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Article ; Online: MEK inhibition invigorates chemoimmunotherapy by tumor mitophagy-induced CXCL10 expression.

Rodriguez, B Leticia / Gibbons, Don L

Cell reports. Medicine

2022 Volume 3, Issue 1, Page(s) 100506

Abstract: A recent study by Limagne et al. ...

Abstract	A recent study by Limagne et al.
MeSH term(s)	Chemokine CXCL10 ; Humans ; Immunotherapy ; Mitogen-Activated Protein Kinase Kinases ; Mitophagy ; Neoplasms/drug therapy ; T-Lymphocytes
Chemical Substances	CXCL10 protein, human ; Chemokine CXCL10 ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
Language	English
Publishing date	2022-01-18
Publishing country	United States
Document type	Journal Article ; Comment
ISSN	2666-3791
ISSN (online)	2666-3791
DOI	10.1016/j.xcrm.2021.100506
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Article ; Online: ZEB1 Is Regulated by K811 Acetylation to Promote Stability, NuRD Complex Interactions, EMT, and NSCLC Metastasis.

Perez-Oquendo, Mabel / Manshouri, Roxsan / Tian, Yanhua / Fradette, Jared J / Rodriguez, B Leticia / Kundu, Samrat T / Gibbons, Don L

Molecular cancer research : MCR

2023 Volume 21, Issue 8, Page(s) 779–794

Abstract: Epithelial-to-mesenchymal transition results in loss of specialized epithelial cell contacts and acquisition of mesenchymal invasive capacity. The transcription repressor zinc finger E-box-binding homeobox 1 (ZEB1) binds to E-boxes of gene promoter ... ...

Abstract	Epithelial-to-mesenchymal transition results in loss of specialized epithelial cell contacts and acquisition of mesenchymal invasive capacity. The transcription repressor zinc finger E-box-binding homeobox 1 (ZEB1) binds to E-boxes of gene promoter regions to suppress the expression of epithelial genes. ZEB1 has inconsistent molecular weights, which have been attributed to posttranslational modifications (PTM). We performed mass spectrometry and identified K811 acetylation as a novel PTM in ZEB1. To define the role of ZEB1 acetylation in regulating function, we generated ZEB1 acetyl-mimetic (K811Q) and acetyl-deficient (K811R) mutant-expressing non-small cell lung cancer cell lines (NSCLC). We demonstrate that the K811R ZEB1 (125 kDa) has a shorter protein half-life than wild-type (WT) ZEB1 and K811Q ZEB1 (∼225 kDa), suggesting that lack of ZEB1 acetylation in the lower molecular weight form affects protein stability. Further, the acetylated form of ZEB1 recruits the nucleosome remodeling and deacetylase (NuRD) complex to bind the promoter of its target genes mir200c-141 and SEMA3F. RNA-sequencing revealed that WT ZEB1 and K811Q ZEB1 downregulate the expression of epithelial genes to promote lung adenocarcinoma invasion and metastasis, whereas the K811R ZEB1 does not. Our findings establish that the K811 acetylation promotes ZEB1 protein stability, interaction with other protein complexes, and subsequent invasion/metastasis of lung adenocarcinoma via epithelial-to-mesenchymal transition. Implications: The molecular mechanisms by which ZEB1 is regulated by K811 acetylation to promote protein stability, NuRD complex and promoter interactions, and function are relevant to the development of treatment strategies to prevent and treat metastasis in patients with NSCLC.
MeSH term(s)	Humans ; Lung Neoplasms/pathology ; Carcinoma, Non-Small-Cell Lung/metabolism ; Mi-2 Nucleosome Remodeling and Deacetylase Complex/genetics ; Mi-2 Nucleosome Remodeling and Deacetylase Complex/metabolism ; Acetylation ; Zinc Finger E-box-Binding Homeobox 1/genetics ; Zinc Finger E-box-Binding Homeobox 1/metabolism ; Protein Processing, Post-Translational ; Adenocarcinoma of Lung/genetics ; Epithelial-Mesenchymal Transition/genetics ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Membrane Proteins/genetics ; Nerve Tissue Proteins/genetics
Chemical Substances	Mi-2 Nucleosome Remodeling and Deacetylase Complex (EC 3.5.1.98) ; Zinc Finger E-box-Binding Homeobox 1 ; ZEB1 protein, human ; SEMA3F protein, human ; Membrane Proteins ; Nerve Tissue Proteins
Language	English
Publishing date	2023-05-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-22-0503
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Zs.A 5744: Show issues

