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Article ; Online: The expanding relevance of nuclear mTOR in carcinogenesis.

Back, Jung H / Kim, Arianna L

2011 Volume 10, Issue 22, Page(s) 3849–3852

Abstract: Deregulated mTOR signaling drives the growth of various human cancers, making mTOR a major target for development of cancer chemotherapeutics. The role of mTOR in carcinogenesis is thought to be largely a consequence of its activity in the cytoplasm ... ...

Abstract	Deregulated mTOR signaling drives the growth of various human cancers, making mTOR a major target for development of cancer chemotherapeutics. The role of mTOR in carcinogenesis is thought to be largely a consequence of its activity in the cytoplasm resulting in increased translation of pro-tumorigenic genes. However, emerging data locate mTOR in various subcellular compartments including Golgi, mitochondria, endoplasmic reticulum, and the nucleus, implying the presence of compartment-specific mTOR substrates and functions. Efforts to identify mTOR substrates in these compartments, and the mechanisms by which mTOR recruits these substrates and affects downstream cellular processes, will add to our understanding of the diversity of roles played by mTOR in carcinogenesis.
MeSH term(s)	Amino Acid Motifs ; Animals ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/pathology ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Humans ; Mice ; Signal Transduction ; TOR Serine-Threonine Kinases/chemistry ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/physiology
Chemical Substances	MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; mTOR protein, mouse (EC 2.7.1.1)
Language	English
Publishing date	2011-11-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/cc.10.22.18329
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Article ; Online: SOX9 Transcriptionally Regulates mTOR-Induced Proliferation of Basal Cell Carcinomas.

Kim, Arianna L / Back, Jung Ho / Chaudhary, Sandeep C / Zhu, Yucui / Athar, Mohammad / Bickers, David R

The Journal of investigative dermatology

2018 Volume 138, Issue 8, Page(s) 1716–1725

Abstract: Currently available smoothened targeted therapies in patients with basal cell nevus syndrome are associated with substantial tumor recurrence and clinical resistance. Strategies bypassing smoothened and/or identifying additional downstream components of ... ...

Abstract	Currently available smoothened targeted therapies in patients with basal cell nevus syndrome are associated with substantial tumor recurrence and clinical resistance. Strategies bypassing smoothened and/or identifying additional downstream components of the Hedgehog pathway could provide novel antitumor targets with a better therapeutic index. Sry-related high mobility group box 9 (SOX9) is a Hedgehog/glioma-associated oncogene homolog-regulated transcription factor known to be overexpressed in basal cell carcinomas (BCCs). A sequence motif search for SOX9-responsive elements identified three motifs in the promoter region of mammalian target of rapamycin (mTOR). In murine BCC cells, SOX9 occupies the mTOR promoter and induces its transcriptional activity. Short hairpin RNA (shRNA)-mediated knockdown of SOX9, as well as smoothened inhibition by itraconazole and vismodegib, reduces mTOR expression and the phosphorylation of known downstream mTOR targets. These effects culminate in diminishing the proliferative capacity of BCC cells, demonstrating a direct mechanistic link between the Hedgehog and mTOR pathways capable of driving BCC growth. Furthermore, rapamycin, a pharmacologic mTOR inhibitor, suppressed the growth of UV-induced BCCs in Ptch1
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Carcinoma, Basal Cell/drug therapy ; Carcinoma, Basal Cell/genetics ; Carcinoma, Basal Cell/pathology ; Carcinoma, Squamous Cell/drug therapy ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/pathology ; Cell Line, Tumor ; Cell Proliferation/genetics ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; HEK293 Cells ; Hedgehog Proteins/metabolism ; Humans ; Mice ; Mice, Hairless ; Neoplasm Recurrence, Local ; Neoplasms, Experimental/drug therapy ; Neoplasms, Experimental/etiology ; Neoplasms, Experimental/pathology ; Phosphorylation/drug effects ; Promoter Regions, Genetic/genetics ; RNA, Small Interfering/metabolism ; SOX9 Transcription Factor/genetics ; SOX9 Transcription Factor/metabolism ; Signal Transduction/genetics ; Skin/pathology ; Skin Neoplasms/drug therapy ; Skin Neoplasms/genetics ; Skin Neoplasms/pathology ; Smoothened Receptor/antagonists & inhibitors ; Smoothened Receptor/metabolism ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism ; Tissue Array Analysis ; Ultraviolet Rays/adverse effects
Chemical Substances	Antineoplastic Agents ; Hedgehog Proteins ; RNA, Small Interfering ; SOX9 Transcription Factor ; SOX9 protein, human ; Smoothened Receptor ; Sox9 protein, mouse ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; mTOR protein, mouse (EC 2.7.1.1)
Language	English
Publishing date	2018-03-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1016/j.jid.2018.01.040
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Article ; Online: Transcriptome Analysis Identifies the Dysregulation of Ultraviolet Target Genes in Human Skin Cancers.

