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Article ; Online: TREM1 activation of myeloid cells promotes antitumor immunity.

Juric, Vladislava / Mayes, Erin / Binnewies, Mikhail / Lee, Tian / Canaday, Pamela / Pollack, Joshua L / Rudolph, Joshua / Du, Xiaoyan / Liu, Victoria M / Dash, Subhadra / Palmer, Rachael / Jahchan, Nadine S / Ramoth, Åsa Johanna / Lacayo, Sergio / Mankikar, Shilpa / Norng, Manith / Brassell, Chris / Pal, Aritra / Chan, Christopher /

Lu, Erick / Sriram, Venkataraman / Streuli, Michel / Krummel, Matthew F / Baker, Kevin P / Liang, Linda

Science translational medicine

2023 Volume 15, Issue 711, Page(s) eadd9990

Abstract: Myeloid cells in the tumor microenvironment (TME) can exist in immunosuppressive and immunostimulatory states that impede or promote antitumor immunity, respectively. Blocking suppressive myeloid cells or increasing stimulatory cells to enhance antitumor ...

Abstract	Myeloid cells in the tumor microenvironment (TME) can exist in immunosuppressive and immunostimulatory states that impede or promote antitumor immunity, respectively. Blocking suppressive myeloid cells or increasing stimulatory cells to enhance antitumor immune responses is an area of interest for therapeutic intervention. Triggering receptor expressed on myeloid cells-1 (TREM1) is a proinflammatory receptor that amplifies immune responses. TREM1 is expressed on neutrophils, subsets of monocytes and tissue macrophages, and suppressive myeloid populations in the TME, including tumor-associated neutrophils, monocytes, and tumor-associated macrophages. Depletion or inhibition of immunosuppressive myeloid cells, or stimulation by TREM1-mediated inflammatory signaling, could be used to promote an immunostimulatory TME. We developed PY159, an afucosylated humanized anti-TREM1 monoclonal antibody with enhanced FcγR binding. PY159 is a TREM1 agonist that induces signaling, leading to up-regulation of costimulatory molecules on monocytes and macrophages, production of proinflammatory cytokines and chemokines, and enhancement of T cell activation in vitro. An antibody against mouse TREM1, PY159m, promoted antitumor efficacy in syngeneic mouse tumor models. These results suggest that PY159-mediated agonism of TREM1 on tumoral myeloid cells can promote a proinflammatory TME and offer a promising strategy for immunotherapy.
MeSH term(s)	Animals ; Mice ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal/therapeutic use ; Disease Models, Animal ; Immunosuppressive Agents ; Macrophages ; Monocytes ; Myeloid Cells ; Triggering Receptor Expressed on Myeloid Cells-1
Chemical Substances	Antibodies, Monoclonal ; Immunosuppressive Agents ; Triggering Receptor Expressed on Myeloid Cells-1 ; TREM1 protein, mouse
Language	English
Publishing date	2023-08-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.add9990
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Article ; Online: Tuning the Tumor Myeloid Microenvironment to Fight Cancer.

Jahchan, Nadine S / Mujal, Adriana M / Pollack, Joshua L / Binnewies, Mikhail / Sriram, Venkataraman / Reyno, Leonard / Krummel, Matthew F

Frontiers in immunology

2019 Volume 10, Page(s) 1611

Abstract: The tumor microenvironment (TME) of diverse cancer types is often characterized by high levels of infiltrating myeloid cells including monocytes, macrophages, dendritic cells, and granulocytes. These cells perform a variety of functions in the TME, ... ...

Abstract	The tumor microenvironment (TME) of diverse cancer types is often characterized by high levels of infiltrating myeloid cells including monocytes, macrophages, dendritic cells, and granulocytes. These cells perform a variety of functions in the TME, varying from immune suppressive to immune stimulatory roles. In this review, we summarize the different myeloid cell populations in the TME and the intratumoral myeloid targeting approaches that are being clinically investigated, and discuss strategies that identify new myeloid subpopulations within the TME. The TME therapies include agents that modulate the functional activities of myeloid populations, that impact recruitment and survival of myeloid subpopulations, and that functionally reprogram or activate myeloid populations. We discuss the benefits, limitations and potential side effects of these therapeutic approaches.
MeSH term(s)	Animals ; Biomarkers ; Cell Differentiation ; Cell Proliferation ; Cell Survival ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Humans ; Immunomodulation ; Macrophages/immunology ; Macrophages/metabolism ; Monocytes/immunology ; Monocytes/metabolism ; Myeloid Cells/immunology ; Myeloid Cells/metabolism ; Neoplasms/etiology ; Neoplasms/pathology ; Neutrophils/immunology ; Neutrophils/metabolism ; Tumor Microenvironment/immunology
Chemical Substances	Biomarkers
Language	English
Publishing date	2019-07-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.01611
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Article ; Online: SnoN in mammalian development, function and diseases.

