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Article ; Online: APC

Tian, Yuhua / Wang, Xin / Cramer, Zvi / Rhoades, Joshua / Estep, Katrina N / Ma, Xianghui / Adams-Tzivelekidis, Stephanie / Katona, Bryson W / Johnson, F Brad / Yu, Zhengquan / Blanco, M Andres / Lengner, Christopher J / Li, Ning

Gut

2023 Volume 72, Issue 12, Page(s) 2294–2306

Abstract: Objective: Colorectal cancer (CRC) is a leading cause of cancer-related deaths, with the majority of cases initiated by inactivation of the APC tumour suppressor. This results in the constitutive activation of canonical WNT pathway transcriptional ... ...

Abstract	Objective: Colorectal cancer (CRC) is a leading cause of cancer-related deaths, with the majority of cases initiated by inactivation of the APC tumour suppressor. This results in the constitutive activation of canonical WNT pathway transcriptional effector ß-catenin, along with induction of WNT feedback inhibitors, including the extracellular palmitoleoyl-protein carboxylesterase NOTUM which antagonises WNT-FZD receptor-ligand interactions. Here, we sought to evaluate the effects of NOTUM activity on CRC as a function of driver mutation landscape. Design: Mouse and human colon organoids engineered with combinations of CRC driver mutations were used for Notum genetic gain-of-function and loss-of-function studies. In vitro assays, in vivo endoscope-guided orthotopic organoid implantation assays and transcriptomic profiling were employed to characterise the effects of Notum activity. Small molecule inhibitors of Notum activity were used in preclinical therapeutic proof-of-principle studies targeting oncogenic Notum activity. Results: NOTUM retains tumour suppressive activity in APC-null adenomas despite constitutive ß-catenin activity. Strikingly, on progression to adenocarcinoma with P53 loss, NOTUM becomes an obligate oncogene. These phenotypes are Wnt-independent, resulting from differential activity of NOTUM on glypican 1 and 4 in early-stage versus late-stage disease, respectively. Ultimately, preclinical mouse models and human organoid cultures demonstrate that pharmacological inhibition of NOTUM is highly effective in arresting primary adenocarcinoma growth and inhibiting metastatic colonisation of distal organs. Conclusions: Our findings that a single agent targeting the extracellular enzyme NOTUM is effective in treating highly aggressive, metastatic adenocarcinomas in preclinical mouse models and human organoids make NOTUM and its glypican targets therapeutic vulnerabilities in advanced CRC.
MeSH term(s)	Humans ; Mice ; Animals ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Mutation ; Wnt Signaling Pathway/genetics ; Catenins/genetics ; Catenins/metabolism ; Catenins/pharmacology ; Adenocarcinoma/drug therapy ; Adenocarcinoma/genetics
Chemical Substances	Tumor Suppressor Protein p53 ; Catenins
Language	English
Publishing date	2023-11-24
Publishing country	England
Document type	Journal Article
ZDB-ID	80128-8
ISSN	1468-3288 ; 0017-5749
ISSN (online)	1468-3288
ISSN	0017-5749
DOI	10.1136/gutjnl-2022-329140
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Article ; Online: Patient-Induced Pluripotent Stem Cell-Derived Hepatostellate Organoids Establish a Basis for Liver Pathologies in Telomeropathies.

Choi, Young-Jun / Kim, Melissa S / Rhoades, Joshua H / Johnson, Nicolette M / Berry, Corbett T / Root, Sarah / Chen, Qijun / Tian, Yuhua / Fernandez, Rafael J / Cramer, Zvi / Adams-Tzivelekidis, Stephanie / Li, Ning / Johnson, F Brad / Lengner, Christopher J

Cellular and molecular gastroenterology and hepatology

2023 Volume 16, Issue 3, Page(s) 451–472

Abstract: Background & aims: Dyskeratosis congenita (DC) is a telomere biology disorder caused primarily by mutations in the DKC1 gene. Patients with DC and related telomeropathies resulting from premature telomere dysfunction experience multiorgan failure. In ... ...