Shen, Yao / Kim, Arianna L / Du, Rong / Liu, Liang

PloS one

2016 Volume 11, Issue 9, Page(s) e0163054

Abstract: Exposure to ultraviolet radiation (UVR) is a major risk factor for both melanoma and non-melanoma skin cancers. In addition to its mutagenic effect, UVR can also induce substantial transcriptional instability in skin cells affecting thousands of genes, ... ...

Abstract	Exposure to ultraviolet radiation (UVR) is a major risk factor for both melanoma and non-melanoma skin cancers. In addition to its mutagenic effect, UVR can also induce substantial transcriptional instability in skin cells affecting thousands of genes, including many cancer genes, suggesting that transcriptional instability may be another important etiological factor in skin photocarcinogenesis. In this study, we performed detailed transcriptomic profiling studies to characterize the kinetic changes in global gene expression in human keratinocytes exposed to different UVR conditions. We identified a subset of UV-responsive genes as UV signature genes (UVSGs) based on 1) conserved UV-responsiveness of this subset of genes among different keratinocyte lines; and 2) UV-induced persistent changes in their mRNA levels long after exposure. Interestingly, 11 of the UVSGs were shown to be critical to skin cancer cell proliferation and survival. Through computational Gene Set Enrichment Analysis, we demonstrated that a significant portion of the UVSGs were dysregulated in human skin squamous cell carcinomas, but not in other human malignancies. This highlights the potential and specificity of the UVSGs in clinical diagnosis of UV damage and stratification of skin cancer risk.
MeSH term(s)	Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/pathology ; Cell Proliferation ; Dose-Response Relationship, Radiation ; Gene Expression Profiling ; Humans ; Skin Neoplasms/genetics ; Skin Neoplasms/pathology ; Transcriptome ; Ultraviolet Rays
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0163054
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Article ; Online: Author Correction: Patched1 haploinsufficiency severely impacts intermediary metabolism in the skin of Ptch1

Li, Changzhao / Mishra, Bharat / Kashyap, Mahendra / Weng, Zhiping / Andrabi, Shaida A / Mukhtar, Shahid M / Kim, Arianna L / Bickers, David R / Kopelovich, Levy / Athar, Mohammad

Scientific reports

2021 Volume 11, Issue 1, Page(s) 20527

Language	English
Publishing date	2021-10-11
Publishing country	England
Document type	Published Erratum
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-98190-7
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Article ; Online: The TINCR ubiquitin-like microprotein is a tumor suppressor in squamous cell carcinoma.

Nature communications

2023 Volume 14, Issue 1, Page(s) 1328

Abstract: The TINCR (Terminal differentiation-Induced Non-Coding RNA) gene is selectively expressed in epithelium tissues and is involved in the control of human epidermal differentiation and wound healing. Despite its initial report as a long non-coding RNA, the ... ...

Abstract	The TINCR (Terminal differentiation-Induced Non-Coding RNA) gene is selectively expressed in epithelium tissues and is involved in the control of human epidermal differentiation and wound healing. Despite its initial report as a long non-coding RNA, the TINCR locus codes for a highly conserved ubiquitin-like microprotein associated with keratinocyte differentiation. Here we report the identification of TINCR as a tumor suppressor in squamous cell carcinoma (SCC). TINCR is upregulated by UV-induced DNA damage in a TP53-dependent manner in human keratinocytes. Decreased TINCR protein expression is prevalently found in skin and head and neck squamous cell tumors and TINCR expression suppresses the growth of SCC cells in vitro and in vivo. Consistently, Tincr knockout mice show accelerated tumor development following UVB skin carcinogenesis and increased penetrance of invasive SCCs. Finally, genetic analyses identify loss-of-function mutations and deletions encompassing the TINCR gene in SCC clinical samples supporting a tumor suppressor role in human cancer. Altogether, these results demonstrate a role for TINCR as protein coding tumor suppressor gene recurrently lost in squamous cell carcinomas.
MeSH term(s)	Animals ; Mice ; Humans ; Ubiquitin/metabolism ; Carcinoma, Squamous Cell/genetics ; Genes, Tumor Suppressor ; Keratinocytes/metabolism ; Head and Neck Neoplasms/genetics ; RNA, Long Noncoding/genetics ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Micropeptides
Chemical Substances	Ubiquitin ; RNA, Long Noncoding
Language	English
Publishing date	2023-03-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-36713-8
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Article ; Online: Targeting the Jak/Signal Transducer and Activator of Transcription 3 Pathway with Ruxolitinib in a Mouse Model of Recessive Dystrophic Epidermolysis Bullosa-Squamous Cell Carcinoma.

