scholarly journals PNO1 promotes cell proliferation in prostate cancer

2020 ◽  
Author(s):  
Jianpeng Hu ◽  
Feilun Cui ◽  
Zhipeng Xv ◽  
Jian Tan ◽  
Zhengyu Wang
Keyword(s):  
Prostate Cancer ◽  
Rna Splicing ◽  
Biological Processes ◽  
Multiple Cancer ◽  
Translational Initiation ◽  
Normal Tissues ◽  
Potential Biomarker ◽  
First Time ◽  
Catabolic Process

Abstract Prostate cancer (PCa) is one of the most commonly diagnosed cancers. The functions of PNO1 in yeasts were involved in regulating ribosome and proteasome biogenesis. However, its roles in PCa remained largely unclear. The present study for the first time demonstrated PNO1 was up-regulated in PCa samples compared to normal tissues. ShRNA mediated knockdown of PNO1 significantly suppressed PCa proliferation and clone formation, however, induced PCa apoptosis. Microarray analysis and bioinformatics analysis revealed PNO1 was involved in regulating multiple cancer related biological processes, such as regulation of DNA repair, single organismal cell-cell adhesion, translational initiation, RNA splicing, transcription, and positive regulation of mRNA catabolic process. OF note, in vivo results showed PNO1 knockdown remarkably reduced the PCa growth rate. Despite more in-depth research is still required, this study showed PNO1 could serve as a potential biomarker for PCa.

scholarly journals PNO1 promotes cell proliferation in prostate cancer

2020 ◽  
Author(s):  
Jianpeng Hu ◽  
Feilun Cui ◽  
Zhipeng Xv ◽  
Jian Tan ◽  
Zhengyu Wang
Keyword(s):  
Prostate Cancer ◽  
Rna Splicing ◽  
Bioinformatic Analysis ◽  
In Vitro Assays ◽  
Multiple Cancer ◽  
Translational Initiation ◽  
Normal Tissues ◽  
Potential Biomarker

Abstract BackgroundProstate cancer (PCa) is one of the most commonly diagnosed cancers. The functions of PNO1 in yeasts were involved in regulating ribosome and proteasome biogenesis. Human PNO1 is crucial to the site 3 cleavage at the 3ʹ-end of 18S pre-rRNA. Previous studies indicated that PNO1 may be related to the progression of cancers. However, the functions of PNO1 in PCa remained unclear. MethodsThe present study evaluated the expression levels of PNO1 in PCa by using GSE45016, GSE55945 and GSE17951 datasets. Then, in vivo and in vitro assays were conducted to detect the biological functions of PNO1 in PCa. Microarray and bioinformatic analysis were carried out to detect the downstream targets and pathways regulated by PNO1.ResultsThe present study for the first time demonstrated PNO1 was up-regulated in PCa samples compared to normal tissues. ShRNA mediated knockdown of PNO1 significantly suppressed PCa proliferation and clone formation, however, induced PCa apoptosis. Microarray analysis and bioinformatics analysis revealed PNO1 was involved in regulating multiple cancer related biological processes, such as regulation of DNA repair, single organismal cell-cell adhesion, translational initiation, RNA splicing, transcription, and positive regulation of mRNA catabolic process. OF note, in vivo results showed PNO1 knockdown remarkably reduced the PCa growth rate. ConclusionsDespite more in-depth research is still required, this study showed PNO1 could serve as a potential biomarker for PCa.

scholarly journals PNO1 promotes cell proliferation in prostate cancer

2019 ◽  
Author(s):  
Jianpeng Hu ◽  
Feilun Cui ◽  
Zhipeng Xv ◽  
Jian Tan ◽  
Zhengyu Wang
Keyword(s):  
Prostate Cancer ◽  
Rna Splicing ◽  
Bioinformatic Analysis ◽  
In Vitro Assays ◽  
Multiple Cancer ◽  
Translational Initiation ◽  
Normal Tissues ◽  
Potential Biomarker

