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Article ; Online: Correction: CYP1B1 promotes tumorigenesis via altered expression of CDC20 and DAPK1 genes in renal cell carcinoma.

Mitsui, Yozo / Chang, Inik / Fukuhara, Shinichiro / Hiraki, Miho / Arichi, Naoko / Yasumoto, Hiroaki / Hirata, Hiroshi / Yamamura, Soichiro / Shahryari, Varahram / Deng, Guoren / Wong, Darryn K / Majid, Shahana / Shiina, Hiroaki / Dahiya, Rajvir / Tanaka, Yuichiro

BMC cancer

2022 Volume 22, Issue 1, Page(s) 813

Language	English
Publishing date	2022-07-25
Publishing country	England
Document type	Published Erratum
ZDB-ID	2041352-X
ISSN	1471-2407 ; 1471-2407
ISSN (online)	1471-2407
ISSN	1471-2407
DOI	10.1186/s12885-022-09907-4
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Article ; Online: Biofabrication of cell-laden allografts of goat urinary bladder scaffold for organ reconstruction/regeneration.

Vishwakarma, Sandeep Kumar / Sarwar, Shahana / Adil, Mohammed Abdul Majid / Khan, Aleem Ahmed

Tissue & cell

2020 Volume 67, Page(s) 101443

Abstract: Introduction: Bladder dysfunction has been considered as one of the most critical health conditions with no proper treatment. Current therapeutic approaches including enterocystoplasty have several limitations. Hence, biofabrication of cell-laden ... ...

Abstract	Introduction: Bladder dysfunction has been considered as one of the most critical health conditions with no proper treatment. Current therapeutic approaches including enterocystoplasty have several limitations. Hence, biofabrication of cell-laden biological allografts using decellularized Goat urinary bladder scaffolds for organ reconstruction/regeneration was major objective of this study. Materials and methods: An efficient method for decellularization of Goat urinary bladder (N = 3) was developed by perfusion of gradient change of detergents through ureter. The retention of organ architecture, extracellular matrix composition, mechanical properties and removal of cellular components was characterized using histological, cellular and molecular analysis. Further, mesenchymal stem cells (MSCs) from human umbilical cord blood (UCB) were used for preparing biological construct of decellularized urinary bladder (DUB) scaffolds to augment the urinary bladder reconstruction/regeneration. Results: The decellularization method adopted in this study generated completely DUB scaffolds within 10 h at 100 mm Hg pressure and constant flow rate of 1 mL/min. The DUB scaffold retains organ architecture, ECM composition, and mechanical strength. No significant amount of residual nucleic acid was observed post-decellularization. Furthermore, MSCs derived from human UCB engrafted and proliferated well on DUB scaffolds in highly aligned manner under xeno-free condition. Conclusion: Biofabricated humanized urinary bladder constructs provides xeno-free allografts for future application in augmenting urinary bladder reconstruction/regeneration with further development.
MeSH term(s)	Allografts/cytology ; Animals ; Cell Proliferation ; Collagen/metabolism ; Glycosaminoglycans/metabolism ; Goats ; Humans ; Immunophenotyping ; Materials Testing ; Microtechnology ; Nucleic Acids/analysis ; Optical Imaging ; Regeneration/physiology ; Tissue Scaffolds/chemistry ; Urinary Bladder/cytology ; Urinary Bladder/physiology ; Urinary Bladder/ultrastructure
Chemical Substances	Glycosaminoglycans ; Nucleic Acids ; Collagen (9007-34-5)
Language	English
Publishing date	2020-09-28
Publishing country	Scotland
Document type	Journal Article
ZDB-ID	204424-9
ISSN	1532-3072 ; 0040-8166
ISSN (online)	1532-3072
ISSN	0040-8166
DOI	10.1016/j.tice.2020.101443
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Article ; Online: Editor's Note: Epigenetic Modifications of

Kawamoto, Ken / Okino, Steven T / Place, Robert F / Urakami, Shinji / Hirata, Hiroshi / Kikuno, Nobuyuki / Kawakami, Toshifumi / Tanaka, Yuichiro / Pookot, Deepa / Chen, Zhong / Majid, Shahana / Enokida, Hideki / Nakagawa, Masayuki / Dahiya, Rajvir

Clinical cancer research : an official journal of the American Association for Cancer Research

2021 Volume 27, Issue 9, Page(s) 2665

Language	English
Publishing date	2021-03-23
Publishing country	United States
Document type	Journal Article ; Expression of Concern
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-21-0847
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Article ; Online: Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients.