Abstract	Background & aims: Dyskeratosis congenita (DC) is a telomere biology disorder caused primarily by mutations in the DKC1 gene. Patients with DC and related telomeropathies resulting from premature telomere dysfunction experience multiorgan failure. In the liver, DC patients present with nodular hyperplasia, steatosis, inflammation, and cirrhosis. However, the mechanism responsible for telomere dysfunction-induced liver disease remains unclear. Methods: We used isogenic human induced pluripotent stem cells (iPSCs) harboring a causal DC mutation in DKC1 or a CRISPR/Cas9 (clustered regularly interspaced short palindromic repeats/Cas9)-corrected control allele to model DC liver pathologies. We differentiated these iPSCs into hepatocytes (HEPs) or hepatic stellate cells (HSCs) followed by generation of genotype-admixed hepatostellate organoids. Single-cell transcriptomics were applied to hepatostellate organoids to understand cell type-specific genotype-phenotype relationships. Results: Directed differentiation of iPSCs into HEPs and stellate cells and subsequent hepatostellate organoid formation revealed a dominant phenotype in the parenchyma, with DC HEPs becoming hyperplastic and also eliciting a pathogenic hyperplastic, proinflammatory response in stellate cells independent of stellate cell genotype. Pathogenic phenotypes in DKC1-mutant HEPs and hepatostellate organoids could be rescued via suppression of serine/threonine kinase AKT (protein kinase B) activity, a central regulator of MYC-driven hyperplasia downstream of DKC1 mutation. Conclusions: Isogenic iPSC-derived admixed hepatostellate organoids offer insight into the liver pathologies in telomeropathies and provide a framework for evaluating emerging therapies.
MeSH term(s)	Humans ; Induced Pluripotent Stem Cells ; Hyperplasia/pathology ; Liver/pathology ; Cell Differentiation/genetics ; Organoids/pathology ; Nuclear Proteins ; Cell Cycle Proteins/genetics
Chemical Substances	DKC1 protein, human ; Nuclear Proteins ; Cell Cycle Proteins
Language	English
Publishing date	2023-06-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2819778-1
ISSN	2352-345X ; 2352-345X
ISSN (online)	2352-345X
ISSN	2352-345X
DOI	10.1016/j.jcmgh.2023.06.003
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Article ; Online: Mapping and modeling human colorectal carcinoma interactions with the tumor microenvironment.

Nature communications

2023 Volume 14, Issue 1, Page(s) 7915

Abstract: The initiation and progression of cancer are intricately linked to the tumor microenvironment (TME). Understanding the function of specific cancer-TME interactions poses a major challenge due in part to the complexity of the in vivo microenvironment. ... ...

Abstract	The initiation and progression of cancer are intricately linked to the tumor microenvironment (TME). Understanding the function of specific cancer-TME interactions poses a major challenge due in part to the complexity of the in vivo microenvironment. Here we predict cancer-TME interactions from single cell transcriptomic maps of both human colorectal cancers (CRCs) and mouse CRC models, ask how these interactions are altered in human tumor organoid (tumoroid) cultures, and functionally recapitulate human myeloid-carcinoma interactions in vitro. Tumoroid cultures suppress gene expression programs involved in inflammation and immune cell migration, providing a reductive platform for re-establishing carcinoma-immune cell interactions in vitro. Introduction of human monocyte-derived macrophages into tumoroid cultures instructs macrophages to acquire immunosuppressive and pro-tumorigenic gene expression programs similar to those observed in vivo. This includes hallmark induction of SPP1, encoding Osteopontin, an extracellular CD44 ligand with established oncogenic effects. Taken together, these findings offer a framework for understanding CRC-TME interactions and provide a reductionist tool for modeling specific aspects of these interactions.
MeSH term(s)	Animals ; Mice ; Humans ; Tumor Microenvironment/genetics ; Macrophages/metabolism ; Carcinogenesis/pathology ; Colorectal Neoplasms/metabolism ; Carcinoma/metabolism
Language	English
Publishing date	2023-11-30
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-43746-6
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Article ; Online: LINGO3 regulates mucosal tissue regeneration and promotes TFF2 dependent recovery from colitis.

Zullo, Kelly M / Douglas, Bonnie / Maloney, Nicole M / Ji, Yingbiao / Wei, Yun / Herbine, Karl / Cohen, Rachel / Pastore, Christopher / Cramer, Zvi / Wang, Xin / Wei, Wenjie / Somsouk, Ma / Hung, Li Yin / Lengner, Christopher / Kohanski, Michael H / Cohen, Noam A / Herbert, De'Broski R

Scandinavian journal of gastroenterology

2021 Volume 56, Issue 7, Page(s) 791–805

Abstract: Aim: ...