Abstract Background Prostate cancer (PCa) is one of the most commonly diagnosed cancers. The functions of PNO1 in yeasts were involved in regulating ribosome and proteasome biogenesis. However, its roles in PCa remained largely unclear. Methods The present study evaluated the expression levels of PNO1 in PCa by using GSE45016, GSE55945 and GSE17951 datasets. Then, in vivo and in vitro assays were conducted to detect the biological functions of PNO1 in PCa. BALB/c mice were used for in vivo assay in this study. Microarray and bioinformatic analysis were carried out to detect the downstream targets and pathways regulated by PNO1. Results The present study for the first time demonstrated PNO1 was up-regulated in PCa samples compared to normal tissues. ShRNA mediated knockdown of PNO1 significantly suppressed PCa proliferation and clone formation, however, induced PCa apoptosis. Microarray analysis and bioinformatics analysis revealed PNO1 was involved in regulating multiple cancer related biological processes, such as regulation of DNA repair, single organismal cell-cell adhesion, translational initiation, RNA splicing, transcription, and positive regulation of mRNA catabolic process. OF note, in vivo results showed PNO1 knockdown remarkably reduced the PCa growth rate. Conclusions Despite more in-depth research is still required, this study showed PNO1 could serve as a potential biomarker for PCa.

scholarly journals NaPi- II b as a potential diagnostic and prognostic biomarker in ovarian cancers

2018 ◽  
Author(s):  
Shoufeng Zhao ◽  
Zhipeng Wang
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cell Line ◽  
Normal Tissues ◽  
Diagnosis And Prognosis ◽  
Kaplan Meier ◽  
Potential Biomarker ◽  
Tumor Types ◽  
First Time ◽  
Kaplan Meier Plotter ◽  
Normal Controls

ABSTRACTOvarian cancer (OC) is commonly diagnosed at an advanced stage due to a lack of effective biomarkers and specificity required for accurate clinical diagnosis. The purpose of this study was to estimate the diagnosis and prognosis of the NaPi- II b in ovarian cancer. Herein, by performing data mining using the databases of Oncomine and Cancer Cell Line Encyclopedia (CCLE), we are for the first time to report that the expression level of NaPi- II b transcripts in a variety of tumor types compared with the normal controls. Based on Kaplan-Meier plotter, we investigated the prognostic values of NaPi- II b specifically high expressed in OC patients. The results of the Oncomine analysis showed that relative expression of NaPi- II b was distinctly high in OC tissues vs. normal tissues. CCLE analysis indicated that the expression of NaPi- II b in OC cell lines expressed the highest level in all cancer lines. In overall survival (OR) analysis, NaPi- II b mRNA high expressions were correlated to worse OR in OC patients. These results indicate that NaPi- II b may be a novel potential biomarker for determining the diagnosis and predicting the prognosis of OC.

scholarly journals Preclinical studies using cisplatin/carboplatin to restore the Enzalutamide sensitivity via degrading the androgen receptor splicing variant 7 (ARv7) to further suppress Enzalutamide resistant prostate cancer

2020 ◽  
Vol 11 (11) ◽  
Author(s):  
Fu-Ju Chou ◽  
ChangYi Lin ◽  
Hao Tian ◽  
WanYing Lin ◽  
Bosen You ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Rna Splicing ◽  
Preclinical Studies ◽  
Castration Resistant Prostate Cancer ◽  
Splicing Variant ◽  
Castration Resistant ◽  
Lncrna Malat1 ◽  
Near Future

Abstract The FDA-approved anti-androgen Enzalutamide (Enz) has been used successfully as the last line therapy to extend castration-resistant prostate cancer (CRPC) patients’ survival by an extra 4.8 months. However, CRPC patients eventually develop Enz-resistance that may involve the induction of the androgen receptor (AR) splicing variant ARv7. Here we found that Cisplatin (Cis) or Carboplatin, currently used in chemotherapy/radiation therapy to suppress tumor progression, could restore the Enz sensitivity in multiple Enz-resistant (EnzR) CRPC cells via directly degrading/suppressing the ARv7. Combining Cis or Carboplatin with Enz therapy can also delay the development of Enz-resistance in CRPC C4-2 cells. Mechanism dissection found that Cis or Carboplatin might decrease the ARv7 expression via multiple mechanisms including targeting the lncRNA-Malat1/SF2 RNA splicing complex and increasing ARv7 degradation via altering ubiquitination. Preclinical studies using in vivo mouse model with implanted EnzR1-C4-2 cells also demonstrated that Cis plus Enz therapy resulted in better suppression of EnzR CRPC progression than Enz treatment alone. These results not only unveil the previously unrecognized Cis mechanism to degrade ARv7 via targeting the Malat1/SF2 complex and ubiquitination signals, it may also provide a novel and ready therapy to further suppress the EnzR CRPC progression in the near future.