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Article ; Online: Autotaxin suppresses cytotoxic T cells via LPAR5 to promote anti-PD-1 resistance in non-small cell lung cancer.

Konen, Jessica M / Rodriguez, B Leticia / Wu, Haoyi / Fradette, Jared J / Gibson, Laura / Diao, Lixia / Wang, Jing / Schmidt, Stephanie / Wistuba, Ignacio I / Zhang, Jianjun / Gibbons, Don L

The Journal of clinical investigation

2023 Volume 133, Issue 17

Abstract: Non-small cell lung cancers that harbor concurrent KRAS and TP53 (KP) mutations are immunologically warm tumors with partial responsiveness to anti-PD-(L)1 blockade; however, most patients observe little or no durable clinical benefit. To identify novel ... ...

Abstract	Non-small cell lung cancers that harbor concurrent KRAS and TP53 (KP) mutations are immunologically warm tumors with partial responsiveness to anti-PD-(L)1 blockade; however, most patients observe little or no durable clinical benefit. To identify novel tumor-driven resistance mechanisms, we developed a panel of KP murine lung cancer models with intrinsic resistance to anti-PD-1 and queried differential gene expression between these tumors and anti-PD-1-sensitive tumors. We found that the enzyme autotaxin (ATX), and the metabolite it produces, lysophosphatidic acid (LPA), were significantly upregulated in resistant tumors and that ATX directly modulated antitumor immunity, with its expression negatively correlating with total and effector tumor-infiltrating CD8+ T cells. Pharmacological inhibition of ATX, or the downstream receptor LPAR5, in combination with anti-PD-1 was sufficient to restore the antitumor immune response and efficaciously control lung tumor growth in multiple KP tumor models. Additionally, ATX was significantly correlated with inflammatory gene signatures, including a CD8+ cytolytic score in multiple lung adenocarcinoma patient data sets, suggesting that an activated tumor-immune microenvironment upregulates ATX and thus provides an opportunity for cotargeting to prevent acquired resistance to anti-PD-1 treatment. These data reveal the ATX/LPA axis as an immunosuppressive pathway that diminishes the immune checkpoint blockade response in lung cancer.
MeSH term(s)	Humans ; Animals ; Mice ; Carcinoma, Non-Small-Cell Lung ; Lung Neoplasms ; T-Lymphocytes, Cytotoxic ; Adenocarcinoma of Lung ; Cell Death ; Tumor Microenvironment ; Receptors, Lysophosphatidic Acid
Chemical Substances	LPAR5 protein, human ; Receptors, Lysophosphatidic Acid
Language	English
Publishing date	2023-09-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI163128
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Article ; Online: Anti-tumor activity of a novel LAIR1 antagonist in combination with anti-PD-1 to treat collagen-rich solid tumors.

Molecular cancer therapeutics

2024

Abstract: We recently reported that resistance to PD-1-blockade in a refractory lung cancer-derived model involved increased collagen deposition and the collagen-binding inhibitory receptor leukocyte-associated immunoglobulin-like receptor 1 (LAIR1), and thus we ... ...

