Inflammation and NF-κB Signaling in Prostate Cancer: Mechanisms and Clinical Implications

Staal, Jens; Beyaert, Rudi

doi:10.3390/cells7090122

Cited by 64 publications

(59 citation statements)

References 190 publications

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“…This process triggers NF-κB signaling activation (23). Previous studies have demonstrated that NF-κB pathways are important for PCa cell growth, invasion, and the development of treatment resistance [14,24]. Moreover, numerous researchers have demonstrated that the HMGB1/NF-κB signaling pathway plays an important role in in ammation and several solid cancers [25][26][27].…”

Section: Discussionmentioning

confidence: 99%

“…The role of the NF-κB signaling pathway has been well established. NF-κB signaling plays a pivotal role in cancer cell proliferation, progression, and metastasis in PCa cells [14]. An association between HMGB1 and the NF-κB signaling pathway has been widely evaluated in several solid cancers and in ammation, but rarely in PCa [15].…”

Section: Suppression Of Hmgb1 Expression Inhibits the Nf-κb Pathway Imentioning

confidence: 99%

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HMGB1/TNFR1/NF-κB Axis in Prostate cancer: Clinical and Biological Correlation

Jung

Kim

et al. 2020

Preprint

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Abstract Background High mobility group box 1 protein (HMGB1) is known to be associated with progression, metastasis, and poor prognosis of several solid tumors, but the role of HMGB1 in prostate cancer (PCa) has remained unclear. Thus, we aimed to evaluate the clinical significance and the biological mechanism of HMGB1 in PCa. Methods To explore the clinical significance of HMGB1 in PCa, we performed IHC analyses using paraffin-embedded tissues from patients with low-, intermediate-, and high-risk PCa and from patients with BPH. Biological role and mechanism of HMGB1 in PCa were analyzed using cell viability, cell cycle, Western blot analyses, proteome profiler antibody array, and co-immunoprecipitation assay. Results We showed that increases in the expression of HMGB1 correlated with an increased risk of aggressive PCa, and high expression of HMGB1 was associated with poor biochemical recurrence-free survival in a Korean cohort. The inhibition of HMGB1 expression significantly reduced cell proliferation and increased cell cycle arrest in the sub-G0 phase. It also inhibited the invasive capacity of PCa cells in vitro. The above processes were mediated through the binding with TNFR1, leading to tumor progression by activation of the NF-κB signaling pathway. Conclusions We identified that HMGB1 is a critical factor in the development and progression of PCa by regulating the HMGB1/TNFR1/NF-κB signaling pathway. HMGB1/TNFR1 could serve as a novel therapeutic target for improving PCa therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Suppression Of Hmgb1 Expression Inhibits the Nf-κb Pathway Imentioning

confidence: 99%

HMGB1/TNFR1/NF-κB Axis in Prostate cancer: Clinical and Biological Correlation

Jung

Kim

et al. 2020

Preprint

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“…Finally, pathway enrichment analysis was performed using common detected genes of the four kits (Supplementary Table S1) of the prostate cancer plasma individual. The most significant p-values (between 1.7 × 10 −16 to 4.9 × 10 −8 ) were obtained with the Spliceosome, Ubiquitin mediated proteolysis, NF-kappa B signalling and Ribosome pathways, all of which are known to be involved in prostate cancer [38][39][40][41] .…”

Section: Detection Of Targeted Variants From the Reference Control Samentioning

confidence: 99%

Comparison of commercially available whole-genome sequencing kits for variant detection in circulating cell-free DNA

