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Article ; Online: Mechanosensitive changes in the expression of genes in colorectal cancer-associated fibroblasts

Bashar Emon / You Jin Song / M. Saddam H. Joy / Mounisha V. Kovour / Kannanganattu V. Prasanth / M. Taher A. Saif

Scientific Data, Vol 10, Iss 1, Pp 1-

2023 Volume 6

Abstract: Abstract Most solid tumors become stiff with progression of cancer. Cancer Associated Fibroblasts (CAFs), most abundant stromal cells in the tumor microenvironment (TME), are known to mediate such stiffening. While the biochemical crosstalk between CAFs ... ...

Abstract	Abstract Most solid tumors become stiff with progression of cancer. Cancer Associated Fibroblasts (CAFs), most abundant stromal cells in the tumor microenvironment (TME), are known to mediate such stiffening. While the biochemical crosstalk between CAFs and cancer cells have been widely investigated, it is not clear if and how CAFs in stiffer TME promote metastatic progression. To gather insights into the process, we controlled the mechanical stiffness of the substrates and collected gene expression data with human colorectal CAFs. We cultured human primary CAFs on 2D polyacrylamide hydrogels with increasing elastic modulus (E) of 1, 10 and 40 kPa, and performed genome-wide transcriptome analyses in these cells to identify expression levels of ~16000 genes. The high-quality RNAseq results can be an excellent data-source for bioinformatic analysis for identifying novel pathways and biomarkers in cancer development and metastatic progression. With thorough analysis and accurate interpretation, this data may help researchers understand the role of mechanical stiffness of the TME in CAF-cancer cell crosstalk.
Keywords	Science ; Q
Language	English
Publishing date	2023-06-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Easy Stress Relief by EZH2

Prasanth, Supriya G / Kannanganattu V. Prasanth

Cell. 2016 Dec. 15, v. 167

2016

Abstract: While we are beginning to appreciate the cellular roles played by long noncoding RNAs, the function of transcripts emerging from repetitive genomic regions remains enigmatic. In this issue, Zovoilis et al. report that the polycomb protein EZH2, upon heat ...

Abstract	While we are beginning to appreciate the cellular roles played by long noncoding RNAs, the function of transcripts emerging from repetitive genomic regions remains enigmatic. In this issue, Zovoilis et al. report that the polycomb protein EZH2, upon heat shock, facilitates transcription of stress-responsive genes by inducing the degradation of the transcriptional repressor B2 repeat RNA.
Keywords	genes ; genomics ; heat stress ; non-coding RNA ; repressor proteins ; transcription (genetics)
Language	English
Dates of publication	2016-1215
Size	p. 1678-1680.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2016.11.051
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Splicing factor SRSF1 deficiency in the liver triggers NASH-like pathology and cell death

Waqar Arif / Bhoomika Mathur / Michael F. Saikali / Ullas V. Chembazhi / Katelyn Toohill / You Jin Song / Qinyu Hao / Saman Karimi / Steven M. Blue / Brian A. Yee / Eric L. Van Nostrand / Sushant Bangru / Grace Guzman / Gene W. Yeo / Kannanganattu V. Prasanth / Sayeepriyadarshini Anakk / Carolyn L. Cummins / Auinash Kalsotra

Nature Communications, Vol 14, Iss 1, Pp 1-

2023 Volume 19

Abstract: Nonalcoholic steatohepatitis (NASH) is an advanced form of fatty liver disease with complex pathogenic mechanisms. Here, the authors report that SRSF1 deficiency in mice livers provokes deleterious R-loop formation and genotoxicity, which impedes ... ...