Abstract	Aim:
MeSH term(s)	Colitis ; Humans ; Intestinal Mucosa ; Organoids ; Trefoil Factor-2 ; Wound Healing
Chemical Substances	TFF2 protein, human ; Trefoil Factor-2
Language	English
Publishing date	2021-05-03
Publishing country	England
Document type	Journal Article
ZDB-ID	82042-8
ISSN	1502-7708 ; 0036-5521
ISSN (online)	1502-7708
ISSN	0036-5521
DOI	10.1080/00365521.2021.1917650
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Article ; Online: Mapping and modeling human colorectal carcinoma interactions with the tumor microenvironment

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

2023 Volume 17

Abstract: Abstract The initiation and progression of cancer are intricately linked to the tumor microenvironment (TME). Understanding the function of specific cancer-TME interactions poses a major challenge due in part to the complexity of the in vivo ... ...

Abstract	Abstract The initiation and progression of cancer are intricately linked to the tumor microenvironment (TME). Understanding the function of specific cancer-TME interactions poses a major challenge due in part to the complexity of the in vivo microenvironment. Here we predict cancer-TME interactions from single cell transcriptomic maps of both human colorectal cancers (CRCs) and mouse CRC models, ask how these interactions are altered in human tumor organoid (tumoroid) cultures, and functionally recapitulate human myeloid-carcinoma interactions in vitro. Tumoroid cultures suppress gene expression programs involved in inflammation and immune cell migration, providing a reductive platform for re-establishing carcinoma-immune cell interactions in vitro. Introduction of human monocyte-derived macrophages into tumoroid cultures instructs macrophages to acquire immunosuppressive and pro-tumorigenic gene expression programs similar to those observed in vivo. This includes hallmark induction of SPP1, encoding Osteopontin, an extracellular CD44 ligand with established oncogenic effects. Taken together, these findings offer a framework for understanding CRC-TME interactions and provide a reductionist tool for modeling specific aspects of these interactions.
Keywords	Science ; Q
Language	English
Publishing date	2023-11-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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Article ; Online: Autophagic state prospectively identifies facultative stem cells in the intestinal epithelium.

EMBO reports

2022 Volume 23, Issue 11, Page(s) e55209

Abstract: The intestinal epithelium exhibits a rapid and efficient regenerative response to injury. Emerging evidence supports a model where plasticity of differentiated cells, particularly those in the secretory lineages, contributes to epithelial regeneration ... ...

Abstract	The intestinal epithelium exhibits a rapid and efficient regenerative response to injury. Emerging evidence supports a model where plasticity of differentiated cells, particularly those in the secretory lineages, contributes to epithelial regeneration upon ablation of injury-sensitive stem cells. However, such facultative stem cell activity is rare within secretory populations. Here, we ask whether specific functional properties predict facultative stem cell activity. We utilize in vivo labeling combined with ex vivo organoid formation assays to evaluate how cell age and autophagic state contribute to facultative stem cell activity within secretory lineages. Strikingly, we find that cell age (time elapsed since cell cycle exit) does not correlate with secretory cell plasticity. Instead, high autophagic vesicle content predicts plasticity and resistance to DNA damaging injury independently of cell lineage. Our findings indicate that autophagic status prior to injury serves as a lineage-agnostic marker for the prospective identification of facultative stem cells.
MeSH term(s)	Prospective Studies ; Stem Cells/metabolism ; Intestinal Mucosa ; Cell Lineage ; Cell Differentiation/genetics
Language	English
Publishing date	2022-09-19
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.15252/embr.202255209
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Zs.A 5433: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Oncofusion-driven de novo enhancer assembly promotes malignancy in Ewing sarcoma via aberrant expression of the stereociliary protein LOXHD1.

Deng, Qu / Natesan, Ramakrishnan / Cidre-Aranaz, Florencia / Arif, Shehbeel / Liu, Ying / Rasool, Reyaz Ur / Wang, Pei / Mitchell-Velasquez, Erick / Das, Chandan Kanta / Vinca, Endrit / Cramer, Zvi / Grohar, Patrick J / Chou, Margaret / Kumar-Sinha, Chandan / Weber, Kristy / Eisinger-Mathason, T S Karin / Grillet, Nicolas / Grünewald, Thomas G. P. / Asangani, Irfan A

Cell reports

2022 Volume 39, Issue 11, Page(s) 110971

Abstract: Ewing sarcoma (EwS) is a highly aggressive tumor of bone and soft tissues that mostly affects children and adolescents. The pathognomonic oncofusion EWSR1::FLI1 transcription factor drives EwS by orchestrating an oncogenic transcription program through ... ...

