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Article ; Online: Near-Infrared Induced miR-34a Delivery from Nanoparticles in Esophageal Cancer Treatment.

Alden, Nick A / Yeingst, Tyus J / Pfeiffer, Hanna M / Celik, Nazmiye / Arrizabalaga, Julien H / Helton, Angelica M / Liu, Yiming / Stairs, Douglas B / Glick, Adam B / Goyal, Neerav / Hayes, Daniel J

Advanced healthcare materials

2024 Volume 13, Issue 10, Page(s) e2303593

Abstract: Current nucleic acid delivery methods have not achieved efficient, non-toxic delivery of miRNAs with tumor-specific selectivity. In this study, a new delivery system based on light-inducible gold-silver-gold, core-shell-shell (CSS) nanoparticles is ... ...

Abstract	Current nucleic acid delivery methods have not achieved efficient, non-toxic delivery of miRNAs with tumor-specific selectivity. In this study, a new delivery system based on light-inducible gold-silver-gold, core-shell-shell (CSS) nanoparticles is presented. This system delivers small nucleic acid therapeutics with precise spatiotemporal control, demonstrating the potential for achieving tumor-specific selectivity and efficient delivery of miRNA mimics. The light-inducible particles leverage the photothermal heating of metal nanoparticles due to the local surface plasmonic resonance for controlled chemical cleavage and release of the miRNA mimic payload. The CSS morphology and composition result in a plasmonic resonance within the near-infrared (NIR) region of the light spectrum. Through this method, exogenous miR-34a-5p mimics are effectively delivered to human squamous cell carcinoma TE10 cells, leading to apoptosis induction without adverse effects on untransformed keratinocytes in vitro. The CSS nanoparticle delivery system is tested in vivo in Foxn1nu athymic nude mice with bilateral human esophageal TE10 cancer cells xenografts. These experiments reveal that this CSS nanoparticle conjugates, when systemically administered, followed by 850 nm light emitting diode irradiation at the tumor site, 6 h post-injection, produce a significant and sustained reduction in tumor volume, exceeding 87% in less than 72 h.
MeSH term(s)	Animals ; Mice ; Humans ; Mice, Nude ; Nanoparticles/chemistry ; MicroRNAs/genetics ; Metal Nanoparticles/chemistry ; Esophageal Neoplasms/drug therapy ; Gold/chemistry ; Cell Line, Tumor
Chemical Substances	MicroRNAs ; Gold (7440-57-5)
Language	English
Publishing date	2024-01-22
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2649576-4
ISSN	2192-2659 ; 2192-2640
ISSN (online)	2192-2659
ISSN	2192-2640
DOI	10.1002/adhm.202303593
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Article ; Online: Targeted deletion of TGFβ1 in basal keratinocytes causes profound defects in stratified squamous epithelia and aberrant melanocyte migration.

Chalmers, Fiona E / Dusold, Justyn E / Shaik, Javed A / Walsh, Hailey A / Glick, Adam B

Developmental biology

2022 Volume 485, Page(s) 9–23

Abstract: Transforming Growth Factor Beta 1 (TGFβ1) is a multifunctional cytokine that regulates proliferation, apoptosis, and epithelial-mesenchymal transition of epithelial cells. While its role in cancer is well studied, less is known about TGFβ1 and regulation ...