Abstract	Nonalcoholic steatohepatitis (NASH) is an advanced form of fatty liver disease with complex pathogenic mechanisms. Here, the authors report that SRSF1 deficiency in mice livers provokes deleterious R-loop formation and genotoxicity, which impedes hepatocellular gene expression, metabolism, and lipid trafficking, resulting in NASH-like pathology.
Keywords	Science ; Q
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: ORCA/LRWD1 Regulates Homologous Recombination at ALT-Telomeres by Modulating Heterochromatin Organization

Rosaline Y.C. Hsu / Yo-Chuen Lin / Christophe Redon / Qinyu Sun / Deepak K. Singh / Yating Wang / Vasudha Aggarwal / Jaba Mitra / Abhijith Matur / Branden Moriarity / Taekjip Ha / Mirit I. Aladjem / Kannanganattu V. Prasanth / Supriya G. Prasanth

iScience, Vol 23, Iss 5, Pp - (2020)

2020

Abstract: Summary: Telomeres are maintained by telomerase or in a subset of cancer cells by a homologous recombination (HR)-based mechanism, Alternative Lengthening of Telomeres (ALT). The mechanisms regulating telomere-homeostasis in ALT cells remain unclear. We ... ...

Abstract	Summary: Telomeres are maintained by telomerase or in a subset of cancer cells by a homologous recombination (HR)-based mechanism, Alternative Lengthening of Telomeres (ALT). The mechanisms regulating telomere-homeostasis in ALT cells remain unclear. We report that a replication initiator protein, Origin Recognition Complex-Associated (ORCA/LRWD1), by localizing at the ALT-telomeres, modulates HR activity. ORCA's localization to the ALT-telomeres is facilitated by its interaction to SUMOylated shelterin components. The loss of ORCA in ALT-positive cells elevates the levels of two mediators of HR, RPA and RAD51, and consistent with this, we observe increased ALT-associated promyelocytic leukemia body formation and telomere sister chromatid exchange. ORCA binds to RPA and modulates the association of RPA to telomeres. Finally, the loss of ORCA causes global chromatin decondensation, including at the telomeres. Our results demonstrate that ORCA acts as an inhibitor of HR by modulating RPA binding to ssDNA and inducing chromatin compaction.
Keywords	Biological Sciences ; Molecular Biology ; Chromosome Organization ; Molecular Structure ; Science ; Q
Subject code	571
Language	English
Publishing date	2020-05-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Long Non-Coding RNA Malat-1 Is Dispensable during Pressure Overload-Induced Cardiac Remodeling and Failure in Mice.

Tim Peters / Steffie Hermans-Beijnsberger / Abdelaziz Beqqali / Nicole Bitsch / Shinichi Nakagawa / Kannanganattu V Prasanth / Leon J de Windt / Ralph J van Oort / Stephane Heymans / Blanche Schroen

PLoS ONE, Vol 11, Iss 2, p e

2016 Volume 0150236

Abstract: Long non-coding RNAs (lncRNAs) are a class of RNA molecules with diverse regulatory functions during embryonic development, normal life, and disease in higher organisms. However, research on the role of lncRNAs in cardiovascular diseases and in ... ...

Abstract	Long non-coding RNAs (lncRNAs) are a class of RNA molecules with diverse regulatory functions during embryonic development, normal life, and disease in higher organisms. However, research on the role of lncRNAs in cardiovascular diseases and in particular heart failure is still in its infancy. The exceptionally well conserved nuclear lncRNA Metastasis associated in lung adenocarcinoma transcript 1 (Malat-1) is a regulator of mRNA splicing and highly expressed in the heart. Malat-1 modulates hypoxia-induced vessel growth, activates ERK/MAPK signaling, and scavenges the anti-hypertrophic microRNA-133. We therefore hypothesized that Malat-1 may act as regulator of cardiac hypertrophy and failure during cardiac pressure overload induced by thoracic aortic constriction (TAC) in mice.Absence of Malat-1 did not affect cardiac hypertrophy upon pressure overload: Heart weight to tibia length ratio significantly increased in WT mice (sham: 5.78±0.55, TAC 9.79±1.82 g/mm; p<0.001) but to a similar extend also in Malat-1 knockout (KO) mice (sham: 6.21±1.12, TAC 8.91±1.74 g/mm; p<0.01) with no significant difference between genotypes. As expected, TAC significantly reduced left ventricular fractional shortening in WT (sham: 38.81±6.53%, TAC: 23.14±11.99%; p<0.01) but to a comparable degree also in KO mice (sham: 37.01±4.19%, TAC: 25.98±9.75%; p<0.05). Histological hallmarks of myocardial remodeling, such as cardiomyocyte hypertrophy, increased interstitial fibrosis, reduced capillary density, and immune cell infiltration, did not differ significantly between WT and KO mice after TAC. In line, the absence of Malat-1 did not significantly affect angiotensin II-induced cardiac hypertrophy, dysfunction, and overall remodeling. Above that, pressure overload by TAC significantly induced mRNA levels of the hypertrophy marker genes Nppa, Nppb and Acta1, to a similar extend in both genotypes. Alternative splicing of Ndrg2 after TAC was apparent in WT (isoform ratio; sham: 2.97±0.26, TAC 1.57±0.40; p<0.0001) and KO mice (sham: 3.64±0.37; TAC: 2.24±0.76; p<0.0001) and interestingly differed between genotypes both at baseline and after pressure overload (p<0.05 each).These findings confirm a role for the lncRNA Malat-1 in mRNA splicing. However, no critical role for Malat-1 was found in pressure overload-induced heart failure in mice, despite its reported role in vascularization, ERK/MAPK signaling, and regulation of miR-133.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: BEND3 represses rDNA transcription by stabilizing a NoRC component via USP21 deubiquitinase

