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Article ; Online: NEDD4 degrades TUSC2 to promote glioblastoma progression.

Rimkus, Tadas K / Arrigo, Austin B / Zhu, Dongqin / Carpenter, Richard L / Sirkisoon, Sherona / Doheny, Daniel / Regua, Angelina T / Wong, Grace L / Manore, Sara / Wagner, Calvin / Lin, Hui-Kuan / Jin, Guangxu / Ruiz, Jimmy / Chan, Michael / Debinski, Waldemar / Lo, Hui-Wen

Cancer letters

2022 Volume 531, Page(s) 124–135

Abstract: Whether tumor suppressor candidate 2 (TUSC2) plays an important role in glioblastoma (GBM) progression is largely unknown. Whether TUSC2 undergoes polyubiquitination is unknown. Herein, we report that TUSC2 protein expression is reduced/lost in GBM ... ...

Abstract	Whether tumor suppressor candidate 2 (TUSC2) plays an important role in glioblastoma (GBM) progression is largely unknown. Whether TUSC2 undergoes polyubiquitination is unknown. Herein, we report that TUSC2 protein expression is reduced/lost in GBM compared to normal brain due to protein destabilization; TUSC2 mRNA is equally expressed in both tissues. NEDD4 E3 ubiquitin ligase polyubiquitinates TUSC2 at residue K71, and the TUSC2-K71R mutant is resistant to NEDD4-mediated proteasomal degradation. Analysis of GBM specimens showed NEDD4 protein is highly expressed in GBM and the level is inversely correlated with TUSC2 protein levels. Furthermore, TUSC2 restoration induces apoptosis and inhibits patient-derived glioma stem cells (PD-GSCs) in vitro and in vivo. Conversely, TUSC2-knockout promotes PD-GSCs in vitro and in vivo. RNA-Seq analysis and subsequent validations showed GBM cells with TUSC2-knockout expressed increased Bcl-xL and were more resistant to apoptosis induced by a Bcl-xL-specific BH3 mimetic. A TUSC2-knockout gene signature created from the RNA-seq data predicts poor patient survival. Together, these findings establish that NEDD4-mediated polyubiquitination is a novel mechanism for TUSC2 degradation in GBM and that TUSC2 loss promotes GBM progression in part through Bcl-xL upregulation.
MeSH term(s)	Brain Neoplasms/pathology ; Cell Line, Tumor ; Genes, Tumor Suppressor ; Glioblastoma/pathology ; Glioma/genetics ; Humans ; Tumor Suppressor Proteins/genetics ; Ubiquitination
Chemical Substances	TUSC2 protein, human ; Tumor Suppressor Proteins
Language	English
Publishing date	2022-02-12
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2022.01.029
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Article: Targeting the Sonic Hedgehog Signaling Pathway: Review of Smoothened and GLI Inhibitors.

Rimkus, Tadas K / Carpenter, Richard L / Qasem, Shadi / Chan, Michael / Lo, Hui-Wen

Cancers

2016 Volume 8, Issue 2

Abstract: The sonic hedgehog (Shh) signaling pathway is a major regulator of cell differentiation, cell proliferation, and tissue polarity. Aberrant activation of the Shh pathway has been shown in a variety of human cancers, including, basal cell carcinoma, ... ...

Abstract	The sonic hedgehog (Shh) signaling pathway is a major regulator of cell differentiation, cell proliferation, and tissue polarity. Aberrant activation of the Shh pathway has been shown in a variety of human cancers, including, basal cell carcinoma, malignant gliomas, medulloblastoma, leukemias, and cancers of the breast, lung, pancreas, and prostate. Tumorigenesis, tumor progression and therapeutic response have all been shown to be impacted by the Shh signaling pathway. Downstream effectors of the Shh pathway include smoothened (SMO) and glioma-associated oncogene homolog (GLI) family of zinc finger transcription factors. Both are regarded as important targets for cancer therapeutics. While most efforts have been devoted towards pharmacologically targeting SMO, developing GLI-targeted approach has its merit because of the fact that GLI proteins can be activated by both Shh ligand-dependent and -independent mechanisms. To date, two SMO inhibitors (LDE225/Sonidegib and GDC-0449/Vismodegib) have received FDA approval for treating basal cell carcinoma while many clinical trials are being conducted to evaluate the efficacy of this exciting class of targeted therapy in a variety of cancers. In this review, we provide an overview of the biology of the Shh pathway and then detail the current landscape of the Shh-SMO-GLI pathway inhibitors including those in preclinical studies and clinical trials.
Language	English
Publishing date	2016-02-15
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers8020022
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Article ; Online: Targeting the Sonic Hedgehog Signaling Pathway