Abstract	Ewing sarcoma (EwS) is a highly aggressive tumor of bone and soft tissues that mostly affects children and adolescents. The pathognomonic oncofusion EWSR1::FLI1 transcription factor drives EwS by orchestrating an oncogenic transcription program through de novo enhancers. By integrative analysis of thousands of transcriptomes representing pan-cancer cell lines, primary cancers, metastasis, and normal tissues, we identify a 32-gene signature (ESS32 [Ewing Sarcoma Specific 32]) that stratifies EwS from pan-cancer. Among the ESS32, LOXHD1, encoding a stereociliary protein, is the most highly expressed gene through an alternative transcription start site. Deletion or silencing of EWSR1::FLI1 bound upstream de novo enhancer results in loss of the LOXHD1 short isoform, altering EWSR1::FLI1 and HIF1α pathway genes and resulting in decreased proliferation/invasion of EwS cells. These observations implicate LOXHD1 as a biomarker and a determinant of EwS metastasis and suggest new avenues for developing LOXHD1-targeted drugs or cellular therapies for this deadly disease.
MeSH term(s)	Adolescent ; Carrier Proteins/genetics ; Cell Line, Tumor ; Child ; Enhancer Elements, Genetic ; Gene Expression Regulation, Neoplastic ; Humans ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; Proteins/metabolism ; Proto-Oncogene Protein c-fli-1/genetics ; Proto-Oncogene Protein c-fli-1/metabolism ; RNA-Binding Protein EWS/genetics ; RNA-Binding Protein EWS/metabolism ; Sarcoma, Ewing/genetics ; Sarcoma, Ewing/pathology
Chemical Substances	Carrier Proteins ; LOXHD1 protein, human ; Oncogene Proteins, Fusion ; Proteins ; Proto-Oncogene Protein c-fli-1 ; RNA-Binding Protein EWS
Language	English
Publishing date	2022-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.110971
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Article ; Online: eIF4A inhibition prevents the onset of cytokine-induced muscle wasting by blocking the STAT3 and iNOS pathways.

Cramer, Zvi / Sadek, Jason / Vazquez, Gabriela Galicia / Di Marco, Sergio / Pause, Arnim / Pelletier, Jerry / Gallouzi, Imed-Eddine

Scientific reports

2018 Volume 8, Issue 1, Page(s) 8414

Abstract: Cachexia is a deadly muscle wasting syndrome that arises under conditions linked to chronic inflammation, such as cancer. Cytokines, including interferon γ (IFNγ), tumor necrosis factor α (TNFα) and interleukin-6 (IL-6), and their downstream effectors ... ...

Abstract	Cachexia is a deadly muscle wasting syndrome that arises under conditions linked to chronic inflammation, such as cancer. Cytokines, including interferon γ (IFNγ), tumor necrosis factor α (TNFα) and interleukin-6 (IL-6), and their downstream effectors such as Signal Transducer and Activator of Transcription 3 (STAT3), have been shown to play a prominent role in muscle wasting. Previously, we demonstrated that Pateamine A (PatA), a compound that targets eukaryotic initiation factor 4A (eIF4A), could prevent muscle wasting by modulating the translation of the inducible Nitric Oxide Synthase (iNOS) mRNA. Here we show that hippuristanol, a compound that impedes eIF4A in a manner distinct from PatA, similarly inhibits the iNOS/NO pathway and cytokine-induced muscle wasting. Furthermore, we show that hippuristanol perturbs the activation of the STAT3 pathway and expression of STAT3-gene targets such as IL-6. The decreased activation of STAT3, which resulted from a decrease in STAT3 protein expression, was due to the inhibition of STAT3 translation as there were no changes in STAT3 mRNA levels. These effects are likely dependent on the inhibition of eIF4A activity since we observed similar results using PatA. Our results identify the inhibition of eIF4A-responsive transcripts, such as STAT3, as a viable approach to alleviate cachexia.
MeSH term(s)	Allosteric Regulation/drug effects ; Animals ; Cell Line ; Cytokines/pharmacology ; Epoxy Compounds/pharmacology ; Eukaryotic Initiation Factor-4A/antagonists & inhibitors ; Interleukin-6/metabolism ; Macrolides/pharmacology ; Mice ; Muscle Fibers, Skeletal/drug effects ; Muscle Fibers, Skeletal/metabolism ; Muscle Fibers, Skeletal/pathology ; Muscular Atrophy/chemically induced ; Muscular Atrophy/metabolism ; Muscular Atrophy/pathology ; Muscular Atrophy/prevention & control ; Nitric Oxide Synthase Type II/metabolism ; STAT3 Transcription Factor/metabolism ; Sterols/pharmacology ; Thiazoles/pharmacology
Chemical Substances	Cytokines ; Epoxy Compounds ; Interleukin-6 ; Macrolides ; STAT3 Transcription Factor ; Sterols ; Thiazoles ; hippuristanol ; pateamine A ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Eukaryotic Initiation Factor-4A (EC 2.7.7.-)
Language	English
Publishing date	2018-05-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-26625-9
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Article ; Online: Oncofusion-driven de novo enhancer assembly promotes malignancy in Ewing sarcoma via aberrant expression of the stereociliary protein LOXHD1