Khan, Abid / Sumanprava Giri / Yating Wang / Arindam Chakraborty / Archit K. Ghosh / Aparna Anantharaman / Vasudha Aggarwal / Kizhakke M. Sathyan / Taekjip Ha / Kannanganattu V. Prasanth / Supriya G. Prasanth

Proceedings of the National Academy of Sciences of the United States of America. 2015 July 7, v. 112, no. 27

2015

Abstract: Ribosome biogenesis dictates the translational capacity of cells. Several mechanisms establish and maintain transcriptional output from eukaryotic ribosomal DNA (rDNA) loci. rDNA silencing is one such mechanism that ensures the inactivity and hence the ... ...

Abstract	Ribosome biogenesis dictates the translational capacity of cells. Several mechanisms establish and maintain transcriptional output from eukaryotic ribosomal DNA (rDNA) loci. rDNA silencing is one such mechanism that ensures the inactivity and hence the maintenance of a silenced state of a subset of rRNA gene copies. Whereas oncogenic agents stimulate rRNA gene transcription, tumor suppressors decrease rRNA gene transcription. We demonstrate in mammalian cells that B ANP, E 5R, and N ac1 (BEN) domain 3 (BEND3), a quadruple BEN domain-containing protein, localizes in nucleoli and binds to ribosomal RNA gene promoters to help repress rRNA genes. Loss of BEND3 increases histone H3K4 trimethylation and, correspondingly, decreases rDNA promoter DNA methylation, consistent with a role for BEND3 in rDNA silencing. BEND3 associates with the nucleolar-remodeling complex (NoRC), and SUMOylated BEND3 stabilizes NoRC component TTF-1âinteracting protein 5 via association with ubiquitin specific protease 21 (USP21) debiquitinase. Our results provide mechanistic insights into how the novel rDNA transcription repressor BEND3 acts together with NoRC to actively coordinate the establishment of rDNA silencing.
Keywords	DNA methylation ; biogenesis ; cell nucleolus ; genes ; histones ; loci ; mammals ; proteinases ; ribosomal DNA ; ribosomal RNA ; ribosomes ; transcription (genetics) ; translation (genetics) ; ubiquitin ; BEND3 ; NoRC ; Tip5 ; transcription repression ; rDNA
Language	English
Dates of publication	2015-0707
Size	p. 8338-8343.
Publishing place	National Academy of Sciences
Document type	Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1424705112
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: The preRC protein ORCA organizes heterochromatin by assembling histone H3 lysine 9 methyltransferases on chromatin

Sumanprava Giri / Vasudha Aggarwal / Julien Pontis / Zhen Shen / Arindam Chakraborty / Abid Khan / Craig Mizzen / Kannanganattu V Prasanth / Slimane Ait-Si-Ali / Taekjip Ha / Supriya G Prasanth

eLife, Vol

2015 Volume 4

Abstract: Heterochromatic domains are enriched with repressive histone marks, including histone H3 lysine 9 methylation, written by lysine methyltransferases (KMTs). The pre-replication complex protein, origin recognition complex-associated (ORCA/LRWD1), ... ...

