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Article ; Online: RNA binding proteins (RBPs) and their role in DNA damage and radiation response in cancer.

Mehta, Meghna / Raguraman, Rajeswari / Ramesh, Rajagopal / Munshi, Anupama

2022 Volume 191, Page(s) 114569

Abstract: Traditionally majority of eukaryotic gene expression is influenced by transcriptional and post-transcriptional events. Alterations in the expression of proteins that act post-transcriptionally can affect cellular signaling and homeostasis. RNA binding ... ...

Abstract	Traditionally majority of eukaryotic gene expression is influenced by transcriptional and post-transcriptional events. Alterations in the expression of proteins that act post-transcriptionally can affect cellular signaling and homeostasis. RNA binding proteins (RBPs) are a family of proteins that specifically bind to RNAs and are involved in post-transcriptional regulation of gene expression and important cellular processes such as cell differentiation and metabolism. Deregulation of RNA-RBP interactions and any changes in RBP expression or function can lead to various diseases including cancer. In cancer cells, RBPs play an important role in regulating the expression of tumor suppressors and oncoproteins involved in various cell-signaling pathways. Several RBPs such as HuR, AUF1, RBM38, LIN28, RBM24, tristetrapolin family and Musashi play critical roles in various types of cancers and their aberrant expression in cancer cells makes them an attractive therapeutic target for cancer treatment. In this review we provide an overview of i). RBPs involved in cancer progression and their mechanism of action ii). the role of RBPs, including HuR, in breast cancer progression and DNA damage response and iii). explore RBPs with emphasis on HuR as therapeutic target for breast cancer therapy.
MeSH term(s)	Humans ; Female ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Gene Expression Regulation ; RNA ; Breast Neoplasms ; DNA Damage
Chemical Substances	RNA-Binding Proteins ; RNA (63231-63-0) ; RBM38 protein, human ; RBM24 protein, human
Language	English
Publishing date	2022-10-14
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	639113-8
ISSN	1872-8294 ; 0169-409X
ISSN (online)	1872-8294
ISSN	0169-409X
DOI	10.1016/j.addr.2022.114569
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Article ; Online: Therapeutic approaches targeting molecular signaling pathways common to diabetes, lung diseases and cancer.

Raguraman, Rajeswari / Srivastava, Akhil / Munshi, Anupama / Ramesh, Rajagopal

Advanced drug delivery reviews

2021 Volume 178, Page(s) 113918

Abstract: Diabetes mellitus (DM), is the most common metabolic disease and is characterized by sustained hyperglycemia. Accumulating evidences supports a strong association between DM and numerous lung diseases including chronic obstructive pulmonary disease (COPD) ...

Abstract	Diabetes mellitus (DM), is the most common metabolic disease and is characterized by sustained hyperglycemia. Accumulating evidences supports a strong association between DM and numerous lung diseases including chronic obstructive pulmonary disease (COPD), fibrosis, and lung cancer (LC). The global incidence of DM-associated lung disorders is rising and several ongoing studies, including clinical trials, aim to elucidate the molecular mechanisms linking DM with lung disorders, in particular LC. Several potential mechanisms, including hyperglycemia, hyperinsulinemia, glycation, inflammation, and hypoxia, are cited as plausible links between DM and LC. In addition, studies also propose a connection between the use of anti-diabetic medications and reduction in the incidence of LC. However, the exact cause for DM associated lung diseases especially LC is not clear and is an area under intense investigation. Herein, we review the biological links reported between DM and lung disorders with an emphasis on LC. Furthermore, we report common signaling pathways (eg: TGF-β, IL-6, HIF-1, PDGF) and miRNAs that are dysregulated in DM and LC and serve as molecular targets for therapy. Finally, we propose a nanomedicine based approach for delivering therapeutics (eg: IL-24 plasmid DNA, HuR siRNA) to disrupt signaling pathways common to DM and LC and thus potentially treat DM-associated LC. Finally, we conclude that the effective modulation of commonly regulated signaling pathways would help design novel therapeutic protocols for treating DM patients diagnosed with LC.
MeSH term(s)	Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Diabetes Mellitus/diagnosis ; Diabetes Mellitus/drug therapy ; Diabetes Mellitus/metabolism ; Humans ; Hypoglycemic Agents/chemistry ; Hypoglycemic Agents/pharmacology ; Hypoxia-Inducible Factor 1, alpha Subunit/antagonists & inhibitors ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Interleukin-6/antagonists & inhibitors ; Interleukin-6/metabolism ; Lung Diseases/diagnosis ; Lung Diseases/drug therapy ; Lung Diseases/metabolism ; Lung Neoplasms/diagnosis ; Lung Neoplasms/drug therapy ; Lung Neoplasms/metabolism ; MicroRNAs ; Nanomedicine ; Platelet-Derived Growth Factor/antagonists & inhibitors ; Platelet-Derived Growth Factor/metabolism ; Signal Transduction/drug effects ; Transforming Growth Factor beta/antagonists & inhibitors ; Transforming Growth Factor beta/metabolism
Chemical Substances	Antineoplastic Agents ; HIF1A protein, human ; Hypoglycemic Agents ; Hypoxia-Inducible Factor 1, alpha Subunit ; IL6 protein, human ; Interleukin-6 ; MicroRNAs ; Platelet-Derived Growth Factor ; Transforming Growth Factor beta
Language	English
Publishing date	2021-08-08
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	639113-8
ISSN	1872-8294 ; 0169-409X
ISSN (online)	1872-8294
ISSN	0169-409X
DOI	10.1016/j.addr.2021.113918
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Article ; Online: Tumor-targeted exosomes for delivery of anticancer drugs.