Jahchan, Nadine S / Luo, Kunxin

Current opinion in pharmacology

2010 Volume 10, Issue 6, Page(s) 670–675

Abstract: SnoN (Ski-novel protein) was discovered as a nuclear proto-oncogene on the basis of its ability to induce transformation of chicken and quail embryonic fibroblasts. As a crucial negative regulator of transforming growth factor-β (TGF-β) signaling and ... ...

Abstract	SnoN (Ski-novel protein) was discovered as a nuclear proto-oncogene on the basis of its ability to induce transformation of chicken and quail embryonic fibroblasts. As a crucial negative regulator of transforming growth factor-β (TGF-β) signaling and also an activator of p53, it plays an important role in regulating cell proliferation, senescence, apoptosis, and differentiation. Recent studies of its expression patterns and functions in mouse models and mammalian cells have revealed important functions of SnoN in normal epithelial development and tumorigenesis. Evidence suggests that SnoN has both pro-oncogenic and anti-oncogenic functions by modulating multiple signaling pathways. These studies suggest that SnoN may have broad functions in the development and homeostasis of embryonic and postnatal tissues.
MeSH term(s)	Animals ; Cell Transformation, Neoplastic/genetics ; Embryonic Development ; Female ; Gene Expression Regulation ; Genes, p53 ; Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Mice ; Molecular Targeted Therapy ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogenes ; Signal Transduction/genetics ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Trans-Activators/physiology ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/metabolism
Chemical Substances	Intracellular Signaling Peptides and Proteins ; Proto-Oncogene Proteins ; SKIL protein, human ; Trans-Activators ; Transforming Growth Factor beta
Language	English
Publishing date	2010-09-06
Publishing country	England
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	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2010.08.006
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Article ; Online: Expression profiles of SnoN in normal and cancerous human tissues support its tumor suppressor role in human cancer.

Jahchan, Nadine S / Ouyang, Gaoliang / Luo, Kunxin

PloS one

2013 Volume 8, Issue 2, Page(s) e55794

Abstract: SnoN is a negative regulator of TGF-β signaling and also an activator of the tumor suppressor p53 in response to cellular stress. Its role in human cancer is complex and controversial with both pro-oncogenic and anti-oncogenic activities reported. To ... ...

Abstract	SnoN is a negative regulator of TGF-β signaling and also an activator of the tumor suppressor p53 in response to cellular stress. Its role in human cancer is complex and controversial with both pro-oncogenic and anti-oncogenic activities reported. To clarify its role in human cancer and provide clinical relevance to its signaling activities, we examined SnoN expression in normal and cancerous human esophageal, ovarian, pancreatic and breast tissues. In normal tissues, SnoN is expressed in both the epithelium and the surrounding stroma at a moderate level and is predominantly cytoplasmic. SnoN levels in all tumor epithelia examined are lower than or similar to that in the matched normal samples, consistent with its anti-tumorigenic activity in epithelial cells. In contrast, SnoN expression in the stroma is highly upregulated in the infiltrating inflammatory cells in high-grade esophageal and ovarian tumor samples, suggesting that SnoN may potentially promote malignant progression through modulating the tumor microenvironment in these tumor types. The overall levels of SnoN expression in these cancer tissues do not correlate with the p53 status. However, in human cancer cell lines with amplification of the snoN gene, a strong correlation between increased SnoN copy number and inactivation of p53 was detected, suggesting that the tumor suppressor SnoN-p53 pathway must be inactivated, either through downregulation of SnoN or inactivation of p53, in order to allow cancer cell to proliferate and survive. These data strongly suggest that SnoN can function as a tumor suppressor at early stages of tumorigenesis in human cancer tissues.
MeSH term(s)	Adult ; Breast/metabolism ; Breast/pathology ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Disease Progression ; Esophageal Neoplasms/genetics ; Esophageal Neoplasms/metabolism ; Esophageal Neoplasms/pathology ; Esophagus/metabolism ; Esophagus/pathology ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Middle Aged ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/metabolism ; Ovarian Neoplasms/pathology ; Ovary/metabolism ; Ovary/pathology ; Pancreas/metabolism ; Pancreas/pathology ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Signal Transduction/physiology ; Transforming Growth Factor beta/metabolism ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Intracellular Signaling Peptides and Proteins ; Proto-Oncogene Proteins ; SKIL protein, human ; Transforming Growth Factor beta ; Tumor Suppressor Protein p53
Language	English
Publishing date	2013-02-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0055794
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Article ; Online: A PHASE IIA STUDY REPOSITIONING DESIPRAMINE IN SMALL CELL LUNG CANCER AND OTHER HIGH-GRADE NEUROENDOCRINE TUMORS.

