Analysis of Fascin-1 in Relation to Gleason Risk Classification and Nuclear ETS-Related Gene Status of Human Prostate Carcinomas: An Immunohistochemical Study of Clinically Annotated Tumours From the Wales Cancer Bank

Jefferies, Matthew; Pope, Christopher S; Kynaston, Howard; Clarke, Alan R.; Martin, Richard M.; Adams, Josephine C.

doi:10.1177/1179299x17710944

Cited by 8 publications

(11 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…TMA demonstrated that the general expression of CEMIP in PCa tissue was substantially higher compared with that in their pericarcinous counterparts. Surprisingly, in the present work, the expression of CEMIP did not seem to be positively statistically correlated with GS, and some reports also observed that the current GS system might occasionally fail to represent-as an indicator-PCa progression and expression of certain oncogenes (31)(32)(33). Of note, CEMIP was indeed more intensively expressed in intermediate-and high-risk patients compared with their low-risk counterparts (data not shown).…”

Section: Discussioncontrasting

confidence: 79%

AMPK/GSK3β/β‐catenin cascade‐triggered overexpression of CEMIP promotes migration and invasion in anoikis‐resistant prostate cancer cells by enhancing metabolic reprogramming

et al. 2018

View full text Add to dashboard Cite

Prostate cancer (PCa) represents one of the most common solid neoplasms, and metastasis is the second leading cause of death in adult males. Anoikis is a programmed cell death that is induced upon cell detachment from the extracellular matrix (ECM), which behaves as a critical protective mechanism for anchorage-independent cell growth and metastasis formation. However, in the absence of ECM attachment, shift of metabolic pattern and tolerance to anoikis facilitate the survival of aggressive cancer cells in the circulatory system as well as their metastasis to distant sites. Few molecular targets in PCa have thus far been reported to prevent anoikis resistance, metabolic reprogramming, and metastasis simultaneously. In the present study, elevated migration, invasion, pyruvate production, lactate generation, ATP level, and impaired detachment-induced apoptosis were found in anoikis-resistant PCa cells, and genome microarray analysis demonstrated that the cell migration-inducing protein (CEMIP) was a potential molecular target for the regulation of the aforementioned malignant behaviors. Additional investigation revealed that the AMPK/glycogen synthase kinase 3β (GSK3β)/β-catenin cascade-triggered CEMIP overexpression in anoikis-resistant PCa cells might be implicated in local progression, metabolic shift, and cellular migration and invasion, whereas knockout of CEMIP by clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 in anoikis-resistant PCa cells reversed the described bioeffects by reducing expressions of matrix metalloproteinase 2 (MMP2), VEGF, pyruvate dehydrogenase kinase isoform 4 (PDK4), and lactate dehydrogenase A. In addition, inhibition of glycolysis by CEMIP-mediated PDK4 down-regulation impaired the migration and invasion of anoikis-resistant PCa cells by attenuating MMP2 and VEGF expressions. Our findings establish that AMPK/GSK3β/β-catenin cascade-triggered CEMIP overexpression might promote migration and invasion in anoikis-resistant PCa cells by enhancing PDK4-associated metabolic reprogramming, which may provide a novel, promising therapeutic target for the treatment of advanced PCa.-Zhang, P., Song, Y., Sun, Y., Li, X., Chen, L., Yang, L., Xing, Y. AMPK/GSK3β/β-catenin cascade-triggered overexpression of CEMIP promotes migration and invasion in anoikis-resistant prostate cancer cells by enhancing metabolic reprogramming.

show abstract

Section: Discussioncontrasting

confidence: 79%

AMPK/GSK3β/β‐catenin cascade‐triggered overexpression of CEMIP promotes migration and invasion in anoikis‐resistant prostate cancer cells by enhancing metabolic reprogramming

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Moreover, it was recently demonstrated that targeted inhibition of FSCN1 could interfere with tumor invasion and metastatic potential [ 58 , 59 ]. The analysis of FSCN1 using immunohistochemistry in prostate carcinoma glands found that only 8% of PCa had more than 10% FSCN1 positivity; FSCN1 expression, however, did not correlate with Gleason score, tumor stage, serum PSA levels or biochemical relapse following surgery [ 43 ]. The analysis of FSCN1 mRNA expression in different PCa datasets showed a quite limited diagnostic role of FSCN1, although increased in metastatic disease [ 60 ].…”

Section: Discussionmentioning

confidence: 99%

“…As reported in recent immunohistochemical analyses of FSCN1 expression in PCa tissue, no correlation was found with Gleason score, tumor stage and PSA values. However, the analysis of FSCN1 using immunohistochemistry in prostate carcinoma glands (several hundred prostate specimens of all Gleason risk scores) found that only 8% of the tumors had more than 10% FSCN1 positivity, and the stromal tumor cells, and stromal levels of FSCN1 were highly increased in high Gleason score [ 43 , 44 ]. We have proposed two objectives to study FSCN1 in PCa.…”