Abstract	Transforming Growth Factor Beta 1 (TGFβ1) is a multifunctional cytokine that regulates proliferation, apoptosis, and epithelial-mesenchymal transition of epithelial cells. While its role in cancer is well studied, less is known about TGFβ1 and regulation of epithelial development. To address this, we deleted TGFβ1 in basal keratinocytes of stratified squamous epithelia. Newborn mice with a homozygous TGFβ1 deletion had significant defects in proliferation and differentiation of the epidermis and oral mucosa, and died shortly after birth. Hair follicles were sparse in TGFβ1 depleted skin and had delayed development. Additionally, the Wnt pathway transcription factor LEF1 was reduced in hair follicle bulbs and nearly absent from the basal epithelial layer. Hemizygous knockout mice survived to adulthood but were runted and had sparse coats. The skin of these mice had irregular hair follicle morphology and aberrant hair cycle progression, as well as abnormally high melanin expression and delayed melanocyte migration. In contrast to newborn TGFβ1 null mice, the epidermis was hyperproliferative, acanthotic and inflamed. Expression of p63, a master regulator of stratified epithelial identity, proliferation and differentiation, was reduced in TGFβ1 null newborn epidermis but expanded in the postnatal acanthotic epidermis of TGFβ1 hemizygous mice. Thus, TGFβ1 is both essential and haploinsufficient with context dependent roles in stratified squamous epithelial development and homeostasis.
MeSH term(s)	Animals ; Carcinoma, Squamous Cell/metabolism ; Cell Differentiation ; Epidermis/metabolism ; Epithelium/metabolism ; Hair Follicle ; Keratinocytes ; Melanocytes ; Mice
Language	English
Publishing date	2022-02-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1114-9
ISSN	1095-564X ; 0012-1606
ISSN (online)	1095-564X
ISSN	0012-1606
DOI	10.1016/j.ydbio.2022.02.009
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Article ; Online: The Role of TGFβ Signaling in Squamous Cell Cancer: Lessons from Mouse Models.

Glick, Adam B

Journal of skin cancer

2012 Volume 2012, Page(s) 249063

Abstract: TGFβ1 is a member of a large growth factor family including activins/inhibins and bone morphogenic proteins (BMPs) that have a potent growth regulatory and immunomodulatory functions in normal skin homeostasis, regulation of epidermal stem cells, ... ...

Abstract	TGFβ1 is a member of a large growth factor family including activins/inhibins and bone morphogenic proteins (BMPs) that have a potent growth regulatory and immunomodulatory functions in normal skin homeostasis, regulation of epidermal stem cells, extracellular matrix production, angiogenesis, and inflammation. TGFβ signaling is tightly regulated in normal tissues and becomes deregulated during cancer development in cutaneous SCC and many other solid tumors. Because of these diverse biological processes regulated by TGFβ1, this cytokine and its signaling pathway appear to function at multiple points during carcinogenesis with distinct effects. The mouse skin carcinogenesis model has been a useful tool to dissect the function of this pathway in cancer pathogenesis, with transgenic and null mice as well as small molecule inhibitors to alter the function of the TGFβ1 pathway and assess the effects on cancer development. This paper will review data on changes in TGFβ1 signaling in human SCC primarily HNSCC and cutaneous SCC and different mouse models that have been generated to investigate the relevance of these changes to cancer. A better understanding of the mechanisms underlying the duality of TGFβ1 action in carcinogenesis will inform potential use of this signaling pathway for targeted therapies.
Language	English
Publishing date	2012-12-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2581531-3
ISSN	2090-2913 ; 2090-2913
ISSN (online)	2090-2913
ISSN	2090-2913
DOI	10.1155/2012/249063
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Article ; Online: The unfolded protein response gene Ire1α is required for tissue renewal and normal differentiation in the mouse tongue and esophagus.

Chalmers, Fiona E / Mogre, Saie / Rimal, Bipin / Son, Jeongin / Patterson, Andrew D / Stairs, Douglas B / Glick, Adam B

Developmental biology

2022 Volume 492, Page(s) 59–70

Abstract: The IRE1α-XBP1s signaling branch of the unfolded protein response is a well-characterized survival pathway that allows cells to adapt to and resolve endoplasmic reticulum stress. Recent data has broadened our understanding of IRE1α-XBP1s signaling beyond ...