Raguraman, Rajeswari / Bhavsar, Dhaval / Kim, Dongin / Ren, Xiaoyu / Sikavitsas, Vassilios / Munshi, Anupama / Ramesh, Rajagopal

Cancer letters

2023 Volume 558, Page(s) 216093

Abstract: Exosomes are small phospholipid bilayer vesicles that are naturally produced by all living cells, both prokaryotes and eukaryotes. The exosomes due to their unique size, reduced immunogenicity, and their ability to mimic synthetic liposomes in carrying ... ...

Abstract	Exosomes are small phospholipid bilayer vesicles that are naturally produced by all living cells, both prokaryotes and eukaryotes. The exosomes due to their unique size, reduced immunogenicity, and their ability to mimic synthetic liposomes in carrying various anticancer drugs have been tested as drug delivery vehicles for cancer treatment. An added advantage of developing exosomes as a drug carrier is the ease of manipulating their intraluminal content and their surface modification to achieve tumor-targeted drug delivery. In the past ten-years, there has been an exponential increase in the number of exosome-related studies in cancer. Preclinical studies demonstrate exosomes-mediated delivery of chemotherapeutics, biologicals and natural products produce potent anticancer activity both, in vitro and in vivo. In contrast, the number of exosome-based clinical trials are few due to challenges in the manufacturing and scalability related to large-scale production of exosomes and their storage and stability. Herein, we discuss recent advances in exosome-based drug delivery for cancer treatment in preclinical and clinical studies and conclude with challenges to be overcome for translating a larger number of exosome-based therapies into the clinic.
MeSH term(s)	Humans ; Exosomes ; Drug Delivery Systems ; Drug Carriers ; Neoplasms/drug therapy ; Antineoplastic Agents/therapeutic use
Chemical Substances	Drug Carriers ; Antineoplastic Agents
Language	English
Publishing date	2023-02-21
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2023.216093
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Article ; Online: AKT1 Transcriptomic Landscape in Breast Cancer Cells.

George, Bijesh / Gui, Bin / Raguraman, Rajeswari / Paul, Aswathy Mary / Nakshatri, Harikrishna / Pillai, Madhavan Radhakrishna / Kumar, Rakesh

Cells

2022 Volume 11, Issue 15

Abstract: Overexpression and hyperactivation of the serine/threonine protein kinase B (AKT) pathway is one of the most common cellular events in breast cancer progression. However, the nature of AKT1-specific genome-wide transcriptomic alterations in breast cancer ...

Abstract	Overexpression and hyperactivation of the serine/threonine protein kinase B (AKT) pathway is one of the most common cellular events in breast cancer progression. However, the nature of AKT1-specific genome-wide transcriptomic alterations in breast cancer cells and breast cancer remains unknown to this point. Here, we delineate the impact of selective AKT1 knock down using gene-specific siRNAs or inhibiting the AKT activity with a pan-AKT inhibitor VIII on the nature of transcriptomic changes in breast cancer cells using the genome-wide RNA-sequencing analysis. We found that changes in the cellular levels of AKT1 lead to changes in the levels of a set of differentially expressed genes and, in turn, imply resulting AKT1 cellular functions. In addition to an expected positive relationship between the status of AKT1 and co-expressed cellular genes, our study unexpectedly discovered an inherent role of AKT1 in inhibiting the expression of a subset of genes in both unstimulated and growth factor stimulated breast cancer cells. We found that depletion of AKT1 leads to upregulation of a subset of genes-many of which are also found to be downregulated in breast tumors with elevated high AKT1 as well as upregulated in breast tumors with no detectable AKT expression. Representative experimental validation studies in two breast cancer cell lines showed a reasonable concurrence between the expression data from the RNA-sequencing and qRT-PCR or data from ex vivo inhibition of AKT1 activity in cancer patient-derived cells. In brief, findings presented here provide a resource for further understanding of AKT1-dependent modulation of gene expression in breast cancer cells and broaden the scope and significance of AKT1 targets and their functions.
MeSH term(s)	Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Female ; Humans ; Proto-Oncogene Proteins c-akt/genetics ; RNA ; Transcriptome
Chemical Substances	RNA (63231-63-0) ; AKT1 protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2022-07-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11152290
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Article: Multiple G-quadruplex binding ligand induced transcriptomic map of cancer cell lines.

