median follow-up of 62 months, 38 (50%) of 76 control patients without ADT experienced BC recurrence, while 19 (22%) of 86 did in ADT group. Thus, patients having received ADT for their PC showed a significantly lower risk of BC recurrence (5-year actuarial recurrence-free survival: 76% v 40%; P < 0.001) and also had a significantly smaller number of recurrence episodes (5-year cumulative recurrence: 0.44 v 1.54; P < 0.001), compared to the control patients. A multivariable analysis revealed ADT as an independent prognosticator (hazard ratio, 0.29; 95% confidence interval, 0.17-0.49) for BC recurrence. This is the first clinical study showing that ADT significantly reduces the risk of BC recurrence.

| S-EPMC4350350 | biostudies-literature

Farnesol prevents aging-related muscle weakness in mice through enhanced farnesylation of Parkin-interacting substrate

Project description:Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is a master regulator of mitochondrial biogenesis. Reduced PGC-1α abundance is linked to skeletal muscle weakness in aging or pathological conditions; thus, elevating PGC-1α abundance might be a promising strategy to treat muscle aging. Here we performed high-throughput screening and identified a natural compound, farnesol, as a potent inducer of PGC-1α. Farnesol administration enhanced oxidative muscle capacity and muscle strength, leading to metabolic rejuvenation in aged mice. Moreover, farensol treatment accelerated the recovery of muscle injury associated with enhanced muscle stem cell function. The protein expression of Parkin-interacting substrate (PARIS/Zfp746), a transcriptional repressor of PGC-1α, was elevated in aged muscles, likely contributing to PGC-1α reduction. The beneficial effect of farnesol on aged muscle was mediated through enhanced PARIS farnesylation, thereby relieving PARIS-mediated PGC-1α suppression. Furthermore, short-term exercise increased PARIS farnesylation in the muscles of young and aged mice, whereas long-term exercise decreased PARIS farnesylation in the muscles of aged mice, leading to the elevation of PGC-1α. Collectively, the current study demonstrated that the PARIS-PGC-1α pathway is linked to muscle aging and that farnesol treatment can restore muscle functionality in aged mice through increased farnesylation of PARIS.

2023-08-12 | GSE240281 | GEO

Regulation of miRNA biogenesis by MCPIP1

Project description:Effect of MCPIP1 knockdown on miRNA expression profile. HepG2 cells were transfected with control siRNA or siRNA against MCPIP1, and subjected to miRNA microarray analysis.

2011-11-05 | E-GEOD-31091 | biostudies-arrayexpress

Extracellular vesicle based therapeutic targeting of b-catenin to modulate anti-cancer immune responses in Hepatocellular Cancer

Project description:Combination therapy with anti PD-1 and β -catenin siRNA delivered using biological nanoparticles provide an effective strategy for the treatment of Hepatocellular carcinoma.

2018-10-02 | GSE120714 | GEO

Expression data from bladder cancer cells T24 - treated with G9a siRNA or negative control siRNA

Project description:Target genes regulated by G9a in bladder cancer cells T24 In this dataset, we include the expression data obtained from bladder cancer cells T24 treated with G9a siRNA or negative control siRNA. These data are used to obtain genes that are differentially expressed in response to G9a konckdown.

2019-05-29 | GSE115341 | GEO

FTO regulated genes in bladder cancer cell

Project description:To investigate the global genes regulated by FTO high-throughput mRNA sequencing (RNA-Seq) was performed to compare the expression profile between 253Jcells transfected with control siRNA or FTO siRNA.

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