Tadas K. Rimkus / Richard L. Carpenter / Shadi Qasem / Michael Chan / Hui-Wen Lo

Cancers, Vol 8, Iss 2, p

Review of Smoothened and GLI Inhibitors

2016 Volume 22

Abstract	The sonic hedgehog (Shh) signaling pathway is a major regulator of cell differentiation, cell proliferation, and tissue polarity. Aberrant activation of the Shh pathway has been shown in a variety of human cancers, including, basal cell carcinoma, malignant gliomas, medulloblastoma, leukemias, and cancers of the breast, lung, pancreas, and prostate. Tumorigenesis, tumor progression and therapeutic response have all been shown to be impacted by the Shh signaling pathway. Downstream effectors of the Shh pathway include smoothened (SMO) and glioma-associated oncogene homolog (GLI) family of zinc finger transcription factors. Both are regarded as important targets for cancer therapeutics. While most efforts have been devoted towards pharmacologically targeting SMO, developing GLI-targeted approach has its merit because of the fact that GLI proteins can be activated by both Shh ligand-dependent and -independent mechanisms. To date, two SMO inhibitors (LDE225/Sonidegib and GDC-0449/Vismodegib) have received FDA approval for treating basal cell carcinoma while many clinical trials are being conducted to evaluate the efficacy of this exciting class of targeted therapy in a variety of cancers. In this review, we provide an overview of the biology of the Shh pathway and then detail the current landscape of the Shh-SMO-GLI pathway inhibitors including those in preclinical studies and clinical trials.
Keywords	sonic hedgehog pathway ; smoothened ; GLI ; tGLI1 ; inhibitors ; PTCH ; targeted therapy ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R
Subject code	616
Language	English
Publishing date	2016-02-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Truncated Glioma-Associated Oncogene Homolog 1 (tGLI1) Mediates Mesenchymal Glioblastoma via Transcriptional Activation of CD44.

Rimkus, Tadas K / Carpenter, Richard L / Sirkisoon, Sherona / Zhu, Dongqin / Pasche, Boris C / Chan, Michael D / Lesser, Glenn J / Tatter, Stephen B / Watabe, Kounosuke / Debinski, Waldemar / Lo, Hui-Wen

Cancer research

2018 Volume 78, Issue 10, Page(s) 2589–2600

Abstract: The molecular pathways driving mesenchymal glioblastoma (GBM) are still not well understood. We report here that truncated glioma-associated oncogene homolog 1 (tGLI1) is a tumor-specific transcription factor that facilitates GBM growth, is enriched in ... ...

Abstract	The molecular pathways driving mesenchymal glioblastoma (GBM) are still not well understood. We report here that truncated glioma-associated oncogene homolog 1 (tGLI1) is a tumor-specific transcription factor that facilitates GBM growth, is enriched in the mesenchymal subtype of GBM and glioma stem cells (GSC), and promotes mesenchymal GSC by upregulating transcription of CD44. In an orthotopic GBM xenograft mouse model, tGLI1-overexpressing tumors grew more aggressively with increased proliferation and angiogenesis compared with control and GLI1-overexpressing xenografts. tGLI1 was highly expressed in GBM clinical specimens but undetectable in normal brains, whereas GLI1 was expressed in both tissues. A t
MeSH term(s)	Animals ; Brain Neoplasms/mortality ; Brain Neoplasms/pathology ; Cell Line, Tumor ; Cell Proliferation ; Female ; Gene Expression Regulation, Neoplastic/genetics ; Glioblastoma/mortality ; Glioblastoma/pathology ; HEK293 Cells ; Humans ; Hyaluronan Receptors/metabolism ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplastic Stem Cells/pathology ; Transcriptional Activation/genetics ; Transplantation, Heterologous ; Zinc Finger Protein GLI1/genetics ; Zinc Finger Protein GLI1/metabolism
Chemical Substances	CD44 protein, human ; GLI1 protein, human ; Hyaluronan Receptors ; Zinc Finger Protein GLI1
Language	English
Publishing date	2018-02-20
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	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-17-2933
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Article ; Online: Interaction between STAT3 and GLI1/tGLI1 oncogenic transcription factors promotes the aggressiveness of triple-negative breast cancers and HER2-enriched breast cancer.