Revikumar, Amjesh / Kashyap, Vivek / Palollathil, Akhina / Aravind, Anjana / Raguraman, Rajeswari / Kumar, Kenkere Mallikarjunaiah Kiran / Vijayakumar, Manavalan / Prasad, Thottethodi Subrahmanya Keshava / Raju, Rajesh

Journal of cell communication and signaling

2021 Volume 16, Issue 1, Page(s) 129–135

Abstract: The G-quadruplexes (G4s) are a class of DNA secondary structures with guanine rich DNA sequences that can fold into four stranded non-canonical structures. At the genomic level, their pivotal role is well established in DNA replication, telomerase ... ...

Abstract	The G-quadruplexes (G4s) are a class of DNA secondary structures with guanine rich DNA sequences that can fold into four stranded non-canonical structures. At the genomic level, their pivotal role is well established in DNA replication, telomerase functions, constitution of topologically associating domains, and the regulation of gene expression. Genome instability mediated by altered G4 formation and assembly has been associated with multiple disorders including cancers and neurodegenerative disorders. Multiple tools have also been developed to predict the potential G4 regions in genomes and the whole genome G4 maps are also being derived through sequencing approaches. Enrichment of G4s in the cis-regulatory elements of genes associated with tumorigenesis has accelerated the quest for identification of G4-DNA binding ligands (G4DBLs) that can selectively bind and regulate the expression of such specific genes. In this context, the analysis of G4DBL responsive transcriptome in diverse cancer cell lines is inevitable for assessment of the specificity of novel G4DBLs. Towards this, we assembled the transcripts differentially regulated by different G4DBLs and have also identified a core set of genes regulated in diverse cancer cell lines in response to 3 or more of these ligands. With the mode of action of G4DBLs towards topology shifts, folding, or disruption of G4 structure being currently visualized, we believe that this dataset will serve as a platform for assembly of G4DBL responsive transcriptome for comparative analysis of G4DBLs in multiple cancer cells based on the expression of specific cis-regulatory G4 associated genes in the future.
Language	English
Publishing date	2021-07-26
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2299380-0
ISSN	1873-961X ; 1873-9601
ISSN (online)	1873-961X
ISSN	1873-9601
DOI	10.1007/s12079-021-00637-z
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Article ; Online: Drug delivery approaches for HuR-targeted therapy for lung cancer.

Raguraman, Rajeswari / Shanmugarama, Santny / Mehta, Meghna / Elle Peterson, Jo / Zhao, Yan D / Munshi, Anupama / Ramesh, Rajagopal

Advanced drug delivery reviews

2021 Volume 180, Page(s) 114068

Abstract: Lung cancer (LC) is often diagnosed at an advanced stage and conventional treatments for disease management have limitations associated with them. Novel therapeutic targets are thus avidly sought for the effective management of LC. RNA binding proteins ( ... ...

Abstract	Lung cancer (LC) is often diagnosed at an advanced stage and conventional treatments for disease management have limitations associated with them. Novel therapeutic targets are thus avidly sought for the effective management of LC. RNA binding proteins (RBPs) have been convincingly established as key players in tumorigenesis, and their dysregulation is linked to multiple cancers, including LC. In this context, we review the role of Human antigen R (HuR), an RBP that is overexpressed in LC, and further associated with various aspects of LC tumor growth and response to therapy. Herein, we describe the role of HuR in LC progression and outline the evidences supporting various pharmacologic and biologic approaches for inhibiting HuR expression and function. These approaches, including use of small molecule inhibitors, siRNAs and shRNAs, have demonstrated favorable results in reducing tumor cell growth, invasion and migration, angiogenesis and metastasis. Hence, HuR has significant potential as a key therapeutic target in LC. Use of siRNA-based approaches, however, have certain limitations that prevent their maximal exploitation as cancer therapies. To address this, in the conclusion of this review, we provide a list of nanomedicine-based HuR targeting approaches currently being employed for siRNA and shRNA delivery, and provide a rationale for the immense potential therapeutic benefits offered by nanocarrier-based HuR targeting and its promise for treating patients with LC.
MeSH term(s)	Animals ; Drug Delivery Systems ; ELAV-Like Protein 1/antagonists & inhibitors ; ELAV-Like Protein 1/genetics ; ELAV-Like Protein 1/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/pathology ; Molecular Targeted Therapy ; Nanomedicine ; RNA, Small Interfering/administration & dosage
Chemical Substances	ELAV-Like Protein 1 ; ELAVL1 protein, human ; RNA, Small Interfering
Language	English
Publishing date	2021-11-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	639113-8
ISSN	1872-8294 ; 0169-409X
ISSN (online)	1872-8294
ISSN	0169-409X
DOI	10.1016/j.addr.2021.114068
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Article ; Online: Gene expression profiling of tumor stroma interactions in retinoblastoma.