Bhagirath, Divya / Dahiya, Rajvir / Majid, Shahana / Tabatabai, Z Laura / Saini, Sharanjot

Journal of visualized experiments : JoVE

2019 , Issue 153

Abstract: Ablation of androgen receptor (AR) signaling by androgen deprivation is the goal of the first line of therapy for prostate cancer that initially results in cancer regression. However, in a significant number of cases, the disease progresses to advanced, ... ...

Abstract	Ablation of androgen receptor (AR) signaling by androgen deprivation is the goal of the first line of therapy for prostate cancer that initially results in cancer regression. However, in a significant number of cases, the disease progresses to advanced, castration-resistant prostate cancer (CRPC), which has limited therapeutic options and is often aggressive. Distant metastasis is mostly observed at this stage of the aggressive disease. CRPC is treated by a second generation of AR pathway inhibitors that improve survival initially, followed by the emergence of therapy resistance. Neuroendocrine prostate cancer (NEPC) is a rare variant of prostate cancer (PCa) that often develops as a result of therapy resistance via a transdifferentiation process known as neuroendocrine differentiation (NED), wherein PCa cells undergo a lineage switch from adenocarcinomas and show increased expression of neuroendocrine (NE) lineage markers. In addition to the genomic alterations that drive the progression and transdifferentiation to NEPC, epigenetic factors and microenvironmental cues are considered essential players in driving disease progression. This manuscript provides a detailed protocol to identify the epigenetic drivers (i.e., small non-coding RNAs) that are associated with advanced PCa. Using purified microRNAs from formalin-fixed paraffin-embedded (FFPE) metastatic tissues and corresponding serum-derived extracellular vesicles (EVs), the protocol describes how to prepare libraries with appropriate quality control for sequencing microRNAs from these sample sources. Isolating RNA from both FFPE and EVs is often challenging because most of it is either degraded or is limited in quantity. This protocol will elaborate on different methods to optimize the RNA inputs and cDNA libraries to yield most specific reads and high-quality data upon sequencing.
MeSH term(s)	Cell Transdifferentiation/physiology ; Exosomes/genetics ; Exosomes/metabolism ; Formaldehyde/administration & dosage ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; MicroRNAs/genetics ; Prostatic Neoplasms, Castration-Resistant/blood ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/pathology ; Sequence Analysis, RNA/methods ; Tissue Fixation/methods
Chemical Substances	MicroRNAs ; Formaldehyde (1HG84L3525)
Language	English
Publishing date	2019-11-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/60549
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Article: Sequencing small non-coding rna from formalin-fixed tissues and serum-derived exosomes from castration-resistant prostate cancer patients

Bhagirath, Divya / Dahiya, Rajvir / Majid, Shahana / Tabatabai, Z. Laura / Saini, Sharanjot

Journal of visualized experiments. 2019 Nov. 19, , no. 153

2019

Abstract	Ablation of androgen receptor (AR) signaling by androgen deprivation is the goal of the first line of therapy for prostate cancer that initially results in cancer regression. However, in a significant number of cases, the disease progresses to advanced, castration-resistant prostate cancer (CRPC), which has limited therapeutic options and is often aggressive. Distant metastasis is mostly observed at this stage of the aggressive disease. CRPC is treated by a second generation of AR pathway inhibitors that improve survival initially, followed by the emergence of therapy resistance. Neuroendocrine prostate cancer (NEPC) is a rare variant of prostate cancer (PCa) that often develops as a result of therapy resistance via a transdifferentiation process known as neuroendocrine differentiation (NED), wherein PCa cells undergo a lineage switch from adenocarcinomas and show increased expression of neuroendocrine (NE) lineage markers. In addition to the genomic alterations that drive the progression and transdifferentiation to NEPC, epigenetic factors and microenvironmental cues are considered essential players in driving disease progression. This manuscript provides a detailed protocol to identify the epigenetic drivers (i.e., small non-coding RNAs) that are associated with advanced PCa. Using purified microRNAs from formalin-fixed paraffin-embedded (FFPE) metastatic tissues and corresponding serum-derived extracellular vesicles (EVs), the protocol describes how to prepare libraries with appropriate quality control for sequencing microRNAs from these sample sources. Isolating RNA from both FFPE and EVs is often challenging because most of it is either degraded or is limited in quantity. This protocol will elaborate on different methods to optimize the RNA inputs and cDNA libraries to yield most specific reads and high-quality data upon sequencing.
Keywords	adenocarcinoma ; androgen receptors ; androgens ; cDNA libraries ; complementary DNA ; disease progression ; epigenetics ; exosomes ; genomics ; metastasis ; microRNA ; non-coding RNA ; patients ; prostatic neoplasms ; quality control ; therapeutics
Language	English
Dates of publication	2019-1119
Size	p. e60549.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/60549
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Article: BRN4