scholarly journals FAM64A Promotes Prostate Cancer Growth In Vivo and In Vitro

2020 ◽  
Author(s):  
Feilun Cui ◽  
Zhipeng Xu ◽  
Yumei Lv ◽  
Jianpeng Hu
Keyword(s):  
Prostate Cancer ◽  
Molecular Mechanisms ◽  
Human Cancer ◽  
Bioinformatic Analysis ◽  
In Vitro Assays ◽  
Multiple Cancer ◽  
Cell Matrix ◽  
Public Datasets

Abstract Background Prostate cancer (PCa) is the most common type of human cancer in males. However, the mechanisms underlying PCa tumorigenesis remained unclear.Methods The present study evaluated the expression levels of FAM64A in PCa by using 5 public datasets, including GSE8511, GSE45016, GSE55945, GSE38241 and GSE17951. Then, in vivo and in vitro assays were conducted to detect the biological functions of FAM64A in PCa. Microarray and bioinformatic analysis were carried out to detect the downstream targets and pathways regulated by FAM64A.Results In this study, we for first time demonstrate FAM64A as a biomarker for PCa. FAM64A was found to be overexpressed in PCa compared to normal samples. Higher FAM64A expression were found in Gleason score (GS) ≥ 8 PCa compared to GS < 8 PCa samples, in N1 staging compared to N1 staging PCa samples, and T3/4 staging compared to T1 staging PCa. Moreover, higher FAM64A expression was correlated to shorter survival time in PCa. Knockdown of FAM64A significantly suppressed PCa cell proliferation and colony formation, however, induced PCa apoptosis in vivo and in vitro. Bioinformatics analysis combined with microarray analysis revealed FAM64A played crucial roles in regulating multiple cancer related pathways, including cell-matrix adhesion and cAMP signaling pathway. Conclusions These results showed FAM64A could serve as a novel biomarker for PCa and will be helpful to understand the underlying FAM64A -related molecular mechanisms in the progression of PCa.

scholarly journals LncRNA LEF1-AS1 promotes metastasis of prostatic carcinoma via the Wnt/β-catenin pathway

2020 ◽  
Author(s):  
Weiyuan Li ◽  
Ganggang Yang ◽  
Dengke Yang ◽  
Dong Li ◽  
Qian Sun
Keyword(s):  
Cell Proliferation ◽  
Migration And Invasion ◽  
Biological Processes ◽  
Sequencing Technology ◽  
Next Generation Sequencing Technology ◽  
Normal Tissues ◽  
Factor C ◽  
Generation Sequencing

Abstract Background Long noncoding RNAs (lncRNAs), which are important functional regulators in cancer, have emerged as critical molecular regulators in various biological processes. However, the mechanisms by which LEF1-AS1 modulates Androgen-Independent Prostate Cancer (AIPC) development remain largely unknown. Methods The LEF1-AS1 expression level was detected in tumour tissues and adjacent normal tissues of AIPC patients by using next-generation sequencing technology and qRT-PCR. Cell proliferation, migration and invasion were assessed by colony formation, EDU assays and transwell assays, respectively. Xenograft assay was conducted to determine the effect of LEF1-AS1 on cell proliferation in vivo. Results LEF1-AS1 promoted the proliferation, migration, invasion and angiogenic ability of AIPC cells in vitro and in vivo. In this mechanism, LEF1-AS1 recruited the transcription factor C-myb to the promoter region of FZD2, which activated FZD2 transcription. Moreover, LEF1-AS1 functioned as a competing endogenous RNA (ceRNA) acting as a sponge for miR-328, which activated CD44. Conclusion Collectively, these data indicate that LEF1-AS1 is a tumour promoter in the development of AIPC and that it may contribute to the improvement of AIPC diagnosis and therapy.

Radiolabeled GRPR Antagonists for Imaging of Disseminated Prostate Cancer - Influence of Labeling Chemistry on Targeting Properties

2020 ◽  
Vol 27 (41) ◽  
pp. 7090-7111 ◽  
Author(s):  
Bogdan Mitran ◽  
Vladimir Tolmachev ◽  
Anna Orlova
Keyword(s):  
Prostate Cancer ◽  
Molecular Imaging ◽  
Rational Design ◽  
Molecular Design ◽  
Short Review ◽  
Special Focus ◽  
Strong Impact ◽  
Blood Proteins ◽  
Normal Tissues