Sirkisoon, Sherona R / Carpenter, Richard L / Rimkus, Tadas / Anderson, Ashley / Harrison, Alexandria / Lange, Allison M / Jin, Guangxu / Watabe, Kounosuke / Lo, Hui-Wen

Oncogene

2018 Volume 37, Issue 19, Page(s) 2502–2514

Abstract: Signal transducer and activator of transcription 3 (STAT3), glioma oncogene homolog 1 (GLI1), and truncated GLI1 (tGLI1) are oncogenic transcription factors playing important roles in breast cancer. tGLI1 is a gain-of-function GLI1 isoform. Whether STAT3 ...

Abstract	Signal transducer and activator of transcription 3 (STAT3), glioma oncogene homolog 1 (GLI1), and truncated GLI1 (tGLI1) are oncogenic transcription factors playing important roles in breast cancer. tGLI1 is a gain-of-function GLI1 isoform. Whether STAT3 physically and/or functionally interacts with GLI1/tGLI1 has not been explored. To address this knowledge gap, we analyzed 47 node-positive breast cancer specimens using immunohistochemical staining and found that phosphorylated-STAT3 (Y705), GLI1, and tGLI1 are co-overexpressed in the majority of triple-negative breast carcinomas (64%) and HER2-enriched (68%) breast carcinomas, and in lymph node metastases (65%). Using gene set enrichment analysis, we analyzed 710 breast tumors and found that STAT3 activation and GLI1/tGLI1 activation signatures are co-enriched in triple-negative subtypes of breast cancers and HER2-enriched subtypes of breast cancers, but not in luminal subtypes of breast cancers. Patients with high levels of STAT3 and GLI1/tGLI1 co-activation in their breast tumors had worse metastasis-free survival compared to those with low levels. Since these proteins co-overexpress in breast tumors, we examined whether they form complexes and observed that STAT3 interacted with both GLI1 and tGLI1. We further found that the STAT3-GLI1 and STAT3-tGLI1 complexes bind to both consensus GLI1-binding and STAT3-binding sites using chromatin immunoprecipitation (ChIP) assay, and that the co-overexpression markedly activated a promoter controlled by GLI1-binding sites. To identify genes that can be directly co-activated by STAT3 and GLI1/tGLI1, we analyzed three ChIP-seq datasets and identified 34 potential target genes. Following validations using reverse transcription polymerase chain reaction and survival analysis, we identified three genes as novel transcriptional targets of STAT3 and GLI1/tGLI1, R-Ras2, Cep70, and UPF3A. Finally, we observed that co-overexpression of STAT3 with GLI1/tGLI1 promoted the ability of breast cancer cells to form mammospheres and that STAT3 only cooperates with tGLI1 in immortalized mammary epithelial cells. In summary, our study identified novel physical and functional cooperation between two families of oncogenic transcription factors, and the interaction contributes to aggressiveness of breast cancer cells and poor prognosis of triple-negative breast cancers and HER2-enriched breast cancers.
MeSH term(s)	Animals ; Brain Neoplasms/genetics ; Brain Neoplasms/metabolism ; Brain Neoplasms/secondary ; Cell Cycle Proteins/genetics ; Cell Line, Tumor ; Female ; Gene Expression Profiling/methods ; Gene Expression Regulation, Neoplastic ; Humans ; Membrane Proteins/genetics ; Mice ; Microtubule-Associated Proteins/genetics ; Monomeric GTP-Binding Proteins/genetics ; Neoplasm Transplantation ; Phosphorylation ; Prognosis ; RNA-Binding Proteins/genetics ; Receptor, ErbB-2/metabolism ; STAT3 Transcription Factor/metabolism ; Spheroids, Cellular/metabolism ; Spheroids, Cellular/pathology ; Survival Analysis ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/metabolism ; Up-Regulation ; Zinc Finger Protein GLI1/metabolism
Chemical Substances	Cell Cycle Proteins ; Cep70 protein, human ; GLI1 protein, human ; Membrane Proteins ; Microtubule-Associated Proteins ; RNA-Binding Proteins ; STAT3 Transcription Factor ; STAT3 protein, human ; UPF3A protein, human ; Zinc Finger Protein GLI1 ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1) ; RRAS2 protein, human (EC 3.6.1) ; Monomeric GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2018-02-16
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	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-018-0132-4
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Article ; Online: Correction: TGLI1 transcription factor mediates breast cancer brain metastasis via activating metastasis-initiating cancer stem cells and astrocytes in the tumor microenvironment.

