// Yin Peng 1,4,* , Xiaojing Zhang 1,3,* , Xianling Feng 1 , Xinmim Fan 1 and Zhe Jin 1,2,3 1 Department of Pathology, The Shenzhen University School of Medicine, Shenzhen, Guangdong, People’s Republic of China 2 Shenzhen Key Laboratory of Micromolecule Innovatal Drugs, The Shenzhen University School of Medicine, Shenzhen, Guangdong, People’s Republic of China 3 Shenzhen Key Laboratory of Translational Medicine in Tumors, The Shenzhen University School of Medicine, Shenzhen, Guangdong, People’s Republic of China 4 Department of Pathology, Wuhan University School of Basic Medical Sciences, Hubei, People’s Republic of China * These authors have contributed equally to this work Correspondence to: Zhe Jin, email: // Keywords : microRNA; Wnt/β-catenin signaling pathway; cancer Received : January 15, 2016 Accepted : October 21, 2016 Published : October 26, 2016 Abstract Mounting evidence has indicated microRNA (miR) dysregulation and the Wnt/β-catenin signaling pathway jointly drive carcinogenesis, cancer metastasis, and drug-resistance The current review will focus on the role of the crosstalk between miRs and the Wnt/β-catenin signaling pathway in cancer development MiRs were found to activate or inhibit the canonical Wnt pathway at various steps On the other hand, Wnt activation increases expression of miR by directly binding to its promoter and activating transcription Moreover, there are mutual feedback loops between some miRs and the Wnt/β-catenin signaling pathway Clinical trials of miR-based therapeutic agents are investigated for solid and hematological tumors, however, challenges concerning low bioavailability and possible side effects must be overcome before the final clinical application This review will describe current understanding of miR crosstalk with the Wnt/β-catenin signaling cascade Better understanding of the regulatory network will provide insight into miR-based therapeutic development

/pdf/the-crosstalk-between-micrornas-and-the-wnt-b-catenin-36qr1422c3.pdf

The crosstalk between microRNAs and the Wnt/β-catenin signaling pathway in cancer

MicroRNA biogenesis, gene silencing mechanisms and role in breast, ovarian and prostate cancer.

Prostate cancer (PCa) is the most prevalent urological cancer that affects aging men in South Africa, and mechanisms underlying prostate tumorigenesis remain elusive. Research advancements in the field of PCa and epigenetics have allowed for the identification of specific alterations that occur beyond genetics but are still critically important in the pathogenesis of tumorigenesis. Anomalous epigenetic changes associated with PCa include histone modifications, DNA methylation, and noncoding miRNA. These mechanisms regulate and silence hundreds of target genes including some which are key components of cellular signalling pathways that, when perturbed, promote tumorigenesis. Elucidation of mechanisms underlying epigenetic alterations and the manner in which these mechanisms interact in regulating gene transcription in PCa are an unmet necessity that may lead to novel chemotherapeutic approaches. This will, therefore, aid in developing combination therapies that will target multiple epigenetic pathways, which can be used in conjunction with the current conventional PCa treatment.

https://downloads.hindawi.com/journals/pc/2016/5653862.pdf

Prostate Cancer: Epigenetic Alterations, Risk Factors, and Therapy.

Objectives Increasing evidence has suggested that microRNA (miRNA) dysregulation may contribute to tumor progression and metastasis. However, the role of miR-613 in bladder cancer was still unknown. Materials and methods qRT-PCR and Western blotting were performed to detect the expression of miR-613 and its direct target gene. CCK-8 analysis, qRT-PCR and cell invasion were performed to measure the cell function. Results We demonstrated that the expression of miR-613 was downregulated in the bladder cancer cell lines. In addition, miR-613 expression was downregulated in the bladder cancer tissues compared to the adjacent normal tissues. Out of 35 bladder cancer tissues, miR-613 was downregulated in 27 cases compared to the adjacent tissues. Ectopic expression of miR-613 suppressed the bladder cancer cell proliferation and invasion. Moreover, miR-613 overexpression enhanced the expression of epithelial biomarker, Ecadherin, and suppressed the expression of mesenchymal biomarker, Vimentin, Snail and N-cadherin. Furthermore, we identified the Sphingosine kinase 1 (SphK1) as the direct target gene of miR-613 in the bladder cancer cell. Restoration of Sphk1 partially rescued miR-613-inhibited bladder cancer cell proliferation, invasion and EMT. Conclusions These data suggested that miR-613 acted a tumor suppressive role in bladder cancer through targeting SphK1 in bladder.

miR-613 inhibits bladder cancer proliferation and migration through targeting SphK1.