Abstract	We recently reported that resistance to PD-1-blockade in a refractory lung cancer-derived model involved increased collagen deposition and the collagen-binding inhibitory receptor leukocyte-associated immunoglobulin-like receptor 1 (LAIR1), and thus we hypothesized that LAIR1 and collagen cooperated to suppress therapeutic response. Here, we report LAIR1 is associated with tumor stroma and is highly expressed by intratumoral myeloid cells in both human tumors and mouse models of cancer. Stroma-associated myeloid cells exhibit a suppressive phenotype and correlate with LAIR1 expression in human cancer. NGM438, a novel humanized LAIR1 antagonist monoclonal antibody, elicits myeloid inflammation and allogeneic T cell responses by binding to LAIR1 and blocking collagen engagement. Further, a mouse-reactive NGM438 surrogate antibody sensitized refractory KP mouse lung tumors to anti-PD-1 therapy and resulted in increased intratumoral CD8+ T cell content and inflammatory gene expression. These data place LAIR1 at the intersection of stroma and suppressive myeloid cells and support the notion that blockade of the LAIR1/collagen axis can potentially address resistance to checkpoint inhibitor therapy in the clinic.
Language	English
Publishing date	2024-04-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-23-0866
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Article ; Online: Molecular targeting of liposomal nanoparticles to tumor microenvironment.

Zhao, Gang / Rodriguez, B Leticia

International journal of nanomedicine

2012 Volume 8, Page(s) 61–71

Abstract: Liposomes are biodegradable and can be used to deliver drugs at a much higher concentration in tumor tissues than in normal tissues. Both passive and active drug delivery by liposomal nanoparticles can significantly reduce the toxic side effects of ... ...

Abstract	Liposomes are biodegradable and can be used to deliver drugs at a much higher concentration in tumor tissues than in normal tissues. Both passive and active drug delivery by liposomal nanoparticles can significantly reduce the toxic side effects of anticancer drugs and enhance the therapeutic efficacy of the drugs delivered. Active liposomal targeting to tumors is achieved by recognizing specific tumor receptors through tumor-specific ligands or antibodies coupled onto the surface of the liposomes, or by stimulus-sensitive drug carriers such as acid-triggered release or enzyme-triggered drug release. Tumors are often composed of tumor cells and nontumor cells, which include endothelial cells, pericytes, fibroblasts, stromal, mesenchymal cells, innate, and adaptive immune cells. These nontumor cells thus form the tumor microenvironment, which could be targeted and modified so that it is unfavorable for tumor cells to grow. In this review, we briefly summarized articles that had taken advantage of liposomal nanoparticles as a carrier to deliver anticancer drugs to the tumor microenvironment, and how they overcame obstacles such as nonspecific uptake, interaction with components in blood, and toxicity. Special attention is devoted to the liposomal targeting of anticancer drugs to the endothelium of tumor neovasculature, tumor associated macrophages, fibroblasts, and pericytes within the tumor microenvironment.
MeSH term(s)	Animals ; Drug Carriers/administration & dosage ; Drug Carriers/pharmacokinetics ; Humans ; Liposomes/administration & dosage ; Liposomes/pharmacokinetics ; Molecular Targeted Therapy ; Nanoparticles/administration & dosage ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Tumor Microenvironment
Chemical Substances	Drug Carriers ; Liposomes
Language	English
Publishing date	2012-12-28
Publishing country	New Zealand
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2364941-0
ISSN	1178-2013 ; 1176-9114
ISSN (online)	1178-2013
ISSN	1176-9114
DOI	10.2147/IJN.S37859
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Article ; Online: Targeting immunosuppressive Ly6C+ classical monocytes reverses anti-PD-1/CTLA-4 immunotherapy resistance.

Rodriguez, B Leticia / Chen, Limo / Li, Yanli / Miao, Shucheng / Peng, David H / Fradette, Jared J / Diao, Lixia / Konen, Jessica M / Alvarez, Frank R Rojas / Solis, Luisa M / Yi, Xiaohui / Padhye, Aparna / Gibson, Laura A / Ochieng, Joshua K / Zhou, Xiaofei / Wang, Jing / Gibbons, Don L

Frontiers in immunology

2023 Volume 14, Page(s) 1161869

Abstract: Introduction: Despite significant clinical advancement with the use of immune checkpoint blockade (ICB) in non-small cell lung cancer (NSCLC) there are still a major subset of patients that develop adaptive/acquired resistance. Understanding resistance ... ...