Sirkisoon, Sherona R / Carpenter, Richard L / Rimkus, Tadas / Doheny, Daniel / Zhu, Dongqin / Aguayo, Noah R / Xing, Fei / Chan, Michael / Ruiz, Jimmy / Metheny-Barlow, Linda J / Strowd, Roy / Lin, Jiayuh / Regua, Angelina T / Arrigo, Austin / Anguelov, Marlyn / Pasche, Boris / Debinski, Waldemar / Watabe, Kounosuke / Lo, Hui-Wen

Oncogene

2021 Volume 40, Issue 12, Page(s) 2338

Language	English
Publishing date	2021-03-02
Publishing country	England
Document type	Published Erratum
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-020-01620-5
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Article ; Online: TGLI1 transcription factor mediates breast cancer brain metastasis via activating metastasis-initiating cancer stem cells and astrocytes in the tumor microenvironment.

Oncogene

2019 Volume 39, Issue 1, Page(s) 64–78

Abstract: Mechanisms for breast cancer metastasis remain unclear. Whether truncated glioma-associated oncogene homolog 1 (TGLI1), a transcription factor known to promote angiogenesis, migration and invasion, plays any role in metastasis of any tumor type has never ...

Abstract	Mechanisms for breast cancer metastasis remain unclear. Whether truncated glioma-associated oncogene homolog 1 (TGLI1), a transcription factor known to promote angiogenesis, migration and invasion, plays any role in metastasis of any tumor type has never been investigated. In this study, results of two mouse models of breast cancer metastasis showed that ectopic expression of TGLI1, but not GLI1, promoted preferential metastasis to the brain. Conversely, selective TGLI1 knockdown using antisense oligonucleotides led to decreased breast cancer brain metastasis (BCBM) in vivo. Immunohistochemical staining showed that TGLI1, but not GLI1, was increased in lymph node metastases compared to matched primary tumors, and that TGLI1 was expressed at higher levels in BCBM specimens compared to primary tumors. TGLI1 activation is associated with a shortened time to develop BCBM and enriched in HER2-enriched and triple-negative breast cancers. Radioresistant BCBM cell lines and specimens expressed higher levels of TGLI1, but not GLI1, than radiosensitive counterparts. Since cancer stem cells (CSCs) are radioresistant and metastasis-initiating cells, we examined TGLI1 for its involvement in breast CSCs and found TGLI1 to transcriptionally activate stemness genes CD44, Nanog, Sox2, and OCT4 leading to CSC renewal, and TGLI1 outcompetes with GLI1 for binding to target promoters. We next examined whether astrocyte-priming underlies TGLI1-mediated brain tropism and found that TGLI1-positive CSCs strongly activated and interacted with astrocytes in vitro and in vivo. These findings demonstrate, for the first time, that TGLI1 mediates breast cancer metastasis to the brain, in part, through promoting metastasis-initiating CSCs and activating astrocytes in BCBM microenvironment.
MeSH term(s)	Animals ; Astrocytes/metabolism ; Astrocytes/pathology ; Brain Neoplasms/genetics ; Brain Neoplasms/pathology ; Brain Neoplasms/radiotherapy ; Brain Neoplasms/secondary ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Breast Neoplasms/radiotherapy ; Cell Line, Tumor ; Female ; Gene Expression Regulation, Neoplastic/genetics ; Heterografts ; Humans ; Hyaluronan Receptors/genetics ; Lymphatic Metastasis ; Mice ; Nanog Homeobox Protein/genetics ; Neoplastic Stem Cells/pathology ; Neoplastic Stem Cells/radiation effects ; Octamer Transcription Factor-3/genetics ; Receptor, ErbB-2/genetics ; SOXB1 Transcription Factors/genetics ; Transcription Factors/genetics ; Tumor Microenvironment/genetics ; Zinc Finger Protein GLI1/genetics ; Zinc Finger Protein GLI1/metabolism