Jacków, Joanna / Rami, Avina / Hayashi, Ryota / Hansen, Corey / Guo, Zongyou / DeLorenzo, Dominick / Pappalardo, Alberto / Alvarez Cespedes, David / Kim, Arianna L / Perez-Lorenzo, Rolando / Owens, David M / Christiano, Angela M

The Journal of investigative dermatology

2020 Volume 141, Issue 4, Page(s) 942–946

MeSH term(s)	Administration, Oral ; Animals ; Carcinoma, Squamous Cell/drug therapy ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/pathology ; Cell Line, Tumor ; Collagen Type VII/genetics ; Epidermolysis Bullosa Dystrophica/complications ; Epidermolysis Bullosa Dystrophica/drug therapy ; Epidermolysis Bullosa Dystrophica/genetics ; Fibroblasts ; Humans ; Janus Kinases/antagonists & inhibitors ; Janus Kinases/metabolism ; Mice ; Mutation ; Pyrazoles/administration & dosage ; Pyrazoles/pharmacology ; STAT3 Transcription Factor/metabolism ; Signal Transduction/drug effects ; Skin Neoplasms/drug therapy ; Skin Neoplasms/genetics ; Skin Neoplasms/pathology ; Xenograft Model Antitumor Assays
Chemical Substances	COL7A1 protein, human ; Collagen Type VII ; Pyrazoles ; STAT3 Transcription Factor ; STAT3 protein, human ; ruxolitinib (82S8X8XX8H) ; Janus Kinases (EC 2.7.10.2)
Keywords	covid19
Language	English
Publishing date	2020-10-16
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1016/j.jid.2020.08.022
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Article ; Online: Sonic hedgehog signaling in Basal cell nevus syndrome.

Athar, Mohammad / Li, Changzhao / Kim, Arianna L / Spiegelman, Vladimir S / Bickers, David R

Cancer research

2014 Volume 74, Issue 18, Page(s) 4967–4975

Abstract: The hedgehog (Hh) signaling pathway is considered to be a major signal transduction pathway during embryonic development, but it usually shuts down after birth. Aberrant Sonic hedgehog (Shh) activation during adulthood leads to neoplastic growth. Basal ... ...

Abstract	The hedgehog (Hh) signaling pathway is considered to be a major signal transduction pathway during embryonic development, but it usually shuts down after birth. Aberrant Sonic hedgehog (Shh) activation during adulthood leads to neoplastic growth. Basal cell carcinoma (BCC) of the skin is driven by this pathway. Here, we summarize information related to the pathogenesis of this neoplasm, discuss pathways that crosstalk with Shh signaling, and the importance of the primary cilium in this neoplastic process. The identification of the basic/translational components of Shh signaling has led to the discovery of potential mechanism-driven druggable targets and subsequent clinical trials have confirmed their remarkable efficacy in treating BCCs, particularly in patients with nevoid BCC syndrome (NBCCS), an autosomal dominant disorder in which patients inherit a germline mutation in the tumor-suppressor gene Patched (Ptch). Patients with NBCCS develop dozens to hundreds of BCCs due to derepression of the downstream G-protein-coupled receptor Smoothened (SMO). Ptch mutations permit transposition of SMO to the primary cilium followed by enhanced expression of transcription factors Glis that drive cell proliferation and tumor growth. Clinical trials with the SMO inhibitor, vismodegib, showed remarkable efficacy in patients with NBCCS, which finally led to its FDA approval in 2012.
MeSH term(s)	Animals ; Basal Cell Nevus Syndrome/drug therapy ; Basal Cell Nevus Syndrome/genetics ; Basal Cell Nevus Syndrome/metabolism ; Basal Cell Nevus Syndrome/pathology ; Cell Growth Processes/physiology ; Disease Models, Animal ; Hedgehog Proteins/metabolism ; Humans ; Receptors, Cell Surface/metabolism ; Signal Transduction
Chemical Substances	Hedgehog Proteins ; Receptors, Cell Surface
Language	English
Publishing date	2014-08-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-14-1666
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Article ; Online: Patched1 haploinsufficiency severely impacts intermediary metabolism in the skin of Ptch1

