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Article ; Online: Thyroid hormone upregulates LAMP2 expression and lysosome activity.

Tseng, Yi-Hsin / Chang, Cheng-Chih / Lin, Kwang-Huei

Biochemical and biophysical research communications

2023 Volume 662, Page(s) 66–75

Abstract: Thyroid hormone ( ... ...

Abstract	Thyroid hormone (T
MeSH term(s)	Animals ; Mice ; Lysosomal-Associated Membrane Protein 2/genetics ; Lysosomal-Associated Membrane Protein 2/metabolism ; Lysosomal Membrane Proteins/genetics ; Lysosomal Membrane Proteins/metabolism ; Lysosomal-Associated Membrane Protein 1/metabolism ; Lysosomes/metabolism ; Thyroid Hormones/metabolism ; Autophagy/physiology
Chemical Substances	Lysosomal-Associated Membrane Protein 2 ; Lysosomal Membrane Proteins ; Lysosomal-Associated Membrane Protein 1 ; Thyroid Hormones
Language	English
Publishing date	2023-04-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2023.04.061
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Article: Mifepristone inhibits hepatoma growth by enhancing the GR-HSP60-survivin interaction to facilitate survivin degradation.

Huang, Ya-Hui / Lin, Kwang-Huei / Lai, Ming-Wei / Yeh, Chau-Ting

Journal of Cancer

2023 Volume 14, Issue 16, Page(s) 3066–3077

Abstract: Silencing of heat shock protein 60 (HSP60) suppresses the growth of hepatocellular carcinoma (HCC). Mifepristone ... ...

Abstract	Silencing of heat shock protein 60 (HSP60) suppresses the growth of hepatocellular carcinoma (HCC). Mifepristone inhibits
Language	English
Publishing date	2023-09-18
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2573318-7
ISSN	1837-9664
ISSN	1837-9664
DOI	10.7150/jca.86611
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Article ; Online: Thyroid hormone upregulates LAMP2 expression and lysosome activity

Tseng, Yi-Hsin / Chang, Cheng-Chih / Lin, Kwang-Huei

Biochemical and Biophysical Research Communications. 2023 Apr. 20,

2023

Abstract: Thyroid hormone (T₃)-induced autophagy and its biological significance have been extensively investigated in recent years. However, limited studies to date have focused on the important role of lysosomes in autophagy. In this study, we explored the ... ...

Abstract	Thyroid hormone (T₃)-induced autophagy and its biological significance have been extensively investigated in recent years. However, limited studies to date have focused on the important role of lysosomes in autophagy. In this study, we explored the effects of T₃ on lysosomal protein expression and trafficking in detail. Our findings showed that T₃ activates rapid lysosomal turnover and expression of numerous lysosomal genes, including TFEB, LAMP2, ARSB, GBA, PSAP, ATP6V0B, ATP6V0D1, ATP6V1E1, CTSB, CTSH, CTSL, and CTSS, in a thyroid hormone receptor-dependent manner. In a murine model, LAMP2 protein was specifically induced in mice with hyperthyroidism. T₃-promoted microtubule assembly was significantly disrupted by vinblastine, resulting in accumulation of the lipid droplet marker PLIN2. In the presence of the lysosomal autophagy inhibitors bafilomycin A1, chloroquine and ammonium chloride, we observed substantial accumulation of LAMP2 but not LAMP1 protein. T₃ further enhanced the protein levels of ectopically expressed LAMP1 and LAMP2. Upon knockdown of LAMP2, cavities of lysosomes and lipid droplets accumulated in the presence of T₃, although the changes in LAMP1 and PLIN2 expression were less pronounced. More specifically, the protective effect of T₃ against ER stress-induced death was abolished by knockdown of LAMP2. Our collective results indicate that T₃ not only promotes lysosomal gene expression but also LAMP protein stability and microtubule assembly, leading to enhancement of lysosomal activity in digesting any additional autophagosomal burden.
Keywords	ammonium chloride ; animal models ; autophagy ; chloroquine ; death ; droplets ; gene expression ; hyperthyroidism ; lipids ; lysosomes ; microtubules ; protective effect ; protein synthesis ; research ; thyroid hormones ; vinblastine ; Thyroid hormone ; Lysosome ; LAMP2 ; Vesicle trafficking ; ER stress
Language	English
Dates of publication	2023-0420
Publishing place	Elsevier Inc.
Document type	Article ; Online
Note	Pre-press version
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2023.04.061
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Reply to Comments: "Molecular Functions of Thyroid Hormone Signaling in Regulation of Cancer Progression and Anti-Apoptosis"

Liu, Yu-Chin / Yeh, Chau-Ting / Lin, Kwang-Huei

International journal of molecular sciences

2020 Volume 21, Issue 10

Abstract: Dear Editor, [ ... ]. ...