Chemical Substances	GLI1 protein, human ; Hyaluronan Receptors ; NANOG protein, human ; Nanog Homeobox Protein ; Octamer Transcription Factor-3 ; POU5F1 protein, human ; SOX2 protein, human ; SOXB1 Transcription Factors ; Transcription Factors ; Zinc Finger Protein GLI1 ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1)
Language	English
Publishing date	2019-08-28
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	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-019-0959-3
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Article ; Online: Combined inhibition of AKT and HSF1 suppresses breast cancer stem cells and tumor growth.

Carpenter, Richard L / Sirkisoon, Sherona / Zhu, Dongqin / Rimkus, Tadas / Harrison, Alexandria / Anderson, Ashley / Paw, Ivy / Qasem, Shadi / Xing, Fei / Liu, Yin / Chan, Michael / Metheny-Barlow, Linda / Pasche, Boris C / Debinski, Waldemar / Watabe, Kounosuke / Lo, Hui-Wen

Oncotarget

2017 Volume 8, Issue 43, Page(s) 73947–73963

Abstract: Breast cancer is the most common cancer in women and the second leading cause of cancer deaths in women. Over 90% of breast cancer deaths are attributable to metastasis. Our lab has recently reported that AKT activates heat shock factor 1 (HSF1), leading ...

Abstract	Breast cancer is the most common cancer in women and the second leading cause of cancer deaths in women. Over 90% of breast cancer deaths are attributable to metastasis. Our lab has recently reported that AKT activates heat shock factor 1 (HSF1), leading to epithelial-to-mesenchymal transition in HER2-positive breast cancer. However, it is unknown whether the AKT-HSF1 pathway plays an important role in other breast cancer subtypes, breast cancer stem cells, or breast cancer growth and metastasis. Herein, we showed AKT and HSF1 to be frequently co-activated in breast cancer cell lines and specimens across different subtypes. Activated AKT (S473) and HSF1 (S326) are strongly associated with shortened time to metastasis. Inhibition of the AKT-HSF1 signaling axis using small molecule inhibitors, HSF1 knockdown or the dominant-negative HSF1 mutant (S326A) reduced the growth of metastatic breast cancer cells and breast cancer stem cells. The combination of small molecule inhibitors targeting AKT (MK-2206) and HSF1 (KRIBB11) resulted in synergistic killing of breast cancer cells and breast cancer stem cells across different molecular subtypes. Using an orthotopic xenograft mouse model, we found that combined targeting of AKT and HSF1 to significantly reduce tumor growth, induce tumor apoptosis, delay time to metastasis, and prolong host survival. Taken together, our results indicate AKT-HSF1 signaling mediates breast cancer stem cells self-renewal, tumor growth and metastasis, and that dual targeting of AKT and HSF1 resulted in synergistic suppression of breast cancer progression thereby supporting future testing of AKT-HSF1 combination therapy for breast cancer patients.
Language	English
Publishing date	2017-09-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.18166
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