Section: Fscn1 In Prostate Cancermentioning

confidence: 99%

Fascin-1 and Its Role As a Serological Marker in Prostate Cancer: a Prospective case–control Study

et al. 2021

View full text Add to dashboard Cite

Aim: This study aims to investigate any modification of serological FSCN1 in prostate cancer patients compared with patients without neoplasia. Material & methods: Clinical data and blood specimens from patients with and without prostate cancer were obtained. A quantitative sandwich ELISA method was used to determine serological values of FSCN1. Results: Although serum values of FSCN1 were dissimilar in the two cohorts of patients (6.90 vs 7.33 ng/ml), the difference was not statistically significant (p = 0.20). Serum values of FSCN1 stratified for Gleason score groups were not significantly distinguishable (p = 0.65). A negative correlation (rho = -0.331; p = 0.009) was reported between FSCN1 and age. Conclusion: Further studies are required to evaluate a possible diagnostic role of FSCN1 in prostate cancer.

show abstract

“…97,98 Limited and hormone-refractory PCas show a significant upregulation of fascin-1 expression than that in benign prostate tissue. 6,68,69,99 In addition, a follow-up of patients undergoing radical prostatectomy has shown high fascin-1 expression to be related to an increased rate of PSA recurrence. 68 High fascin-1 expression is related to Gleason score and bone metastases, 69 thus confirming its role in PCa progression.…”

Section: Fascin-1 and Pcamentioning

confidence: 99%

“…However, PSA cannot accurately distinguish between inert tumors and aggressive disease. 6 Therefore, new clinical prognostic PCa biomarkers are needed to better differentiate inert prostate tumors from PCa. 7,8 Fascin-1 is a 55 kDa cytoskeleton protein, which binds to F-actin and participates in cell division, cell migration, and intercellular interactions.…”

Section: Introductionmentioning

confidence: 99%

The Role of Fascin-1 in Human Urologic Cancers: A Promising Biomarker or Therapeutic Target?

Zhang,

Bian,

Gao

et al. 2023

Technol Cancer Res Treat

View full text Add to dashboard Cite

Human cancer statistics show that an increased incidence of urologic cancers such as bladder cancer, prostate cancer, and renal cell carcinoma. Due to the lack of early markers and effective therapeutic targets, their prognosis is poor. Fascin-1 is an actin-binding protein, which functions in the formation of cell protrusions by cross-linking with actin filaments. Studies have found that fascin-1 expression is elevated in most human cancers and is related to outcomes such as neoplasm metastasis, reduced survival, and increased aggressiveness. Fascin-1 has been considered as a potential therapeutic target for urologic cancers, but there is no comprehensive review to evaluate these studies. This review aimed to provide an enhanced literature review, outline, and summarize the mechanism of fascin-1 in urologic cancers and discuss the therapeutic potential of fascin-1 and the possibility of its use as a potential marker. We also focused on the correlation between the overexpression of fascin-1 and clinicopathological parameters. Mechanistically, fascin-1 is regulated by several regulators and signaling pathways (such as long noncoding RNA, microRNA, c-Jun N-terminal kinase, and extracellular regulated protein kinases). The overexpression of fascin-1 is related to clinicopathologic parameters such as pathological stage, bone or lymph node metastasis, and reduced disease-free survival. Several fascin-1 inhibitors (G2, NP-G2-044) have been evaluated in vitro and in preclinical models. The study proved the promising potential of fascin-1 as a newly developing biomarker and a potential therapeutic target that needs further investigation. The data also highlight the inadequacy of fascin-1 to serve as a novel biomarker for prostate cancer.

show abstract

Analysis of Fascin-1 in Relation to Gleason Risk Classification and Nuclear ETS-Related Gene Status of Human Prostate Carcinomas: An Immunohistochemical Study of Clinically Annotated Tumours From the Wales Cancer Bank

Cited by 8 publications

References 28 publications

AMPK/GSK3β/β‐catenin cascade‐triggered overexpression of CEMIP promotes migration and invasion in anoikis‐resistant prostate cancer cells by enhancing metabolic reprogramming

AMPK/GSK3β/β‐catenin cascade‐triggered overexpression of CEMIP promotes migration and invasion in anoikis‐resistant prostate cancer cells by enhancing metabolic reprogramming

Fascin-1 and Its Role As a Serological Marker in Prostate Cancer: a Prospective case–control Study

The Role of Fascin-1 in Human Urologic Cancers: A Promising Biomarker or Therapeutic Target?

Contact Info

Product

Resources

About