Abstract	The IRE1α-XBP1s signaling branch of the unfolded protein response is a well-characterized survival pathway that allows cells to adapt to and resolve endoplasmic reticulum stress. Recent data has broadened our understanding of IRE1α-XBP1s signaling beyond a stress response and revealed a physiological mechanism required for the differentiation and maturation of a wide variety of cell types. Here we provide evidence that the IRE1α-XBP1s signaling pathway is required for the proliferation and maturation of basal keratinocytes in the mouse tongue and esophageal epithelium. Mice with conditional targeted deletion of either Ire1α or Xbp1 in keratin 14 expressing basal keratinocytes displayed severe thinning of the lingual and esophageal mucosa that rendered them unable to eat. In IRE1α null epithelium harvested at an earlier timepoint, genes regulating cell proliferation, cell-cell adhesion, and keratinization were significantly downregulated; indirect immunofluorescence revealed fewer proliferating basal keratinocytes, downregulation of E-cadherin, and thinning of the loricrin-positive granular and cornified layers. The number of Tp63-positive basal keratinocytes was reduced in the absence of IRE1α, and expression of the Wnt pathway transcription factor LEF1, which is required for the proliferation of lingual transit amplifying cells, was also significantly downregulated at the transcript and protein level. Together these results reveal an essential role for IRE1α-XBP1s in the maintenance of the stratified squamous epithelial tissue of the tongue and esophagus.
MeSH term(s)	Mice ; Animals ; Endoribonucleases/genetics ; Endoribonucleases/metabolism ; Protein Serine-Threonine Kinases/genetics ; Unfolded Protein Response/genetics ; Endoplasmic Reticulum Stress/genetics ; Esophagus ; Tongue/metabolism
Chemical Substances	Endoribonucleases (EC 3.1.-) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2022-09-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	1114-9
ISSN	1095-564X ; 0012-1606
ISSN (online)	1095-564X
ISSN	0012-1606
DOI	10.1016/j.ydbio.2022.09.009
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Article ; Online: The Endoplasmic Reticulum Stress Sensor IRE1α Regulates the UV DNA Repair Response through the Control of Intracellular Calcium Homeostasis.

Son, Jeongin / Mogre, Saie / Chalmers, Fiona E / Ibinson, Jack / Worrell, Stephen / Glick, Adam B

The Journal of investigative dermatology

2021 Volume 142, Issue 6, Page(s) 1682–1691.e7

Abstract: The unfolded protein response is activated by UVB irradiation, but the role of a key mediator, IRE1α, is not clear. In this study, we show that mice with an epidermal IRE1α deletion are sensitized to UV with increased apoptosis, rapid loss of UV-induced ... ...

Abstract	The unfolded protein response is activated by UVB irradiation, but the role of a key mediator, IRE1α, is not clear. In this study, we show that mice with an epidermal IRE1α deletion are sensitized to UV with increased apoptosis, rapid loss of UV-induced cyclopyrimidine dimer‒positive keratinocytes, and sloughing of the epidermis. In vitro, Ire1α-deficient keratinocytes have increased UVB sensitivity, reduced cyclopyrimidine dimer repair, and reduced accumulation of γH2AX and phosphorylated ATR, suggesting defective activation of nucleotide excision repair. Knockdown of XBP1 or pharmacologic inhibition of the IRE1α ribonuclease did not phenocopy Ire1α deficiency. The altered UV response was linked to elevated intracellular calcium levels and ROS, and this was due to dysregulation of the endoplasmic reticulum calcium channel InsP3R. Pharmacologic, genetic, and biochemical studies linked the regulation of the Ins3PR, intracellular calcium, and normal UV DNA damage response to CIB1 and the IRE1α‒TRAF2‒ASK1 complex. These results suggest a model where IRE1α activation state drives CIB1 binding either to the InsP3R or ASK1 to regulate endoplasmic reticulum calcium efflux, ROS, and DNA repair responses after UV irradiation.
MeSH term(s)	Animals ; Calcium/metabolism ; DNA Repair ; Endoplasmic Reticulum Stress/genetics ; Endoribonucleases/genetics ; Endoribonucleases/metabolism ; Homeostasis ; Mice ; Protein Serine-Threonine Kinases/genetics ; Reactive Oxygen Species/metabolism ; Unfolded Protein Response ; X-Box Binding Protein 1/genetics ; X-Box Binding Protein 1/metabolism
Chemical Substances	Reactive Oxygen Species ; X-Box Binding Protein 1 ; Ern1 protein, mouse (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Endoribonucleases (EC 3.1.-) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-11-20
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1016/j.jid.2021.11.010
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Article ; Online: Delivery of Therapeutic miR-148b Mimic via Poly(β Amino Ester) Polyplexes for Post-transcriptional Gene Regulation and Apoptosis of A549 Cells.