// Martin F. Orth 1 , Alex Cazes 1 , Elke Butt 1 and Thomas G. P. Grunewald 2 1 Institute for Clinical Biochemistry and Pathobiochemistry, University Clinic of Wurzburg, Grombuhlstrasse, Wurzburg, Germany 2 Laboratory for Pediatric Sarcoma Biology, Institute of Pathology of the LMU Munich, Thalkirchner Strasse, Munich, Germany Correspondence: Thomas Grunewald, email: // Keywords : LASP1, cancer, biomarker, microRNA, nucleo-cytoplasmic Received : December 16, 2014 Accepted : December 28, 2014 Published : December 31, 2014 Abstract The gene encoding the LIM and SH3 domain protein (LASP1) was cloned two decades ago from a cDNA library of breast cancer metastases. As the first protein of a class comprising one N-terminal LIM and one C-terminal SH3 domain, LASP1 founded a new LIM-protein subfamily of the nebulin group. Since its discovery LASP1 proved to be an extremely versatile protein because of its exceptional structure allowing interaction with various binding partners, its ubiquitous expression in normal tissues, albeit with distinct expression patterns, and its ability to transmit signals from the cytoplasm into the nucleus. As a result, LASP1 plays key roles in cell structure, physiological processes, and cell signaling. Furthermore, LASP1 overexpression contributes to cancer aggressiveness hinting to a potential value of LASP1 as a cancer biomarker. In this review we summarize published data on structure, regulation, function, and expression pattern of LASP1, with a focus on its role in human cancer and as a biomarker protein. In addition, we provide a comprehensive transcriptome analysis of published microarrays (n=2,780) that illustrates the expression profile of LASP1 in normal tissues and its overexpression in a broad range of human cancer entities.

/pdf/an-update-on-the-lim-and-sh3-domain-protein-1-lasp1-a-4i236f1le7.pdf

An update on the LIM and SH3 domain protein 1 (LASP1): a versatile structural, signaling, and biomarker protein

MicroRNA-613 represses prostate cancer cell proliferation and invasion through targeting Frizzled7.

Background 
LIM and SH3 protein 1 (LASP-1) is a specific focal adhesion protein that is known to be involved in numerous biological and pathological processes. LASP-1 overexpression has been described in several types of cancers, but its expression and role in clear cell renal cell cancer (ccRCC) remains unknown.


Methods 
Using immunohistochemistry, we analyzed LASP-1 protein expression in 216 clinicopathologically characterized ccRCC cases. We also examined LASP-1 expression in 20 paired ccRCC tissues and in 2 cell lines by real-time PCR and Western blot. Using RNA interference, we investigated the effects of LASP-1 depletion on tumor cell behavior in vitro. Statistical analyses were used to determine the associations between LASP-1 levels, tumor features and patient outcomes.


Results 
LASP-1 overexpression was observed in ccRCC tissues (P<0.0001) compared to adjuvant nontumorous tissues, and its expression levels were closely correlated with overall survival and recurrence-free survival (P = 0.044 and 0.006, respectively) in patients with ccRCC. RNA interference-mediated silencing of the LASP-1 gene in 786–0 ccRCC cells significantly inhibited cell migration.


Conclusions 
The results of the present study indicate that LASP-1 may serve as a prognostic biomarker for ccRCC patients and may be a promising target for the treatment of ccRCC.

LIM and SH3 domain protein 1 (LASP-1) overexpression was associated with aggressive phenotype and poor prognosis in clear cell renal cell cancer.

In the last few decades, microRNAs (miRNAs) are possible to effectively control and treat cancer. However, the function of miR-613 in renal cell carcinoma (RCC) is not very clear up to now. Here, the direction of this research was to investigate the influence of miR-613 for the proliferation, invasion and migration of RCC, and the underlying molecular mechanism. First, the mRNA and protein expression levels of miR-613 were determined in RCC tissues and cancer cells (786-O and ACHN). Using bioinformatics and literature review, anexelekto (AXL), as the target of miR-613 in renal cell carcinoma, was screened. Phenotype experiment and mechanism experiment illustrated the targeting relationship between miR-613 and AXL in cancer cells. Furthermore, a rescue assay with AXL overexpression was performed to make a profound study whether miR-613 disturbs RCC proliferation, invasion, and migration through direct regulation of AXL. Finally, through experiment in vivo, we observe the influence of miR-613 overexpression for tumor. These results were as follows. The present findings proved, in RCC, that the production of miR-613 was at a low level. Except for this point, this current research confirmed, in RCC cells, that the upregulation of miR-613 can control proliferation, metastasis, and invasion by reducing AXL levels and controlling the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway.