Abstract	Heterochromatic domains are enriched with repressive histone marks, including histone H3 lysine 9 methylation, written by lysine methyltransferases (KMTs). The pre-replication complex protein, origin recognition complex-associated (ORCA/LRWD1), preferentially localizes to heterochromatic regions in post-replicated cells. Its role in heterochromatin organization remained elusive. ORCA recognizes methylated H3K9 marks and interacts with repressive KMTs, including G9a/GLP and Suv39H1 in a chromatin context-dependent manner. Single-molecule pull-down assays demonstrate that ORCA-ORC (Origin Recognition Complex) and multiple H3K9 KMTs exist in a single complex and that ORCA stabilizes H3K9 KMT complex. Cells lacking ORCA show alterations in chromatin architecture, with significantly reduced H3K9 di- and tri-methylation at specific chromatin sites. Changes in heterochromatin structure due to loss of ORCA affect replication timing, preferentially at the late-replicating regions. We demonstrate that ORCA acts as a scaffold for the establishment of H3K9 KMT complex and its association and activity at specific chromatin sites is crucial for the organization of heterochromatin structure.
Keywords	ORCA/LRWD1 ; heterochromatin ; lysine methyl transferase ; single-molecule pull down ; replication ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2015-04-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A small protein encoded by a putative lncRNA regulates apoptosis and tumorigenicity in human colorectal cancer cells

Xiao Ling Li / Lőrinc Pongor / Wei Tang / Sudipto Das / Bruna R Muys / Matthew F Jones / Sarah B Lazar / Emily A Dangelmaier / Corrine CR Hartford / Ioannis Grammatikakis / Qinyu Hao / Qinyu Sun / Aaron Schetter / Jennifer L Martindale / BinWu Tang / Lisa M Jenkins / Ana I Robles / Robert L Walker / Stefan Ambs /

Raj Chari / Svetlana A Shabalina / Myriam Gorospe / S Perwez Hussain / Curtis C Harris / Paul S Meltzer / Kannanganattu V Prasanth / Mirit I Aladjem / Thorkell Andresson / Ashish Lal

eLife, Vol

2020 Volume 9

Abstract: Long noncoding RNAs (lncRNAs) are often associated with polysomes, indicating coding potential. However, only a handful of endogenous proteins encoded by putative lncRNAs have been identified and assigned a function. Here, we report the discovery of a ... ...

Abstract	Long noncoding RNAs (lncRNAs) are often associated with polysomes, indicating coding potential. However, only a handful of endogenous proteins encoded by putative lncRNAs have been identified and assigned a function. Here, we report the discovery of a putative gastrointestinal-tract-specific lncRNA (LINC00675) that is regulated by the pioneer transcription factor FOXA1 and encodes a conserved small protein of 79 amino acids which we termed FORCP (FOXA1-Regulated Conserved Small Protein). FORCP transcript is undetectable in most cell types but is abundant in well-differentiated colorectal cancer (CRC) cells where it functions to inhibit proliferation, clonogenicity, and tumorigenesis. The epitope-tagged and endogenous FORCP protein predominantly localizes to the endoplasmic reticulum (ER). In response to ER stress, FORCP depletion results in decreased apoptosis. Our findings on the initial characterization of FORCP demonstrate that FORCP is a novel, conserved small protein encoded by a mis-annotated lncRNA that regulates apoptosis and tumorigenicity in well-differentiated CRC cells.
Keywords	lncRNA ; ORF ; FOXA1 ; LINC00675 ; CRC ; micropeptide ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2020-10-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The S-phase-induced lncRNA SUNO1 promotes cell proliferation by controlling YAP1/Hippo signaling pathway