Abstract	Introduction: Despite significant clinical advancement with the use of immune checkpoint blockade (ICB) in non-small cell lung cancer (NSCLC) there are still a major subset of patients that develop adaptive/acquired resistance. Understanding resistance mechanisms to ICB is critical to developing new therapeutic strategies and improving patient survival. The dynamic nature of the tumor microenvironment and the mutational load driving tumor immunogenicity limit the efficacy to ICB. Recent studies indicate that myeloid cells are drivers of ICB resistance. In this study we sought to understand which immune cells were contributing to resistance and if we could modify them in a way to improve response to ICB therapy. Results: Our results show that combination anti-PD-1/CTLA-4 produces an initial antitumor effect with evidence of an activated immune response. Upon extended treatment with anti-PD-1/CTLA-4 acquired resistance developed with an increase of the immunosuppressive populations, including T-regulatory cells, neutrophils and monocytes. Addition of anti-Ly6C blocking antibody to anti-PD-1/CTLA-4 was capable of completely reversing treatment resistance and restoring CD8 T cell activity in multiple KP lung cancer models and in the autochthonous lung cancer Kras Conclusions: Therapeutically we found that addition of anti-Ly6C to the combination of anti-PD-1/CTLA-4 was capable of complete tumor eradication. Classical Ly6C+ monocytes differentiate into immunosuppressive cells, while blockade of classical monocytes drives dendritic cell differentiation/maturation to reinvigorate the anti-tumor T cell response. These findings support that immunotherapy resistance is associated with infiltrating monocytes and that controlling the differentiation process of monocytes can enhance the therapeutic potential of ICB.
MeSH term(s)	Humans ; Monocytes ; CTLA-4 Antigen ; Carcinoma, Non-Small-Cell Lung/therapy ; Lung Neoplasms/therapy ; Immunotherapy/methods ; Tumor Microenvironment
Chemical Substances	CTLA-4 Antigen
Language	English
Publishing date	2023-06-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1161869
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Article ; Online: Impad1 and Syt11 work in an epistatic pathway that regulates EMT-mediated vesicular trafficking to drive lung cancer invasion and metastasis.

Bajaj, Rakhee / Rodriguez, B Leticia / Russell, William K / Warner, Amanda N / Diao, Lixia / Wang, Jing / Raso, Maria G / Lu, Wei / Khan, Khaja / Solis, Luisa S / Batra, Harsh / Tang, Ximing / Fradette, Jared F / Kundu, Samrat T / Gibbons, Don L

Cell reports

2022 Volume 40, Issue 13, Page(s) 111429

Abstract: Lung cancer is a highly aggressive and metastatic disease responsible for approximately 25% of all cancer-related deaths in the United States. Using high-throughput in vitro and in vivo screens, we have previously established Impad1 as a driver of lung ... ...

Abstract	Lung cancer is a highly aggressive and metastatic disease responsible for approximately 25% of all cancer-related deaths in the United States. Using high-throughput in vitro and in vivo screens, we have previously established Impad1 as a driver of lung cancer invasion and metastasis. Here we elucidate that Impad1 is a direct target of the epithelial microRNAs (miRNAs) miR-200 and miR∼96 and is de-repressed during epithelial-to-mesenchymal transition (EMT); thus, we establish a mode of regulation of the protein. Impad1 modulates Golgi apparatus morphology and vesicular trafficking through its interaction with a trafficking protein, Syt11. These changes in Golgi apparatus dynamics alter the extracellular matrix and the tumor microenvironment (TME) to promote invasion and metastasis. Inhibiting Impad1 or Syt11 disrupts the cancer cell secretome, regulates the TME, and reverses the invasive or metastatic phenotype. This work identifies Impad1 as a regulator of EMT and secretome-mediated changes during lung cancer progression.
MeSH term(s)	Cell Line, Tumor ; Cell Movement ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms/pathology ; MicroRNAs/metabolism ; Neoplasm Invasiveness/genetics ; Neoplasm Metastasis ; Synaptotagmins/metabolism ; Tumor Microenvironment
Chemical Substances	MicroRNAs ; SYT11 protein, human ; Synaptotagmins (134193-27-4)
Language	English
Publishing date	2022-09-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.111429
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Article ; Online: A novel ex vivo tumor system identifies Src-mediated invasion and metastasis in mesenchymal tumor cells in non-small cell lung cancer.