Abstract	Dear Editor, [...].
MeSH term(s)	Apoptosis ; Disease Progression ; Humans ; Neoplasms/pathology ; Protein Isoforms/chemistry ; Protein Isoforms/metabolism ; Receptors, Thyroid Hormone/chemistry ; Receptors, Thyroid Hormone/metabolism ; Signal Transduction ; Thyroid Hormones/metabolism
Chemical Substances	Protein Isoforms ; Receptors, Thyroid Hormone ; Thyroid Hormones
Language	English
Publishing date	2020-05-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21103554
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Cancer Stem Cell Functions in Hepatocellular Carcinoma and Comprehensive Therapeutic Strategies.

Liu, Yu-Chin / Yeh, Chau-Ting / Lin, Kwang-Huei

Cells

2020 Volume 9, Issue 6

Abstract: Hepatocellular carcinoma (HCC) is a significant cause of cancer-related mortality owing to resistance to traditional treatments and tumor recurrence after therapy, which leads to poor therapeutic outcomes. Cancer stem cells (CSC) are a small subset of ... ...

Abstract	Hepatocellular carcinoma (HCC) is a significant cause of cancer-related mortality owing to resistance to traditional treatments and tumor recurrence after therapy, which leads to poor therapeutic outcomes. Cancer stem cells (CSC) are a small subset of tumor cells with the capability to influence self-renewal, differentiation, and tumorigenesis. A number of surface markers for liver cancer stem cell (LCSC) subpopulations (EpCAM, CD133, CD44, CD13, CD90, OV-6, CD47, and side populations) in HCC have been identified. LCSCs play critical roles in regulating HCC stemness, self-renewal, tumorigenicity, metastasis, recurrence, and therapeutic resistance via genetic mutations, epigenetic disruption, signaling pathway dysregulation, or alterations microenvironment. Accumulating studies have shown that biomarkers for LCSCs contribute to diagnosis and prognosis prediction of HCC, supporting their utility in clinical management and development of therapeutic strategies. Preclinical and clinical analyses of therapeutic approaches for HCC using small molecule inhibitors, oncolytic measles viruses, and anti-surface marker antibodies have demonstrated selective, efficient, and safe targeting of LCSC populations. The current review focuses on recent reports on the influence of LCSCs on HCC stemness, tumorigenesis, and multiple drug resistance (MDR), along with LCSC-targeted therapeutic strategies for HCC.
MeSH term(s)	Animals ; Biomarkers, Tumor/metabolism ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/pathology ; Carcinoma, Hepatocellular/therapy ; Cell Communication/genetics ; Cell Plasticity/genetics ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/pathology ; Liver Neoplasms/therapy ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Tumor Microenvironment
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2020-05-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9061331
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Article: Thyroid Hormone in Hepatocellular Carcinoma: Cancer Risk, Growth Regulation, and Anticancer Drug Resistance.

Lin, Yang-Hsiang / Lin, Kwang-Huei / Yeh, Chau-Ting

Frontiers in medicine

2020 Volume 7, Page(s) 174

Abstract: Thyroid hormone (TH) and its receptor (TR) are involved in differentiation, metabolic process, and growth regulation in hepatocellular carcinoma (HCC). The TH/TR complexes are ligand-dependent transcriptional factors, functioning through binding to ... ...

Abstract	Thyroid hormone (TH) and its receptor (TR) are involved in differentiation, metabolic process, and growth regulation in hepatocellular carcinoma (HCC). The TH/TR complexes are ligand-dependent transcriptional factors, functioning through binding to thyroid hormone response elements (TREs) upstream of the target genes. To date, deciphering the biological effects of TH in cancer progression remains challenging. Several lines of evidence suggest a growth inhibitory effect of TH in liver cancer. Mutation and aberrant expression of TRs are highly correlated with several types of cancers including HCC. Several reports show that TH inhibits cell growth in liver cancer through regulation of cell-cycle-related genes and non-coding RNAs. A case-control study indicates that hypothyroidism is associated with an increased risk of HCC. Moreover, TH/TR suppresses hepatocarcinogenesis via selective autophagy. Conversely, other groups have indicated that TH promotes cancer cell proliferation.
Language	English
Publishing date	2020-05-22
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2775999-4
ISSN	2296-858X
ISSN	2296-858X
DOI	10.3389/fmed.2020.00174
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Article ; Online: Correction: Lin, K.-H., et al. Molecular Functions of Thyroid Hormone Signaling in Regulation of Cancer Progression and Anti-Apoptosis.