Bhagirath, Divya / Yang, Thao Ly / Tabatabai, Z Laura / Majid, Shahana / Dahiya, Rajvir / Tanaka, Yuichiro / Saini, Sharanjot

Clinical cancer research : an official journal of the American Association for Cancer Research

2019 Volume 25, Issue 21, Page(s) 6532–6545

Abstract: Purpose: Neuroendocrine prostate cancer (NEPC), an aggressive variant of castration-resistant prostate cancer (CRPC), often emerges after androgen receptor-targeted therapies such as enzalutamide or : Results: We identify for the first time that: (i) ...

Abstract	Purpose: Neuroendocrine prostate cancer (NEPC), an aggressive variant of castration-resistant prostate cancer (CRPC), often emerges after androgen receptor-targeted therapies such as enzalutamide or Results: We identify for the first time that: (i) Conclusions: Our study identifies a novel TF that drives NEPC and suggests that as adaptive mechanism to enzalutamide treatment, prostate cancer cells express and secrete
MeSH term(s)	Aged ; Aged, 80 and over ; Animals ; Carcinogenesis/genetics ; Carcinoma, Neuroendocrine/genetics ; Carcinoma, Neuroendocrine/pathology ; Cell Differentiation/genetics ; Cell Line, Tumor ; Disease Progression ; Extracellular Vesicles/genetics ; Gene Expression Regulation, Neoplastic/genetics ; Heterografts ; Homeodomain Proteins/genetics ; Humans ; Male ; Mice ; Middle Aged ; POU Domain Factors/genetics ; Prostate/metabolism ; Prostate/pathology ; Prostatic Neoplasms, Castration-Resistant/epidemiology ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/pathology ; Receptors, Androgen/genetics
Chemical Substances	AR protein, human ; Homeodomain Proteins ; POU Domain Factors ; POU3F4 protein, human ; Receptors, Androgen ; transcription factor Brn-2
Language	English
Publishing date	2019-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-19-0498
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Article: Biomarkers of Prostatic Cancer: An Attempt to Categorize Patients into Prostatic Carcinoma, Benign Prostatic Hyperplasia, or Prostatitis Based on Serum Prostate Specific Antigen, Prostatic Acid Phosphatase, Calcium, and Phosphorus.

Sarwar, Shahana / Adil, Mohammed Abdul Majid / Nyamath, Parveen / Ishaq, Mohammed

Prostate cancer

2017 Volume 2017, Page(s) 5687212

Abstract: Prostatitis, BPH, and P.Ca are the most frequent pathologies of the prostate gland that are responsible for morbidity in men. Raised levels of PSA are seen in different pathological conditions involving the prostate. PAP levels are altered in ... ...

Abstract	Prostatitis, BPH, and P.Ca are the most frequent pathologies of the prostate gland that are responsible for morbidity in men. Raised levels of PSA are seen in different pathological conditions involving the prostate. PAP levels are altered in inflammatory or infectious or abnormal growth of the prostate tissue. Serum calcium and phosphorus levels were also found to be altered in prostate cancer and BPH. The present study was carried out to study the levels of PSA, PAP, calcium, and phosphorus in serum of patients with Prostatitis, BPH, or P.Ca and also to evaluate the relationship between them. Males in the age group of 50-85 years with LUTS disease symptoms and with PSA levels more than 4 ng/mL were included. A total of 114 patients were analyzed including 30 controls. Prostatitis in 35.7% of cases, BPH in 35.7% of the cases, and P.Ca in 28.57% of the cases were observed. Thus, the nonmalignant cases constitute a majority. PSA, a marker specific for prostatic conditions, was significantly high in all the diseases compared to controls. A rise in serum PSA and PAP indicates prostatitis or, in combination with these two tests, decreased serum calcium shows advanced disease.
Language	English
Publishing date	2017-01-12
Publishing country	Egypt
Document type	Journal Article
ZDB-ID	2627965-4
ISSN	2090-312X ; 2090-3111
ISSN (online)	2090-312X
ISSN	2090-3111
DOI	10.1155/2017/5687212
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Article ; Online: MicroRNAs and epithelial-mesenchymal transition in prostate cancer.