Raguraman, Rajeswari / Parameswaran, Sowmya / Kanwar, Jagat Rakesh / Vasudevan, Madavan / Chitipothu, Srujana / Kanwar, Rupinder Kaur / Krishnakumar, Subramanian

Experimental eye research

2020 Volume 197, Page(s) 108067

Abstract: We aimed to identify the critical molecular pathways altered upon tumor stroma interactions in retinoblastoma (RB). In vitro 2 D cocultures of RB tumor cells (Weri-Rb-1 and NCC-RbC-51) with primary bone marrow stromal cells (BMSC) was established. Global ...

Abstract	We aimed to identify the critical molecular pathways altered upon tumor stroma interactions in retinoblastoma (RB). In vitro 2 D cocultures of RB tumor cells (Weri-Rb-1 and NCC-RbC-51) with primary bone marrow stromal cells (BMSC) was established. Global gene expression patterns in coculture samples were assessed using Affymetrix Prime view human gene chip microarray and followed with bioinformatics analyses. Key upregulated genes from Weri-Rb-1 + BMSC and NCC-RbC-51 + BMSC coculture were validated using qRT-PCR to ascertain their role in RB progression. Whole genome microarray experiments identified significant (P ≤ 0.05, 1.1 log 2 FC) transcriptome level changes induced upon coculture of RB cells with BMSC. A total of 1155 genes were downregulated and 1083 upregulated in Weri-Rb-1 + BMSC coculture. Similarly, 1865 genes showed downregulation and 1644 genes were upregulation in NCC-RbC-51 + BMSC coculture. The upregulated genes were significantly associated with pathways of focal adhesion, PI3K-Akt signalling, ECM-receptor interaction, JAK-STAT, TGF-β signalling thus contributing to RB progression. Validation of key genes by qRT-PCR revealed significant overexpression of IL8, IL6, MYC and SMAD3 in the case of Weri-Rb-1 + BMSC coculture and IL6 in the case of NCC-RbC-51 + BMSC coculture. The microarray expression study on in vitro RB coculture models revealed the pathways that could be involved in the progression of RB. The gene signature obtained in a stimulated model when a growing tumor interacts with its microenvironment may provide new horizons for potential targeted therapy in RB.
MeSH term(s)	Biomarkers, Tumor/biosynthesis ; Biomarkers, Tumor/genetics ; Cell Cycle ; Cell Line, Tumor ; Cell Proliferation ; Disease Progression ; Gene Expression Profiling/methods ; Gene Expression Regulation, Neoplastic ; Humans ; Retinal Neoplasms/genetics ; Retinal Neoplasms/metabolism ; Retinal Neoplasms/pathology ; Retinoblastoma/genetics ; Retinoblastoma/metabolism ; Retinoblastoma/pathology ; Signal Transduction ; Up-Regulation
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2020-06-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80122-7
ISSN	1096-0007 ; 0014-4835
ISSN (online)	1096-0007
ISSN	0014-4835
DOI	10.1016/j.exer.2020.108067
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Article: Targeting HMGA2 in Retinoblastoma Cells in vitro Using the Aptamer Strategy.

Nalini, Venkatesan / Deepa, Perinkulam Ravi / Raguraman, Rajeswari / Khetan, Vikas / Reddy, Maddy Ashwin / Krishnakumar, Subramanian

Ocular oncology and pathology

2016 Volume 2, Issue 4, Page(s) 262–269

Abstract: High-mobility group A2 (HMGA2) protein regulates retinoblastoma (RB) cancer cell proliferation. Here, a stable phosphorothioate-modified HMGA2 aptamer was used to block HMGA2 protein function in RB cells. HMGA2-aptamer internalisation in RB cells (Y79, ... ...