Riess, Jonathan W / Jahchan, Nadine S / Das, Millie / Zach Koontz, M / Kunz, Pamela L / Wakelee, Heather A / Schatzberg, Alan / Sage, Julien / Neal, Joel W

Cancer treatment and research communications

2020 Volume 23, Page(s) 100174

Abstract: Background: A bioinformatics approach identified antitumor effects of tricyclic antidepressants (TCAs) in small cell lung cancer (SCLC) and other high-grade neuroendocrine carcinomas (grade 3 neuroendocrine carcinomas) (G3NEC) that was subsequently ... ...

Abstract	Background: A bioinformatics approach identified antitumor effects of tricyclic antidepressants (TCAs) in small cell lung cancer (SCLC) and other high-grade neuroendocrine carcinomas (grade 3 neuroendocrine carcinomas) (G3NEC) that was subsequently validated in preclinical models with a putative mechanism of action via inhibition of neuroendocrine signaling pathways. This study was undertaken to reposition the candidate TCA desipramine in a clinical trial in SCLC and G3NEC. Methods: In this prospective, phase IIa intrapatient dose escalation clinical trial, patients were required to have failed at least one prior chemotherapy for metastatic SCLC or G3NEC. Treatment with desipramine began at 75 mg nightly with escalation in increments of 75 mg weekly to a maximum of 450 mg daily. Results: Six patients were enrolled, 3 with SCLC, and 3 with G3NEC (lung, rectal, and pancreas). Tolerability of desipramine was worse than predicted. Of the 6 patients enrolled: 1 patient achieved 300 mg daily, 2 patients reached 150 mg daily, 1 patient reached 75 mg daily, and 2 patients were unable to tolerate any stable dose. Reasons for discontinuation included drug-related grade 3 colon pseudo-obstruction, unrelated GI bleed, and grade 1-2 neurocognitive adverse events. Median clinical or radiographic progression free survival was 1.2 months (range 0.2-3.3) and median overall survival from study entry was 2.7 months (range 1.3-5.6). Conclusions: No clinical or radiographic benefit was observed using desipramine to treat SCLC and G3NEC, so this trial was terminated. Intolerable low and medium grade neurocognitive side effects led to intermittent treatment and early discontinuation in most patients; given this limitation, doses achieved may be inadequate compared to the preclinical studies. Microabstract: A bioinformatics approach previously identified a potential antitumor effect of tricyclic antidepressants (TCAs) in small cell lung cancer (SCLC) and other high-grade neuroendocrine carcinomas (grade 3 neuroendocrine carcinoma) (G3NEC), which was validated in preclinical models. In this prospective, phase IIa clinical trial, patients were required to have failed at least one prior chemotherapy for metastatic SCLC or G3NEC (Ki-67 ≥ 20% or ≥ 20 mitoses/10 HPF). Treatment with desipramine began at 75 mg nightly with escalation by 75 mg weekly to a maximum dose of 450 mg daily. Six patients were enrolled on this clinical trial, 3 with SCLC, and 3 with G3NEC (lung, rectal, and pancreatic). Tolerability of desipramine was worse than predicted. In the 6 patients enrolled: 1 patient achieved 300 mg daily, 2 patients reached 150 mg daily, 1 patient reached 75 mg daily, and 2 patients were unable to tolerate any stable dose. Reasons for discontinuation included drug-related grade 3 colon pseudo-obstruction, unrelated GI bleed, and grade 1-2 drug related dizziness, confusion, and somnolence. Though numbers are small, median clinical or radiographic progression free survival was 1.2 months (range 0.2-3.3) and median overall survival from study entry was 2.7 months (range 1.3-5.6). Although preclinical evidence was promising, no clinical or radiographic benefit was observed using desipramine to treat SCLC and G3NEC, so this trial was terminated.
Language	English
Publishing date	2020-04-20
Publishing country	England
Document type	Journal Article
ISSN	2468-2942
ISSN (online)	2468-2942
DOI	10.1016/j.ctarc.2020.100174
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Article ; Online: Expression profiles of SnoN in normal and cancerous human tissues support its tumor suppressor role in human cancer.