Sekhon, Kirandeep / Bucay, Nathan / Majid, Shahana / Dahiya, Rajvir / Saini, Sharanjot

Oncotarget

2016 Volume 7, Issue 41, Page(s) 67597–67611

Abstract: Prostate cancer (PCa) is a leading cause of male cancer-related deaths. A significant fraction of prostate tumors are very aggressive, often metastasizing to bone, causing significant morbidity and mortality. Also, PCa is associated with high rates of ... ...

Abstract	Prostate cancer (PCa) is a leading cause of male cancer-related deaths. A significant fraction of prostate tumors are very aggressive, often metastasizing to bone, causing significant morbidity and mortality. Also, PCa is associated with high rates of recurrence, often attributed to the existence of cancer stem cells. Epithelial-mesenchymal transition (EMT), a process characterized by decreased expression of epithelial genes and increased expression of mesenchymal genes, plays a critical role in tumor invasion, metastasis and recurrence. In PCa, EMT has been implicated particularly in the context of metastatic disease and microRNAs have emerged as critical post-transcriptional regulators of PCa EMT. In this review, we summarize the role of miRNAs in PCa EMT that play a role in progression, metastasis and recurrence. Studies till date suggest that microRNAs mediate efficient and reversible control of PCa EMT via multiple mechanisms including either by (i) directly repressing single or multiple EMT-TFs or regulating cytoskeletal components (epithelial/mesenchymal genes) or (ii) regulating key signaling pathways involved in EMT. Oncogenic microRNAs often act as EMT promoters by repressing epithelial characteristics and tumor suppressive miRNAs act by inhibiting mesenchymal progression. Further, EMT is mechanistically linked to stem cell signatures in PCa and several miRNAs implicated in EMT have been reported to influence PCa stem cells. Loss of EMT-inhibiting miRNAs and/or gain of EMT promoting miRNAs lead to induction of PCa EMT, leading to tumor progression, metastasis and recurrence. Restoring expression of tumor suppressive miRNAs and inhibiting oncogenic miRNAs represent potential therapeutic opportunities to prevent disease metastasis and recurrence.
Language	English
Publishing date	2016-10-11
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.11708
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Article ; Online: A lncRNA TCL6-miR-155 Interaction Regulates the Src-Akt-EMT Network to Mediate Kidney Cancer Progression and Metastasis.

Kulkarni, Priyanka / Dasgupta, Pritha / Hashimoto, Yutaka / Shiina, Marisa / Shahryari, Varahram / Tabatabai, Z Laura / Yamamura, Soichiro / Tanaka, Yuichiro / Saini, Sharanjot / Dahiya, Rajvir / Majid, Shahana

Cancer research

2021 Volume 81, Issue 6, Page(s) 1500–1512

Abstract: Metastasis is the leading cause of mortality from kidney cancer, and understanding the underlying mechanism of this event will provide better strategies for its management. Here we investigated the biological, functional, and clinical significance of ... ...

Abstract	Metastasis is the leading cause of mortality from kidney cancer, and understanding the underlying mechanism of this event will provide better strategies for its management. Here we investigated the biological, functional, and clinical significance of lncTCL6 and its interacting miR-155 in clear cell renal cell carcinoma (ccRCC). We employed a comprehensive approach to investigate the lncTCL6-miR-155-Src/Akt-mediated epithelial-to-mesenchymal transition (EMT) pathway as a novel regulatory mechanism in ccRCC progression. Expression analyses revealed that lncTCL6 is downregulated in ccRCC compared with normal tissues. Overexpression of lncTCL6 in ccRCC cell lines impaired their oncogenic functions, such as cell proliferation and migration/invasion, and induced cell-cycle arrest and apoptosis; conversely, depletion of lncTCL6 rescued these phenotypic effects. Furthermore, lncTCL6 directly interacted with miR-155. Unlike lncTCL6, miR-155 was overexpressed in ccRCC. Stable knockdown of miR-155 phenocopied the effects of lncTCL6 overexpression. Conversely, reconstitution of miR-155 and suppression of lncTCL6 in noncancerous renal cell HK2 induced tumorigenic characteristics. Patients with higher expression of lncTCL6 and lower expression of miR-155 had better survival probability. When overexpressed, lncTCL6 recruited STAU1 and mediated decay of Src mRNA, followed by a marked downregulation of an integrated network of Src target genes involved in migration, invasion, and EMT. However, the interaction between miR-155 and lncTCL6 attenuated the regulatory role of lncTCL6 on Src-mediated EMT. In conclusion, this study is the first report documenting the lncTCL6-miR155-Src/Akt/EMT network as a novel regulatory mechanism in aggressive ccRCC and a promising therapeutic target to inhibit renal cancer. SIGNIFICANCE: This study's investigation of noncoding RNA interactions in renal cell carcinoma identify miRNA-155-lncRNA TCL6-mediated regulation of the Src-Akt-EMT network as a novel mechanism of disease progression and metastasis.
MeSH term(s)	Aged ; Animals ; Carcinogenesis/genetics ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/mortality ; Carcinoma, Renal Cell/secondary ; Carcinoma, Renal Cell/surgery ; Cell Line, Tumor ; Down-Regulation ; Epithelial-Mesenchymal Transition/genetics ; Follow-Up Studies ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Humans ; Kaplan-Meier Estimate ; Kidney/pathology ; Kidney/surgery ; Kidney Neoplasms/genetics ; Kidney Neoplasms/mortality ; Kidney Neoplasms/pathology ; Kidney Neoplasms/surgery ; Male ; Mice ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Middle Aged ; Nephrectomy ; Proto-Oncogene Proteins c-akt/metabolism ; RNA, Long Noncoding/metabolism ; Signal Transduction/genetics ; Treatment Outcome ; Xenograft Model Antitumor Assays ; src-Family Kinases/metabolism
Chemical Substances	MIRN155 microRNA, human ; MicroRNAs ; RNA, Long Noncoding ; long noncoding RNA TCL6, human ; src-Family Kinases (EC 2.7.10.2) ; AKT1 protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2021-01-26
Publishing country	United States
Document type	Journal Article ; Observational Study ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-20-0832
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Article ; Online: Role of a novel race-related tumor suppressor microRNA located in frequently deleted chromosomal locus 8p21 in prostate cancer progression.