Qinyu Hao / Xinying Zong / Qinyu Sun / Yo-Chuen Lin / You Jin Song / Seyedsasan Hashemikhabir / Rosaline YC Hsu / Mohammad Kamran / Ritu Chaudhary / Vidisha Tripathi / Deepak Kumar Singh / Arindam Chakraborty / Xiao Ling Li / Yoon Jung Kim / Arturo V Orjalo / Maria Polycarpou-Schwarz / Branden S Moriarity / Lisa M Jenkins / Hans E Johansson /

Yuelin J Zhu / Sven Diederichs / Anindya Bagchi / Tae Hoon Kim / Sarath C Janga / Ashish Lal / Supriya G Prasanth / Kannanganattu V Prasanth

eLife, Vol

2020 Volume 9

Abstract: Cell cycle is a cellular process that is subject to stringent control. In contrast to the wealth of knowledge of proteins controlling the cell cycle, very little is known about the molecular role of lncRNAs (long noncoding RNAs) in cell-cycle progression. ...

Abstract	Cell cycle is a cellular process that is subject to stringent control. In contrast to the wealth of knowledge of proteins controlling the cell cycle, very little is known about the molecular role of lncRNAs (long noncoding RNAs) in cell-cycle progression. By performing genome-wide transcriptome analyses in cell-cycle-synchronized cells, we observed cell-cycle phase-specific induction of >2000 lncRNAs. Further, we demonstrate that an S-phase-upregulated lncRNA, SUNO1, facilitates cell-cycle progression by promoting YAP1-mediated gene expression. SUNO1 facilitates the cell-cycle-specific transcription of WTIP, a positive regulator of YAP1, by promoting the co-activator, DDX5-mediated stabilization of RNA polymerase II on chromatin. Finally, elevated SUNO1 levels are associated with poor cancer prognosis and tumorigenicity, implying its pro-survival role. Thus, we demonstrate the role of a S-phase up-regulated lncRNA in cell-cycle progression via modulating the expression of genes controlling cell proliferation.
Keywords	human cancer cell lines ; U2OS ; HCT116 ; lncRNA ; cell cycle ; WTIP ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2020-10-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Prosurvival long noncoding RNA PINCR regulates a subset of p53 targets in human colorectal cancer cells by binding to Matrin 3

Ritu Chaudhary / Berkley Gryder / Wendy S Woods / Murugan Subramanian / Matthew F Jones / Xiao Ling Li / Lisa M Jenkins / Svetlana A Shabalina / Min Mo / Mary Dasso / Yuan Yang / Lalage M Wakefield / Yuelin Zhu / Susan M Frier / Branden S Moriarity / Kannanganattu V Prasanth / Pablo Perez-Pinera / Ashish Lal

eLife, Vol

2017 Volume 6

Abstract: Thousands of long noncoding RNAs (lncRNAs) have been discovered, yet the function of the vast majority remains unclear. Here, we show that a p53-regulated lncRNA which we named PINCR (p53-induced noncoding RNA), is induced ~100-fold after DNA damage and ... ...

Abstract	Thousands of long noncoding RNAs (lncRNAs) have been discovered, yet the function of the vast majority remains unclear. Here, we show that a p53-regulated lncRNA which we named PINCR (p53-induced noncoding RNA), is induced ~100-fold after DNA damage and exerts a prosurvival function in human colorectal cancer cells (CRC) in vitro and tumor growth in vivo. Targeted deletion of PINCR in CRC cells significantly impaired G1 arrest and induced hypersensitivity to chemotherapeutic drugs. PINCR regulates the induction of a subset of p53 targets involved in G1 arrest and apoptosis, including BTG2, RRM2B and GPX1. Using a novel RNA pulldown approach that utilized endogenous S1-tagged PINCR, we show that PINCR associates with the enhancer region of these genes by binding to RNA-binding protein Matrin 3 that, in turn, associates with p53. Our findings uncover a critical prosurvival function of a p53/PINCR/Matrin 3 axis in response to DNA damage in CRC cells.
Keywords	p53 ; lncRNA ; Matrin 3 ; RP3-326I13.1 ; PINCR ; DNA damage ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	572
Language	English
Publishing date	2017-06-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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