Abstract	High-mobility group A2 (HMGA2) protein regulates retinoblastoma (RB) cancer cell proliferation. Here, a stable phosphorothioate-modified HMGA2 aptamer was used to block HMGA2 protein function in RB cells. HMGA2-aptamer internalisation in RB cells (Y79, Weri Rb1) and non-neoplastic human retinal cells (MIO-M1) were optimised. Aptamer induced dose-dependent cytotoxicity in RB cancer cells (0.25-1.5 µM). Increased expression of
Language	English
Publishing date	2016-07-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2806965-1
ISSN	2296-4657 ; 2296-4681
ISSN (online)	2296-4657
ISSN	2296-4681
DOI	10.1159/000447300
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Article: Evidence of Tumour Microenvironment and Stromal Cellular Components in Retinoblastoma.

Raguraman, Rajeswari / Parameswaran, Sowmya / Kanwar, Jagat Rakesh / Khetan, Vikas / Rishi, Pukhraj / Kanwar, Rupinder Kaur / Krishnakumar, Subramanian

Ocular oncology and pathology

2018 Volume 5, Issue 2, Page(s) 85–93

Abstract: Background: The tumour microenvironment (TME) consisting of tumour cells and multiple stromal cell types regulate tumour growth, invasion and metastasis. While the concept of TME and presence of stromal cellular components is widely established in ... ...

Abstract	Background: The tumour microenvironment (TME) consisting of tumour cells and multiple stromal cell types regulate tumour growth, invasion and metastasis. While the concept of TME and presence of stromal cellular components is widely established in cancers, its significance in the paediatric intraocular malignancy, retinoblastoma (RB), remains unknown. Methods: The study qualitatively identified the presence of multiple stromal cellular subtypes in RB TME by immunohistochemistry. Results: Results of the study identified the presence of stromal cell types such as endothelial cells, tumour-associated macrophages, fibroblasts, cancer-associated fibroblasts, retinal astrocytes and glia in RB TME. The extent of stromal marker positivity, however, did not correlate with histopathological features of RB. Conclusions: The findings of the study convincingly suggest the presence of a stromal component in RB tumours. The interactions between stromal cells and tumour cells might be of profound importance in RB progression.
Language	English
Publishing date	2018-07-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2806965-1
ISSN	2296-4657 ; 2296-4681
ISSN (online)	2296-4657
ISSN	2296-4681
DOI	10.1159/000488709
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Article: Targeting HMGA2 in Retinoblastoma Cells in vitro Using the Aptamer Strategy

Nalini, Venkatesan / Deepa, Perinkulam Ravi / Raguraman, Rajeswari / Khetan, Vikas / Reddy, Maddy Ashwin / Krishnakumar, Subramanian

Ocular Oncology and Pathology

2016 Volume 2, Issue 4, Page(s) 262–269

Institution	Department of Larsen & Toubro Ocular Pathology, The Kamalnayan Bajaj Institute for Research in Vision & Ophthalmology, Vision Research Foundation, Chennai Birla Institute of Technology and Science (BITS), and Department of Biological Sciences, Birla Institute of Technology and Science (BITS), Pilani, and Department of Vitreoretina and Oncology, Medical Research Foundation, Sankara Nethralaya, Chennai, India Department of Ophthalmology, Barts Health NHS Trust, London, UK
Abstract	High-mobility group A2 (HMGA2) protein regulates retinoblastoma (RB) cancer cell proliferation. Here, a stable phosphorothioate-modified HMGA2 aptamer was used to block HMGA2 protein function in RB cells. HMGA2-aptamer internalisation in RB cells (Y79, Weri Rb1) and non-neoplastic human retinal cells (MIO-M1) were optimised. Aptamer induced dose-dependent cytotoxicity in RB cancer cells (0.25-1.5 µM). Increased expression of TGFβSMAD4 CDH1BAXCASP 3 PARP mRNA and decreased SNAI1 Bcl2 mRNA levels in aptamer-treated RB cells suggests the activation of TGFβ-SMAD4-mediated apoptotic pathway. Synergistic effect with etoposide was observed in aptamer treated RB cells (p value ≤0.05). No significant toxicity was observed in non-neoplastic retinal cells.
Keywords	HMGA2 ; HMGA2-aptamer ; Retinoblastoma ; Etoposide
Language	English
Publishing date	2016-07-02
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Basic Science Research
ZDB-ID	2806965-1
ISSN	2296-4657 ; 2296-4681
ISSN (online)	2296-4657
ISSN	2296-4681
DOI	10.1159/000447300
Database	Karger publisher's database

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