Li, Changzhao / Mishra, Bharat / Kashyap, Mahendra / Weng, Zhiping / Andrabi, Shaida A / Mukhtar, Shahid M / Kim, Arianna L / Bickers, David R / Kopelovich, Levy / Athar, Mohammad

Scientific reports

2019 Volume 9, Issue 1, Page(s) 13072

Abstract: The study of dominantly heritable cancers has provided insights about tumor development. Gorlin syndrome (GS) is an autosomal dominant disorder wherein affected individuals develop multiple basal cell carcinomas (BCCs) of the skin. We developed a murine ... ...

Abstract	The study of dominantly heritable cancers has provided insights about tumor development. Gorlin syndrome (GS) is an autosomal dominant disorder wherein affected individuals develop multiple basal cell carcinomas (BCCs) of the skin. We developed a murine model of Ptch1 haploinsufficiency on an ornithine decarboxylase (ODC) transgenic background (Ptch1
MeSH term(s)	Animals ; Computational Biology/methods ; Energy Metabolism/genetics ; Gene Expression Profiling ; Haploinsufficiency ; Heterozygote ; Lipid Metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Ornithine Decarboxylase/genetics ; Patched-1 Receptor/genetics ; Pentose Phosphate Pathway ; Phenotype ; Skin/metabolism ; Skin Neoplasms/genetics ; Skin Neoplasms/metabolism ; Skin Neoplasms/pathology ; Transcriptome
Chemical Substances	Patched-1 Receptor ; Ptch1 protein, mouse ; Ornithine Decarboxylase (EC 4.1.1.17)
Language	English
Publishing date	2019-09-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-49470-w
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Article ; Online: AKT1 Activation is Obligatory for Spontaneous BCC Tumor Growth in a Murine Model that Mimics Some Features of Basal Cell Nevus Syndrome.

Kim, Arianna L / Back, Jung Ho / Zhu, Yucui / Tang, Xiuwei / Yardley, Nathan P / Kim, Katherine J / Athar, Mohammad / Bickers, David R

Cancer prevention research (Philadelphia, Pa.)

2016 Volume 9, Issue 10, Page(s) 794–802

Abstract: Patients with basal cell nevus syndrome (BCNS), also known as Gorlin syndrome, develop numerous basal cell carcinomas (BCC) due to germline mutations in the tumor suppressor PTCH1 and aberrant activation of Hedgehog (Hh) signaling. Therapies targeted at ... ...

Abstract	Patients with basal cell nevus syndrome (BCNS), also known as Gorlin syndrome, develop numerous basal cell carcinomas (BCC) due to germline mutations in the tumor suppressor PTCH1 and aberrant activation of Hedgehog (Hh) signaling. Therapies targeted at components of the Hh pathway, including the smoothened (SMO) inhibitor vismodegib, can ablate these tumors clinically, but tumors recur upon drug discontinuation. Using SKH1-Ptch1
MeSH term(s)	Animals ; Basal Cell Nevus Syndrome/metabolism ; Basal Cell Nevus Syndrome/pathology ; Carcinoma, Basal Cell/metabolism ; Carcinoma, Basal Cell/pathology ; Cell Line ; Disease Models, Animal ; Humans ; Keratinocytes/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Proto-Oncogene Proteins c-akt/metabolism ; Skin Neoplasms/metabolism ; Skin Neoplasms/pathology
Chemical Substances	Akt1 protein, mouse (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2016-07-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2434717-6
ISSN	1940-6215 ; 1940-6207
ISSN (online)	1940-6215
ISSN	1940-6207
DOI	10.1158/1940-6207.CAPR-16-0066
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Article: Targeting the JAK/STAT3 pathway with Ruxolitinib in a mouse model of recessive dystrophic epidermolysis bullosa-squamous cell carcinoma

Jacków, Joanna / Rami, Avina / Hayashi, Ryota / Hansen, Corey / Guo, Zongyou / DeLorenzo, Dominick / Pappalardo, Alberto / Cespedes, David Alvarez / Kim, Arianna L / Perez-Lorenzo, Rolando / Owens, David M / Christiano, Angela M

J. invest. dermatol

Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #33069729
Database	COVID19

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