Qu Deng / Ramakrishnan Natesan / Florencia Cidre-Aranaz / Shehbeel Arif / Ying Liu / Reyaz ur Rasool / Pei Wang / Erick Mitchell-Velasquez / Chandan Kanta Das / Endrit Vinca / Zvi Cramer / Patrick J. Grohar / Margaret Chou / Chandan Kumar-Sinha / Kristy Weber / T.S. Karin Eisinger-Mathason / Nicolas Grillet / Thomas Grünewald / Irfan A. Asangani

Cell Reports, Vol 39, Iss 11, Pp 110971- (2022)

2022

Abstract: Summary: Ewing sarcoma (EwS) is a highly aggressive tumor of bone and soft tissues that mostly affects children and adolescents. The pathognomonic oncofusion EWSR1::FLI1 transcription factor drives EwS by orchestrating an oncogenic transcription program ... ...

Abstract	Summary: Ewing sarcoma (EwS) is a highly aggressive tumor of bone and soft tissues that mostly affects children and adolescents. The pathognomonic oncofusion EWSR1::FLI1 transcription factor drives EwS by orchestrating an oncogenic transcription program through de novo enhancers. By integrative analysis of thousands of transcriptomes representing pan-cancer cell lines, primary cancers, metastasis, and normal tissues, we identify a 32-gene signature (ESS32 [Ewing Sarcoma Specific 32]) that stratifies EwS from pan-cancer. Among the ESS32, LOXHD1, encoding a stereociliary protein, is the most highly expressed gene through an alternative transcription start site. Deletion or silencing of EWSR1::FLI1 bound upstream de novo enhancer results in loss of the LOXHD1 short isoform, altering EWSR1::FLI1 and HIF1α pathway genes and resulting in decreased proliferation/invasion of EwS cells. These observations implicate LOXHD1 as a biomarker and a determinant of EwS metastasis and suggest new avenues for developing LOXHD1-targeted drugs or cellular therapies for this deadly disease.
Keywords	CP: Cancer ; CP: Molecular biology ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: β-Hydroxybutyrate suppresses colorectal cancer.

Dmitrieva-Posocco, Oxana / Wong, Andrea C / Lundgren, Patrick / Golos, Aleksandra M / Descamps, Hélène C / Dohnalová, Lenka / Cramer, Zvi / Tian, Yuhua / Yueh, Brian / Eskiocak, Onur / Egervari, Gabor / Lan, Yemin / Liu, Jinping / Fan, Jiaxin / Kim, Jihee / Madhu, Bhoomi / Schneider, Kai Markus / Khoziainova, Svetlana / Andreeva, Natalia /

Wang, Qiaohong / Li, Ning / Furth, Emma E / Bailis, Will / Kelsen, Judith R / Hamilton, Kathryn E / Kaestner, Klaus H / Berger, Shelley L / Epstein, Jonathan A / Jain, Rajan / Li, Mingyao / Beyaz, Semir / Lengner, Christopher J / Katona, Bryson W / Grivennikov, Sergei I / Thaiss, Christoph A / Levy, Maayan

Nature

2022 Volume 605, Issue 7908, Page(s) 160–165

Abstract: Colorectal cancer (CRC) is among the most frequent forms of cancer, and new strategies for its prevention and therapy are urgently ... ...

Abstract	Colorectal cancer (CRC) is among the most frequent forms of cancer, and new strategies for its prevention and therapy are urgently needed
MeSH term(s)	3-Hydroxybutyric Acid/metabolism ; 3-Hydroxybutyric Acid/pharmacology ; Animals ; Cell Proliferation ; Cell Transformation, Neoplastic ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/prevention & control ; Humans ; Signal Transduction
Chemical Substances	3-Hydroxybutyric Acid (TZP1275679)
Language	English
Publishing date	2022-04-27
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-022-04649-6
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