Alden, Nick A / Arrizabalaga, Julien H / Liu, Yiming / Amin, Shantu / Gowda, Krishne / Yao, Shun / Archetti, Marco / Glick, Adam B / Hayes, Daniel J

Langmuir : the ACS journal of surfaces and colloids

2022 Volume 38, Issue 32, Page(s) 9833–9843

Abstract: In this study, we utilized selectively modified, biodegradable polymer-based polyplexes to deliver custom, exogenous miR-148b mimics to induce apoptosis in human lung cancer (A549) cells. The gene regulatory effects of the payload miRNA mimics (miR-148b- ... ...

Abstract	In this study, we utilized selectively modified, biodegradable polymer-based polyplexes to deliver custom, exogenous miR-148b mimics to induce apoptosis in human lung cancer (A549) cells. The gene regulatory effects of the payload miRNA mimics (miR-148b-3p) were first evaluated through bioinformatic analyses to uncover specific gene targets involved in critical carcinogenic pathways. Hyperbranched poly(β amino ester) polyplexes (hPBAE) loaded with custom miR-148b mimics were then developed for targeted therapy. When evaluated
MeSH term(s)	A549 Cells ; Apoptosis ; Cell Proliferation ; Esters ; Humans ; MicroRNAs/genetics ; Poly A ; Polymers
Chemical Substances	Esters ; MicroRNAs ; Polymers ; poly(beta-amino ester) ; Poly A (24937-83-5)
Language	English
Publishing date	2022-08-02
Publishing country	United States
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	2005937-1
ISSN	1520-5827 ; 0743-7463
ISSN (online)	1520-5827
ISSN	0743-7463
DOI	10.1021/acs.langmuir.2c00913
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Article: Biology of Stress Responses in Aging.

Maragkakis, Manolis / Malla, Sulochan / Hatzoglou, Maria / Trifunovic, Aleksandra / Glick, Adam B / Finkel, Toren / Longo, Valter D / Kaushik, Susmita / Muñoz-Cánoves, Pura / Lithgow, Gordon J / Naidoo, Nirinjini / Booth, Lauren N / Payea, Matthew J / Herman, Allison B / de Cabo, Rafael / Wilson, David M / Ferrucci, Luigi / Gorospe, Myriam

Aging Biology

2023 Volume 1

Abstract: ... On April ... ...

Abstract	On April 28
Language	English
Publishing date	2023-06-27
Publishing country	United States
Document type	Journal Article
DOI	10.59368/agingbio.20230001
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Article ; Online: TGFβ1 regulates HRas-mediated activation of IRE1α through the PERK-RPAP2 axis in keratinocytes.

Mogre, Saie / Blazanin, Nicholas / Walsh, Hailey / Ibinson, Jack / Minnich, Chase / Andrew Hu, Chih-Chi / Glick, Adam B

Molecular carcinogenesis

2022 Volume 61, Issue 10, Page(s) 958–971

Abstract: Transforming Growth Factor β1 (TGFβ1) is a critical regulator of tumor progression in response to HRas. Recently, TGFβ1 has been shown to trigger ER stress in many disease models; however, its role in oncogene-induced ER stress is unclear. Oncogenic HRas ...