miR-613 suppresses renal cell carcinoma proliferation, invasion and migration by regulating the AXL/AKT pathway

Poly (ADP-ribose) polymerase (PARP) inhibitors (PARPi), have gained approval for treating patients with castration-resistant prostate cancer (CRPC). Maternally expressed gene 3 (MEG3), a long non-coding RNA (lncRNA), plays a role in inhibiting tumorigenesis through regulating DNA repair genes. This study aimed to investigate the association between the anti-prostate cancer (PCa) effect of niraparib, a representative PARPi, and MEG3 expression, as well as explore the downstream pathway involved.The levels of MEG3, miR-181-5p, GATA binding protein 6 (GATA6) in clinical samples from PCa patients were accessed by RT-qPCR. PC3 cells were treated with niraparib, and the expression of MEG3, miR-181-5p, GATA6 expression was tested. PC3 cell proliferation, migration, and invasion were tested by CCK-8, wound healing, and Transwell assays, respectively. The bindings between miR-181-5p and MEG3/GATA6 were determined by dual-luciferase reporter gene assay. Furthermore, rescue experiments were conducted to investigate the underlying mechanism of MEG3/miR-181-5p/GATA6 axis in PCa progression. Additionally, mice were injected with PC3 cells transfected with sh-MEG3 and treated with niraparib, and the xenograft tumor growth was observed.MEG3 and GATA6 were upregulated and miR-181-5p was downregulated in PCa patients. Niraparib treatment substantially upregulated MEG3 and GATA6, and downregulated miR-181-5p expression in PCa cells. Niraparib effectively restrained PC3 cell proliferation, migration, and invasion. MiR-181-5p targeted to MEG3, and the inhibitory effects of MEG3 overexpression on PC3 cell proliferation and metastasis were abrogated by miR-181-5p overexpression. Moreover, GATA6 was identified as a target of miR-181-5p, and GATA6 silencing abolished the inhibitory effects of miR-181-5p inhibition on PC3 cell proliferation and metastasis. Besides, MEG3 silencing could abrogate niraparib-mediated tumor growth inhibition in mice.Niraparib restrains prostate cancer cell proliferation and metastasis and tumor growth in mice by regulating the lncRNA MEG3/miR-181-5p/GATA6 pathway. 

Niraparib restrains prostate cancer cell proliferation and metastasis and tumor growth in mice by regulating the lncRNA MEG3/miR-181-5p/GATA6 pathway

OBJECTIVE
This study aims to establish and validate a predictive model for bone metastasis in prostate cancer patients based on multiple immune inflammatory parameters.


METHODS
In this retrospective study, 162 prostate cancer patients who met the inclusion criteria were selected by Urology Surgery, Shaanxi Provincial People's Hospital. Based on the medical record number of patients and the random number table method, 40 patients were randomly included in a validation group, and the rest were in a modeling group. The patients in the modeling group were divided into a metastatic group (n=67) and a non-metastatic group (n=55) according to the whole-body bone imaging results.


RESULTS
The predictive model was established based on the results of Logistics regression analysis: Logit (P) = -5.341 + 0.930*total Gleason score + 1.426*total prostate specific antigen + 0.836*neutrophil-lymphocyte ratio + 0.896*platelet lymphocyte ratio + 0.641*lymphocyte/monocyte ratio + 0.750*albumin/globulin ratio. ROC analysis showed that the areas under the curve of the predictive model for bone metastasis in the modeling and validation groups were 0.896 and 0.870, respectively. Hosmer-Lemeshow test showed that P=0.253, indicating a high degree of the fitting. External verification results showed that the C-index for predicting prostate cancer bone metastasis in the predictive model established in this study was 0.760 (95% CI: 0.670-0.851).


CONCLUSION
The bone metastasis predictive model based on the multiple immune inflammatory parameters (neutrophil-lymphocyte ratio, platelet lymphocyte ratio, lymphocyte/monocyte ratio and albumin/globulin ratio) in prostate cancer patients can reasonably predict the occurrence of bone metastasis and is well worth clinical application.

Establishment and validation of a predictive model for bone metastasis in prostate cancer patients based on multiple immune inflammatory parameters.

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