Mauger

Horgues

Pierre-Jean

et al. 2020

Sci Rep

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circulating cell-free DnA (ccfDnA) has great potential for non-invasive diagnosis, prognosis and monitoring treatment of disease. However, a sensitive and specific whole-genome sequencing (WGS) method is required to identify novel genetic variations (i.e., SnVs, cnVs and inDeLS) on ccfDnA that can be used as clinical biomarkers. In this article, five WGS methods were compared: ThruPLEX Plasma-seq, QIAseq cfDNA All-in-One, NEXTFLEX Cell Free DNA-seq, Accel-NGS 2 S PCR FREE DNA and Accel-NGS 2 S PLUS DNA. The Accel PCR-free kit did not produce enough material for sequencing. The other kits had significant common number of SNVs, INDELs and CNVs and showed similar results for SnVs and cnVs. the detection of variants and genomic signatures depends more upon the type of plasma sample rather than the WGS method used. Accel detected several variants not observed by the other kits. ThruPLEX seemed to identify more low-abundant SNVs and SNV signatures were similar to signatures observed with the QIAseq kit. Accel and NEXTFLEX had similar CNV and SNV signatures. These results demonstrate the importance of establishing a standardized workflow for identifying noninvasive candidate biomarkers. Moreover, the combination of variants discovered in ccfDNA using WGS has the potential to identify enrichment pathways, while the analysis of signatures could identify new subgroups of patients. The analysis of circulating cell-free DNA (ccfDNA) from plasma bears great promise for diagnosis, prognosis and monitoring the treatment of cancer 1. In the context of precision medicine, the identification of novel non-invasive biomarkers is crucial but the analysis of ccfDNA is still a challenge. Indeed, ccfDNA is low concentrated, highly fragmented and the abundance depends on the type and the stage of cancer and the pre-analytical steps 2,3-5. Due to its properties, a complete workflow for sample preparation, library preparation, sequencing and data analysis should be performed to ensure standardization of sample analysis especially in the case of clinical cohorts 4,6,7. Pre-analytical steps including sample collection, storage, processing and extraction were compared to maximize the yield and size of ccfDNA 3,5,8-12. Furthermore, size analysis and quantification methods were used to evaluate the extracted ccfDNA. Sensitive approaches such as quantitative PCR, digital PCR, mass spectrometry and next generation sequencing (NGS) are commonly applied to analyze extracted ccfDNA 2. With the improvement of NGS analysis, whole-genome sequencing (WGS) is a great approach to identify all types of genomic alteration including single nucleotide variant (SNV), insertion and deletion (INDEL), copy number variation (CNV) and structural variant (SV) for the identification of candidate biomarkers in cancer 13. In particular, several specific and sensitive low-coverage sequencing approaches have been applied for the analysis of CNVs from cancer plasma samples 14-20. In addition, recent WGS studies allowed the analysis of nucleosome

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“…These molecules can dimerise to form all possible combinations of homo and heterodimers. Among the NF-κB family subunits, NF-κB2 (p52/p100), RelA, RelB, and c-Rel have described are implicated in PCa [165]. Other studies reported that RelA (NF-κB/p65) is constitutively activated in human PCa and transgenic TRAMP [166].…”

Section: Nuclear Factor Kappa-b (Nf-κb)mentioning

confidence: 99%

Mechanism of Anti-Cancer Activity of Curcumin on Androgen-Dependent and Androgen-Independent Prostate Cancer

et al. 2020

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Prostate cancer (PCa) is a heterogeneous disease and ranked as the second leading cause of cancer-related deaths in males worldwide. The global burden of PCa keeps rising regardless of the emerging cutting-edge technologies for treatment and drug designation. There are a number of treatment options which are effectively treating localised and androgen-dependent PCa (ADPC) through hormonal and surgery treatments. However, over time, these cancerous cells progress to androgen-independent PCa (AIPC) which continuously grow despite hormone depletion. At this particular stage, androgen depletion therapy (ADT) is no longer effective as these cancerous cells are rendered hormone-insensitive and capable of growing in the absence of androgen. AIPC is a lethal type of disease which leads to poor prognosis and is a major contributor to PCa death rates. A natural product-derived compound, curcumin has been identified as a pleiotropic compound which capable of influencing and modulating a diverse range of molecular targets and signalling pathways in order to exhibit its medicinal properties. Due to such multi-targeted behaviour, its benefits are paramount in combating a wide range of diseases including inflammation and cancer disease. Curcumin exhibits anti-cancer properties by suppressing cancer cells growth and survival, inflammation, invasion, cell proliferation as well as possesses the ability to induce apoptosis in malignant cells. In this review, we investigate the mechanism of curcumin by modulating multiple signalling pathways such as androgen receptor (AR) signalling, activating protein-1 (AP-1), phosphatidylinositol 3-kinases/the serine/threonine kinase (PI3K/Akt/mTOR), wingless (Wnt)/ß-catenin signalling, and molecular targets including nuclear factor kappa-B (NF-κB), B-cell lymphoma 2 (Bcl-2) and cyclin D1 which are implicated in the development and progression of both types of PCa, ADPC and AIPC. In addition, the role of microRNAs and clinical trials on the anti-cancer effects of curcumin in PCa patients were also reviewed.

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Inflammation and NF-κB Signaling in Prostate Cancer: Mechanisms and Clinical Implications

Cited by 64 publications

References 190 publications

HMGB1/TNFR1/NF-κB Axis in Prostate cancer: Clinical and Biological Correlation

HMGB1/TNFR1/NF-κB Axis in Prostate cancer: Clinical and Biological Correlation

Comparison of commercially available whole-genome sequencing kits for variant detection in circulating cell-free DNA

Mechanism of Anti-Cancer Activity of Curcumin on Androgen-Dependent and Androgen-Independent Prostate Cancer

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