Nadine S Jahchan / Gaoliang Ouyang / Kunxin Luo

PLoS ONE, Vol 8, Iss 2, p e

2013 Volume 55794

Abstract	SnoN is a negative regulator of TGF-β signaling and also an activator of the tumor suppressor p53 in response to cellular stress. Its role in human cancer is complex and controversial with both pro-oncogenic and anti-oncogenic activities reported. To clarify its role in human cancer and provide clinical relevance to its signaling activities, we examined SnoN expression in normal and cancerous human esophageal, ovarian, pancreatic and breast tissues. In normal tissues, SnoN is expressed in both the epithelium and the surrounding stroma at a moderate level and is predominantly cytoplasmic. SnoN levels in all tumor epithelia examined are lower than or similar to that in the matched normal samples, consistent with its anti-tumorigenic activity in epithelial cells. In contrast, SnoN expression in the stroma is highly upregulated in the infiltrating inflammatory cells in high-grade esophageal and ovarian tumor samples, suggesting that SnoN may potentially promote malignant progression through modulating the tumor microenvironment in these tumor types. The overall levels of SnoN expression in these cancer tissues do not correlate with the p53 status. However, in human cancer cell lines with amplification of the snoN gene, a strong correlation between increased SnoN copy number and inactivation of p53 was detected, suggesting that the tumor suppressor SnoN-p53 pathway must be inactivated, either through downregulation of SnoN or inactivation of p53, in order to allow cancer cell to proliferate and survive. These data strongly suggest that SnoN can function as a tumor suppressor at early stages of tumorigenesis in human cancer tissues.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2013-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Axon-like protrusions promote small cell lung cancer migration and metastasis.

Yang, Dian / Qu, Fangfei / Cai, Hongchen / Chuang, Chen-Hua / Lim, Jing Shan / Jahchan, Nadine / Grüner, Barbara M / S Kuo, Christin / Kong, Christina / Oudin, Madeleine J / Winslow, Monte M / Sage, Julien

eLife

2019 Volume 8

Abstract: Metastasis is the main cause of death in cancer patients but remains a poorly understood process. Small cell lung cancer (SCLC) is one of the most lethal and most metastatic cancer types. SCLC cells normally express neuroendocrine and neuronal gene ... ...

Abstract	Metastasis is the main cause of death in cancer patients but remains a poorly understood process. Small cell lung cancer (SCLC) is one of the most lethal and most metastatic cancer types. SCLC cells normally express neuroendocrine and neuronal gene programs but accumulating evidence indicates that these cancer cells become relatively more neuronal and less neuroendocrine as they gain the ability to metastasize. Here we show that mouse and human SCLC cells in culture and in vivo can grow cellular protrusions that resemble axons. The formation of these protrusions is controlled by multiple neuronal factors implicated in axonogenesis, axon guidance, and neuroblast migration. Disruption of these axon-like protrusions impairs cell migration in culture and inhibits metastatic ability in vivo. The co-option of developmental neuronal programs is a novel molecular and cellular mechanism that contributes to the high metastatic ability of SCLC.
MeSH term(s)	Animals ; Cell Movement ; Cell Surface Extensions/metabolism ; Humans ; Lung Neoplasms/physiopathology ; Mice ; Neoplasm Metastasis/physiopathology ; Small Cell Lung Carcinoma/physiopathology ; Tumor Cells, Cultured
Language	English
Publishing date	2019-12-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.50616
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Article ; Online: SnoN regulates mammary gland alveologenesis and onset of lactation by promoting prolactin/Stat5 signaling.

Jahchan, Nadine S / Wang, Douglas / Bissell, Mina J / Luo, Kunxin

Development (Cambridge, England)

2012 Volume 139, Issue 17, Page(s) 3147–3156

Abstract: Mammary epithelial cells undergo structural and functional differentiation at late pregnancy and parturition to produce and secrete milk. Both TGF-β and prolactin pathways are crucial regulators of this process. However, how the activities of these two ... ...

