Expression of Two Testis-specific Genes, SPATA19 and LEMD1, in Prostate Cancer

Ghafouri‐Fard, Soudeh; Ashtiani, Zahra Ousati; Golian, Bareto Sabah; Hasheminasab, Sayed-Mohammad; Modarressi, Mohammad Hossein

doi:10.1016/j.arcmed.2010.04.003

Cited by 53 publications

(43 citation statements)

References 20 publications

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“…MiR-135b is located on the negative strand of 1q32.1 and overlaps with exon 1 of the LEM domain-containing 1 (LEMD1) gene ( Figure S2G). LEMD1 is overexpressed in prostate cancer (Ghafouri-Fard et al, 2010) and anaplastic cell lymphoma (Matsuyama et al, 2011). Gene expression analysis suggests that only a (657 nt) LEMD1 isoform is expressed in CRC (Yuki et al, 2004).…”

Section: Mir-135b Overexpression Is Associated With Mutations In Specmentioning

confidence: 99%

microRNA-135b promotes cancer progression acting as a downstream effector of oncogenic pathways in colon cancer

Valeri¹,

Braconi²,

Gasparini³

et al. 2013

The Lancet

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SUMMARYMicroRNA deregulation is frequent in human colorectal cancers (CRCs), but little is known as to whether it represents a bystander event or actually drives tumor progression in vivo. We show that miR-135b overexpression is triggered in mice and humans by APC loss, PTEN/PI3K pathway deregulation, and SRC overexpression and promotes tumor transformation and progression. We show that miR-135b upregulation is common in sporadic and inflammatory bowel disease-associated human CRCs and correlates with tumor stage and poor clinical outcome. Inhibition of miR-135b in CRC mouse models reduces tumor growth by controlling genes involved in proliferation, invasion, and apoptosis. We identify miR-135b as a key downsteam effector of oncogenic pathways and a potential target for CRC treatment.

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Section: Mir-135b Overexpression Is Associated With Mutations In Specmentioning

confidence: 99%

microRNA-135b promotes cancer progression acting as a downstream effector of oncogenic pathways in colon cancer

Valeri¹,

Braconi²,

Gasparini³

et al. 2013

The Lancet

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“…The causes of prostate cancer, which is a heterogeneous disease, are unknown but are thought to include environmental, nutritional, hormonal, and genetic factors. Molecular mechanism of prostate cancer is poorly understood; however, several molecular abnormalities such as chromosomal loss or gain, gene amplification, mutations leading to increase, decrease or induction of gene expression, mutations leading to changes in function of the proteins and some polymorphisms have been described (Roylance et al, 1997;Ousati Ashtiani et al, 2009;Ghafouri-Fard et al, 2010;Ashtiani et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial D-Loop Polymorphism and Microsatellite Instability in Prostate Cancer and Benign Hyperplasia Patients

Ashtiani

Heidari²,

Hasheminasab³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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In this study mitochondrial D-Loop variations in Iranian prostate cancer and benign prostatic hyperplasia (BPH) patients were investigated. Tumour samples and corresponding non-cancerous prostate tissue from 40 prostate cancer patients and 40 age-matched BPH patients were collected. The entire mtD-loop region (16024-576) was amplified using the PCR method and products were gel-purified and subjected to direct nucleotide sequencing. A total of 129 variations were found, the most frequent being 263AgG and 310TgC among both BPH and prostate cancer patients. Variation of 309 CgT was significantly more frequent in prostate cancer patients (P value<0.05). Four novel variations were observed on comparison with the MITOMAP database. Novel variations were np16154delT, np366GgA, np389GgA and 56insT. There was no correspondence between the different variations and the age of subjects. Considering that D-loop variations were frequent in both BPH and prostate cancer patients in our study, the fact that both groups had high average age can be a possible contributing factor. D-loop polymorphisms and microsatellite instability can influence cell physiology and result in a benign or malignant phenotype. Significantly higher frequency of 309 CgT variation in cancer patients is a notable finding and must be a focus of attention in future studies.

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“…After literature screening, 12 reviews [7,8,9,10,11,12,13,14,15,16,17,18] and 137 research papers [19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82,83,84,85,86,87,88,89,90,91,92,93,94,95,96,97,98,99,100,101,102...…”

Section: Resultsmentioning

confidence: 99%

Trends in Gene Expression Profiling for Prostate Cancer Risk Assessment: A Systematic Review

et al. 2017

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Objectives: The aim of the study is to review biotechnology advances in gene expression profiling on prostate cancer (PCa), focusing on experimental platform development and gene discovery, in relation to different study designs and outcomes in order to understand how they can be exploited to improve PCa diagnosis and clinical management. Methods: We conducted a systematic literature review on gene expression profiling studies through PubMed/MEDLINE and Web of Science between 2000 and 2016. Tissue biopsy and clinical gene profiling studies with different outcomes (e.g., recurrence, survival) were included. Results: Over 3,000 papers were screened and 137 full-text articles were selected. In terms of technology used, microarray is still the most popular technique, increasing from 50 to 70% between 2010 and 2015, but there has been a rise in the number of studies using RNA sequencing (13% in 2015). Sample sizes have increased, as well as the number of genes that can be screened all at once, but we have also observed more focused targeting in more recent studies. Qualitative analysis on the specific genes found associated with PCa risk or clinical outcomes revealed a large variety of gene candidates, with a few consistent cross-studies. Conclusions: The last 15 years of research in gene expression in PCa have brought a large volume of data and information that has been decoded only in part, but advancements in high-throughput sequencing technology are increasing the amount of data that can be generated. The variety of findings warrants the execution of both validation studies and meta-analyses. Genetic biomarkers have tremendous potential for early diagnosis of PCa and, if coupled with other diagnostics (e.g., imaging), can effectively be used to concretize less-invasive, personalized prediction of PCa risk and progression.

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Expression of Two Testis-specific Genes, SPATA19 and LEMD1, in Prostate Cancer

Cited by 53 publications

References 20 publications

microRNA-135b promotes cancer progression acting as a downstream effector of oncogenic pathways in colon cancer

microRNA-135b promotes cancer progression acting as a downstream effector of oncogenic pathways in colon cancer

Mitochondrial D-Loop Polymorphism and Microsatellite Instability in Prostate Cancer and Benign Hyperplasia Patients

Trends in Gene Expression Profiling for Prostate Cancer Risk Assessment: A Systematic Review

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