Padhye, Aparna / Ungewiss, Christin / Fradette, Jared J / Rodriguez, B Leticia / Albritton, Jacob L / Miller, Jordan S / Gibbons, Don L

Scientific reports

2019 Volume 9, Issue 1, Page(s) 4819

Abstract: Lung cancer is the foremost cause of cancer related deaths in the U.S. It is a heterogeneous disease composed of genetically and phenotypically distinct tumor cells surrounded by heterotypic cells and extracellular matrix dynamically interacting with the ...

Abstract	Lung cancer is the foremost cause of cancer related deaths in the U.S. It is a heterogeneous disease composed of genetically and phenotypically distinct tumor cells surrounded by heterotypic cells and extracellular matrix dynamically interacting with the tumor cells. Research in lung cancer is often restricted to patient-derived tumor specimens, in vitro cell cultures and limited animal models, which fail to capture the cellular or microenvironment heterogeneity of the tumor. Therefore, our knowledge is primarily focused on cancer-cell autonomous aberrations. For a fundamental understanding of lung cancer progression and an exploration of therapeutic options, we focused our efforts to develop an Ex Vivo Tumor platform to culture tumors in 3D matrices, which retains tumor cell heterogeneity arising due to in vivo selection pressure and environmental influences and recapitulate responses of tumor cells to external manipulations. To establish this model, implanted syngeneic murine tumors from a mutant KRAS/p53 model were harvested to yield multicellular tumor aggregates followed by culture in 3D extracellular matrices. Using this system, we identified Src signaling as an important driver of invasion and metastasis in lung cancer and demonstrate that EVTs are a robust experimental tool bridging the gap between conventional in vitro and in vivo models.
MeSH term(s)	Animals ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/pathology ; Cell Culture Techniques ; Cell Line, Tumor ; Epithelial-Mesenchymal Transition/genetics ; Extracellular Matrix/genetics ; Gene Expression Regulation, Neoplastic/genetics ; Genes, src/genetics ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Mice ; Neoplasm Invasiveness/genetics ; Neoplasm Invasiveness/pathology ; Neoplasm Metastasis/genetics ; Neoplasm Metastasis/pathology ; Rats ; Signal Transduction/genetics ; Spheroids, Cellular/pathology ; Tumor Microenvironment/genetics
Language	English
Publishing date	2019-03-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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/s41598-019-41301-2
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Article ; Online: p53 loss activates prometastatic secretory vesicle biogenesis in the Golgi.

Tan, Xiaochao / Banerjee, Priyam / Shi, Lei / Xiao, Guan-Yu / Rodriguez, B Leticia / Grzeskowiak, Caitlin L / Liu, Xin / Yu, Jiang / Gibbons, Don L / Russell, William K / Creighton, Chad J / Kurie, Jonathan M

Science advances

2021 Volume 7, Issue 25

Abstract: Cancer cells exhibit hyperactive secretory states that maintain cancer cell viability and remodel the tumor microenvironment. However, the oncogenic signals that heighten secretion remain unclear. Here, we show that p53 loss activates prometastatic ... ...