Abstract	Mammary epithelial cells undergo structural and functional differentiation at late pregnancy and parturition to produce and secrete milk. Both TGF-β and prolactin pathways are crucial regulators of this process. However, how the activities of these two antagonistic pathways are orchestrated to initiate lactation has not been well defined. Here, we show that SnoN, a negative regulator of TGF-β signaling, coordinates TGF-β and prolactin signaling to control alveologenesis and lactogenesis. SnoN expression is induced at late pregnancy by the coordinated actions of TGF-β and prolactin. The elevated SnoN promotes Stat5 signaling by enhancing its stability, thereby sharply increasing the activity of prolactin signaling at the onset of lactation. SnoN-/- mice display severe defects in alveologenesis and lactogenesis, and mammary epithelial cells from these mice fail to undergo proper morphogenesis. These defects can be rescued by an active Stat5. Thus, our study has identified a new player in the regulation of milk production and revealed a novel function of SnoN in mammary alveologenesis and lactogenesis in vivo through promotion of Stat5 signaling.
MeSH term(s)	Animals ; Blotting, Western ; Cell Differentiation/physiology ; Cells, Cultured ; DNA Primers/genetics ; Female ; Gene Expression Regulation, Developmental/physiology ; Immunohistochemistry ; Lactation/physiology ; Mammary Glands, Animal/cytology ; Mammary Glands, Animal/growth & development ; Mice ; Mice, Knockout ; Pregnancy ; Prolactin/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; STAT5 Transcription Factor/metabolism ; Signal Transduction/physiology ; Transforming Growth Factor beta/metabolism
Chemical Substances	DNA Primers ; Proto-Oncogene Proteins ; STAT5 Transcription Factor ; Skil protein, mouse ; Transforming Growth Factor beta ; Prolactin (9002-62-4)
Language	English
Publishing date	2012-07-25
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	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.079616
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Article ; Online: Targeting TREM2 on tumor-associated macrophages enhances immunotherapy.

Cell reports

2021 Volume 37, Issue 3, Page(s) 109844

Abstract: Converting checkpoint inhibitor (CPI)-resistant individuals to being responsive requires identifying suppressive mechanisms. We identify ... ...

Abstract	Converting checkpoint inhibitor (CPI)-resistant individuals to being responsive requires identifying suppressive mechanisms. We identify TREM2
MeSH term(s)	Animals ; Antineoplastic Agents, Immunological/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; CD8-Positive T-Lymphocytes/drug effects ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Cell Line, Tumor ; Coculture Techniques ; Drug Resistance, Neoplasm ; Female ; HEK293 Cells ; Humans ; Immune Checkpoint Inhibitors/pharmacology ; Lymphocyte Activation/drug effects ; Lymphocytes, Tumor-Infiltrating/drug effects ; Lymphocytes, Tumor-Infiltrating/immunology ; Lymphocytes, Tumor-Infiltrating/metabolism ; Membrane Glycoproteins/antagonists & inhibitors ; Membrane Glycoproteins/metabolism ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neoplasms/drug therapy ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/pathology ; Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Programmed Cell Death 1 Receptor/immunology ; Programmed Cell Death 1 Receptor/metabolism ; Receptors, Immunologic/antagonists & inhibitors ; Receptors, Immunologic/metabolism ; Signal Transduction ; Tumor Cells, Cultured ; Tumor Microenvironment ; Tumor-Associated Macrophages/drug effects ; Tumor-Associated Macrophages/immunology ; Tumor-Associated Macrophages/metabolism ; Mice
Chemical Substances	Antineoplastic Agents, Immunological ; Immune Checkpoint Inhibitors ; Membrane Glycoproteins ; PDCD1 protein, human ; Pdcd1 protein, mouse ; Programmed Cell Death 1 Receptor ; Receptors, Immunologic ; TREM2 protein, human ; Trem2 protein, mouse
Language	English
Publishing date	2021-10-19
Publishing country	United States
Document type	Journal Article ; 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.2021.109844
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Article ; Online: Axon-like protrusions promote small cell lung cancer migration and metastasis

Dian Yang / Fangfei Qu / Hongchen Cai / Chen-Hua Chuang / Jing Shan Lim / Nadine Jahchan / Barbara M Grüner / Christin S Kuo / Christina Kong / Madeleine J Oudin / Monte M Winslow / Julien Sage

eLife, Vol

2019 Volume 8

Abstract	Metastasis is the main cause of death in cancer patients but remains a poorly understood process. Small cell lung cancer (SCLC) is one of the most lethal and most metastatic cancer types. SCLC cells normally express neuroendocrine and neuronal gene programs but accumulating evidence indicates that these cancer cells become relatively more neuronal and less neuroendocrine as they gain the ability to metastasize. Here we show that mouse and human SCLC cells in culture and in vivo can grow cellular protrusions that resemble axons. The formation of these protrusions is controlled by multiple neuronal factors implicated in axonogenesis, axon guidance, and neuroblast migration. Disruption of these axon-like protrusions impairs cell migration in culture and inhibits metastatic ability in vivo. The co-option of developmental neuronal programs is a novel molecular and cellular mechanism that contributes to the high metastatic ability of SCLC.
Keywords	SCLC ; neuroendocrine ; neuronal ; protrusions ; migration ; metastasis ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2019-12-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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