Bhagirath, Divya / Yang, Thao Ly / Tabatabai, Z Laura / Shahryari, Varahram / Majid, Shahana / Dahiya, Rajvir / Tanaka, Yuichiro / Saini, Sharanjot

Carcinogenesis

2019 Volume 40, Issue 5, Page(s) 633–642

Abstract: The prostate cancer (PCa) genome is characterized by deletions of chromosome 8p21-22 region that increase significantly with tumor grade and are associated with poor prognosis. We proposed and validated a novel, paradigm-shifting hypothesis that this ... ...

Abstract	The prostate cancer (PCa) genome is characterized by deletions of chromosome 8p21-22 region that increase significantly with tumor grade and are associated with poor prognosis. We proposed and validated a novel, paradigm-shifting hypothesis that this region is associated with a set of microRNA genes-miR-3622, miR-3622b, miR-383-that are lost in PCa and play important mechanistic roles in PCa progression and metastasis. Extending our hypothesis, in this study, we evaluated the role of a microRNA gene located in chromosome 8p-miR-4288-by employing clinical samples and cell lines. Our data suggests that (i) miR-4288 is widely downregulated in primary prostate tumors and cell lines; (ii) miR-4288 expression is lost in metastatic castration-resistant PCa; (ii) miR-4288 downregulation is race-related PCa alteration that is prevalent in Caucasian patients and not in African Americans; (iii) in Caucasians, miR-4288 was found to be associated with increasing tumor grade and high serum prostate-specific antigen, suggesting that miR-4288 downregulation/loss may be associated with tumor progression specifically in Caucasians; (iv) miR-4288 possess significant potential as a molecular biomarker to predict aggressiveness/metastasis; and (v) miR-4288 is anti-proliferative, is anti-invasive and inhibits epithelial-to-mesenchymal transition; and (vi) miR-4288 directly represses expression of metastasis/invasion-associated genes MMP16 and ROCK1. Thus, the present study demonstrates a tumor suppressor role for a novel miRNA located with a frequently lost region in PCa, strengthening our hypothesis that this locus is causally related to PCa disease progression via loss of microRNA genes. Our study suggests that miR-4288 may be a novel biomarker and therapeutic target, particularly in Caucasians.
MeSH term(s)	Adult ; Aged ; Apoptosis ; Cell Movement ; Cell Proliferation ; Chromosome Deletion ; Chromosomes, Human, Pair 8/genetics ; Disease Progression ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Humans ; Male ; MicroRNAs/genetics ; Middle Aged ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; Tumor Cells, Cultured
Chemical Substances	MIRN4288 microRNA, human ; MicroRNAs
Language	English
Publishing date	2019-03-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	603134-1
ISSN	1460-2180 ; 0143-3334
ISSN (online)	1460-2180
ISSN	0143-3334
DOI	10.1093/carcin/bgz058
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