Abstract	Cancer cells exhibit hyperactive secretory states that maintain cancer cell viability and remodel the tumor microenvironment. However, the oncogenic signals that heighten secretion remain unclear. Here, we show that p53 loss activates prometastatic secretory vesicle biogenesis in the Golgi. p53 loss up-regulates the expression of a Golgi scaffolding protein, progestin and adipoQ receptor 11 (PAQR11), which recruits an adenosine diphosphate ribosylation factor 1-containing protein complex that loads cargos into secretory vesicles. PAQR11-dependent secretion of a protease, PLAU, prevents anoikis and initiates autocrine activation of a PLAU receptor/signal transducer and activator of transcription-3-dependent pathway that up-regulates PAQR11 expression, thereby completing a feedforward loop that amplifies prometastatic effector protein secretion. Pharmacologic inhibition of PLAU receptor impairs the growth and metastasis of p53-deficient cancers. Blockade of PAQR11-dependent secretion inhibits immunosuppressive processes in the tumor microenvironment. Thus, Golgi reprogramming by p53 loss is a key driver of hypersecretion in cancer.
MeSH term(s)	Animals ; Biological Transport ; Carrier Proteins/metabolism ; Golgi Apparatus/metabolism ; Mice ; Protein Transport ; Receptors, Progesterone/metabolism ; Secretory Vesicles/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Carrier Proteins ; Receptors, Progesterone ; Tumor Suppressor Protein p53
Language	English
Publishing date	2021-06-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abf4885
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Article ; Online: A protumorigenic secretory pathway activated by p53 deficiency in lung adenocarcinoma.

Tan, Xiaochao / Shi, Lei / Banerjee, Priyam / Liu, Xin / Guo, Hou-Fu / Yu, Jiang / Bota-Rabassedas, Neus / Rodriguez, B Leticia / Gibbons, Don L / Russell, William K / Creighton, Chad J / Kurie, Jonathan M

The Journal of clinical investigation

2020 Volume 131, Issue 1

Abstract: Therapeutic strategies designed to target TP53-deficient cancer cells remain elusive. Here, we showed that TP53 loss initiated a pharmacologically actionable secretory process that drove lung adenocarcinoma (LUAD) progression. Molecular, biochemical, and ...

Abstract	Therapeutic strategies designed to target TP53-deficient cancer cells remain elusive. Here, we showed that TP53 loss initiated a pharmacologically actionable secretory process that drove lung adenocarcinoma (LUAD) progression. Molecular, biochemical, and cell biological studies showed that TP53 loss increased the expression of Golgi reassembly and stacking protein 55 kDa (G55), a Golgi stacking protein that maintains Golgi organelle integrity and is part of a GOLGIN45 (G45)-myosin IIA-containing protein complex that activates secretory vesicle biogenesis in the Golgi. TP53 loss activated G55-dependent secretion by relieving G55 and myosin IIA from miR-34a-dependent silencing. G55-dependent secreted proteins enhanced the proliferative and invasive activities of TP53-deficient LUAD cells and promoted angiogenesis and CD8+ T cell exhaustion in the tumor microenvironment. A small molecule that blocks G55-G45 interactions impaired secretion and reduced TP53-deficient LUAD growth and metastasis. These results identified a targetable secretory vulnerability in TP53-deficient LUAD cells.
MeSH term(s)	Adenocarcinoma of Lung/genetics ; Adenocarcinoma of Lung/metabolism ; Adenocarcinoma of Lung/pathology ; Animals ; Cell Line, Tumor ; Golgi Apparatus/genetics ; Golgi Apparatus/metabolism ; Golgi Apparatus/pathology ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Mice ; Neoplasm Metastasis ; Tumor Suppressor Protein p53/deficiency ; Tumor Suppressor Protein p53/metabolism ; Vesicular Transport Proteins/genetics ; Vesicular Transport Proteins/metabolism
Chemical Substances	Golgin45 protein, mouse ; Trp53 protein, mouse ; Tumor Suppressor Protein p53 ; Vesicular Transport Proteins
Language	English
Publishing date	2020-09-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI137186
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