Background: Radionuclide molecular imaging of Gastrin-Releasing Peptide Receptor (GRPR) expression promises unparalleled opportunities for visualizing subtle prostate tumors, which due to small size, adjacent benign tissue, or a challenging location would otherwise remain undetected by conventional imaging. Achieving high imaging contrast is essential for this purpose and the molecular design of any probe for molecular imaging of prostate cancer should be aimed at obtaining as high tumor-to-organ ratios as possible. Objective: This short review summarizes the key imaging modalities currently used in prostate cancer, with a special focus on radionuclide molecular imaging. Emphasis is laid mainly on the issue of radiometals labeling chemistry and its influence on the targeting properties and biodistribution of radiolabeled GRPR antagonists for imaging of disseminated prostate cancer. Methods: A comprehensive literature search of the PubMed/MEDLINE, and Scopus library databases was conducted to find relevant articles. Results: The combination of radionuclide, chelator and required labeling chemistry was shown to have a significant influence on the stability, binding affinity and internalization rate, off-target interaction with normal tissues and blood proteins, interaction with enzymes, activity uptake and retention in excretory organs and activity uptake in tumors of radiolabeled bombesin antagonistic analogues. Conclusion: Labeling chemistry has a very strong impact on the biodistribution profile of GRPRtargeting peptide based imaging probes and needs to be considered when designing a targeting probe for high contrast molecular imaging. Taking into account the complexity of in vivo interactions, it is not currently possible to accurately predict the optimal labeling approach. Therefore, a detailed in vivo characterization and optimization is essential for the rational design of imaging agents.

The emergence of aqueous chemiluminescence: new promising class of phenoxy 1,2-dioxetane luminophores

2018 ◽  
Vol 54 (17) ◽  
pp. 2073-2085 ◽  
Author(s):  
Samer Gnaim ◽  
Ori Green ◽  
Doron Shabat
Keyword(s):  
Biological Processes ◽  
Single Entity ◽  
First Time

For the first time, science now have a single-entity chemiluminescent luminophore that can serve to prepare effective diagnostic probes to evaluate biological processesin vitroandin vivo.

scholarly journals WNT4 secreted by tumor tissues promotes tumor progression in colorectal cancer by activation of the Wnt/β-catenin signalling pathway

2020 ◽  
Author(s):  
Dongmei Yang ◽  
Qing Li ◽  
Renduo Shang ◽  
Liwen Yao ◽  
Lianlian Wu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Resection ◽  
Signalling Pathway ◽  
Tumor Xenograft ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Normal Tissues ◽  
Potential Biomarker ◽  
Wnt Ligands

Abstract Background: Wingless and Int-related protein (Wnt) ligands are aberrantly expressed in patients with colorectal cancer (CRC). However, the aberrant level of Wnt ligands in serum have not been explored. Here, we aimed to identify the levels of WNT4 in serum and explored its oncogenic role in CRC Methods: The Oncomine database was used to analyze the relationship between WNT4 and the prognosis of CRC. ELISA was performed to measure WNT4 levels in serum and conditioned medium from fresh CRC tissues and adjacent normal tissues. Western blot and immunohistochemistry were carried out to measure the expression of WNT4 in human CRC tissues and adjacent normal tissues. The migration and invasion of CRC cells were determined by trans-well assay, and the effects of WNT4 on CRC invasion and metastasis in vivo were verified by tumor xenograft in nude mice. Cancer-associated fibroblasts (CAFs) and angiogenesis in subcutaneous nodules were detected by immunofluorescence (IF). In addition, the suspended spheres formation and tube formation assay were performed to explore the effects of WNT4 on CAFs and angiogenesis respectively. Results: WNT4 was significantly upregulated in serum of CRC patients, and CRC tissues were identified as an important source of elevated WNT4 levels in CRC patients. Interestingly, elevated levels of WNT4 in serum were downregulated after tumor resection. Furthermore, we found that WNT4 contributed to epithelial-to-mesenchymal transition (EMT) and activated fibroblasts by activating the WNT4/β-catenin pathway in vitro and in vivo. Moreover, angiogenesis was induced via the WNT4/β-catenin/Ang2 pathway. Those effects could be reversed by ICG-001, a β-catenin/TCF inhibitor. Conclusion: Our findings indicated that serum levels of WNT4 may be a potential biomarker for CRC. WNT4 secreted by colorectal cancer tissues promote the progression of CRC by inducing EMT, activate fibroblasts and promote angiogenesis through the canonical Wnt/β-catenin signalling pathway.

Sign in / Sign up

Export Citation Format

Share Document