Abstract	Transforming Growth Factor β1 (TGFβ1) is a critical regulator of tumor progression in response to HRas. Recently, TGFβ1 has been shown to trigger ER stress in many disease models; however, its role in oncogene-induced ER stress is unclear. Oncogenic HRas induces the unfolded protein response (UPR) predominantly via the Inositol-requiring enzyme 1α (IRE1α) pathway to initiate the adaptative responses to ER stress, with importance for both proliferation and senescence. Here, we show a role of the UPR sensor proteins IRE1α and (PKR)-like endoplasmic reticulum kinase (PERK) to mediate the tumor-suppressive roles of TGFβ1 in mouse keratinocytes expressing mutant forms of HRas. TGFβ1 suppressed IRE1α phosphorylation and activation by HRas both in in vitro and in vivo models while simultaneously activating the PERK pathway. However, the increase in ER stress indicated an uncoupling of ER stress and IRE1α activation by TGFβ1. Pharmacological and genetic approaches demonstrated that TGFβ1-dependent dephosphorylation of IRE1α was mediated by PERK through RNA Polymerase II Associated Protein 2 (RPAP2), a PERK-dependent IRE1α phosphatase. In addition, TGFβ1-mediated growth arrest in oncogenic HRas keratinocytes was partially dependent on PERK-induced IRE1α dephosphorylation and inactivation. Together, these results demonstrate a critical cross-talk between UPR proteins that is important for TGFβ1-mediated tumor suppressive responses.
MeSH term(s)	Animals ; Endoplasmic Reticulum Stress/genetics ; Endoribonucleases/genetics ; Endoribonucleases/metabolism ; Inositol ; Keratinocytes/metabolism ; Mice ; Protein Serine-Threonine Kinases/genetics ; RNA Polymerase II ; Transforming Growth Factor beta1/genetics ; Transforming Growth Factor beta1/metabolism ; Unfolded Protein Response ; eIF-2 Kinase/metabolism
Chemical Substances	Transforming Growth Factor beta1 ; Inositol (4L6452S749) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; eIF-2 Kinase (EC 2.7.11.1) ; RNA Polymerase II (EC 2.7.7.-) ; Endoribonucleases (EC 3.1.-)
Language	English
Publishing date	2022-08-17
Publishing country	United States
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	1004029-8
ISSN	1098-2744 ; 0899-1987
ISSN (online)	1098-2744
ISSN	0899-1987
DOI	10.1002/mc.23453
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Article: Targeted deletion of TGFβ1 in basal keratinocytes causes profound defects in stratified squamous epithelia and aberrant melanocyte migration

Chalmers, Fiona E. / Dusold, Justyn E. / Shaik, Javed A. / Walsh, Hailey A. / Glick, Adam B.

Developmental biology. 2022 May, v. 485

2022

Abstract	Transforming Growth Factor Beta 1 (TGFβ1) is a multifunctional cytokine that regulates proliferation, apoptosis, and epithelial-mesenchymal transition of epithelial cells. While its role in cancer is well studied, less is known about TGFβ1 and regulation of epithelial development. To address this, we deleted TGFβ1 in basal keratinocytes of stratified squamous epithelia. Newborn mice with a homozygous TGFβ1 deletion had significant defects in proliferation and differentiation of the epidermis and oral mucosa, and died shortly after birth. Hair follicles were sparse in TGFβ1 depleted skin and had delayed development. Additionally, the Wnt pathway transcription factor LEF1 was reduced in hair follicle bulbs and nearly absent from the basal epithelial layer. Hemizygous knockout mice survived to adulthood but were runted and had sparse coats. The skin of these mice had irregular hair follicle morphology and aberrant hair cycle progression, as well as abnormally high melanin expression and delayed melanocyte migration. In contrast to newborn TGFβ1 null mice, the epidermis was hyperproliferative, acanthotic and inflamed. Expression of p63, a master regulator of stratified epithelial identity, proliferation and differentiation, was reduced in TGFβ1 null newborn epidermis but expanded in the postnatal acanthotic epidermis of TGFβ1 hemizygous mice. Thus, TGFβ1 is both essential and haploinsufficient with context dependent roles in stratified squamous epithelial development and homeostasis.
Keywords	adulthood ; apoptosis ; cytokines ; hair follicles ; homeostasis ; homozygosity ; keratinocytes ; melanin ; melanocytes ; mucosa ; neonates ; transcription factors
Language	English
Dates of publication	2022-05
Size	p. 9-23.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1114-9
ISSN	1095-564X ; 0012-1606
ISSN (online)	1095-564X
ISSN	0012-1606
DOI	10.1016/j.ydbio.2022.02.009
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: The Role of TGF Signaling in Squamous Cell Cancer

Adam B. Glick

Journal of Skin Cancer, Vol

Lessons from Mouse Models

2012 Volume 2012

Keywords	Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Oncology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Language	English
Publishing date	2012-01-01T00:00:00Z
Publisher	Hindawi Publishing Corporation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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