Liu, Yu-Chin / Yeh, Chau-Ting / Lin, Kwang-Huei

International journal of molecular sciences

2020 Volume 21, Issue 9

Abstract: The authors wish to make the following corrections to this paper [ ... ]. ...

Abstract	The authors wish to make the following corrections to this paper [...].
Language	English
Publishing date	2020-04-30
Publishing country	Switzerland
Document type	Journal Article ; Published Erratum
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21093185
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Article ; Online: Thyroid hormones suppress FOXM1 expression to reduce liver cancer progression.

Wu, Cheng-Heng / Yeh, Chau-Ting / Lin, Kwang-Huei

Oncology reports

2020 Volume 44, Issue 4, Page(s) 1686–1698

Abstract: Thyroid hormones (TH) are multifunctional mediators that fine‑tune several physiological processes, including metabolic rate, digestive function and tissue development via interactions with type II nuclear thyroid hormone receptors (TR). Upon binding of ... ...

Abstract	Thyroid hormones (TH) are multifunctional mediators that fine‑tune several physiological processes, including metabolic rate, digestive function and tissue development via interactions with type II nuclear thyroid hormone receptors (TR). Upon binding of TH, TRs interact specifically with thyroid hormone response elements of target gene promoter regions to regulate their transcription. Earlier studies suggested a correlation between aberrant TR regulation and hepatocellular carcinoma (HCC). THs are involved in a crosstalk between hepatoma and stromal cells, and disruption of TH signaling is associated with tumorigenesis. Previous cDNA microarray analysis of target gene expression following T3 treatment of wild‑type TR‑expressing hepatoma cells led to the identification of forkhead box M1 (FOXM1) as a factor negatively regulated by T3 and associated with poor prognosis in several cancer types. Increased FOXM1 expression during late stages of HCC was associated with poorer overall and recurrence‑free survival in patients with HCC. However, the specific mechanisms underlying FOXM1 activity in liver cancer progression remain to be elucidated. Experiments from the present study showed that TH/TR signaling suppresses FOXM1 mRNA and protein expression. Depletion of FOXM1 induced inhibition of the cell growth rate and a decline in oncogenic cyclin D1, cyclin E and CDK2 expression. Conversely, overexpression of FOXM1 enhanced cell proliferation and expression of oncogenic factors, which was decreased upon FOXM1 depletion. Re‑expression of FOXM1 partially rescued suppression of cell proliferation induced by T3. Collectively, the present findings suggest that TH/TR participates in HCC progression via modulation of FOXM1 expression.
MeSH term(s)	Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/pathology ; Cell Proliferation/drug effects ; Cyclin D1/genetics ; Cyclin E/genetics ; Cyclin-Dependent Kinase 2/genetics ; Disease Progression ; Forkhead Box Protein M1/genetics ; Gene Expression Regulation, Neoplastic/drug effects ; Hep G2 Cells ; Humans ; Liver/drug effects ; Liver/pathology ; Liver Neoplasms/drug therapy ; Liver Neoplasms/genetics ; Liver Neoplasms/pathology ; Thyroid Hormone Receptors beta/genetics ; Triiodothyronine/pharmacology
Chemical Substances	CCND1 protein, human ; Cyclin E ; FOXM1 protein, human ; Forkhead Box Protein M1 ; Thyroid Hormone Receptors beta ; Triiodothyronine (06LU7C9H1V) ; Cyclin D1 (136601-57-5) ; CDK2 protein, human (EC 2.7.11.22) ; Cyclin-Dependent Kinase 2 (EC 2.7.11.22)
Language	English
Publishing date	2020-08-05
Publishing country	Greece
Document type	Journal Article
ZDB-ID	1222484-4
ISSN	1791-2431 ; 1021-335X
ISSN (online)	1791-2431
ISSN	1021-335X
DOI	10.3892/or.2020.7716
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Association between Inflammation and Function of Cell Adhesion Molecules Influence on Gastrointestinal Cancer Development.

Huang, Hsiang-Wei / Chang, Cheng-Chih / Wang, Chia-Siu / Lin, Kwang-Huei

Cells

2021 Volume 10, Issue 1

Abstract: Gastrointestinal cancer is highly associated with inflammatory processes inducing the release of cytokines from cancer or immune cells, including interferons, interleukins, chemokines, colony-stimulating factors, and growth factors, which promote or ... ...

Abstract	Gastrointestinal cancer is highly associated with inflammatory processes inducing the release of cytokines from cancer or immune cells, including interferons, interleukins, chemokines, colony-stimulating factors, and growth factors, which promote or suppress tumor progression. Inflammatory cytokines within the tumor microenvironment promote immune cell infiltration. Infiltrating immune, and tumor-surrounding stromal cells support tumor growth, angiogenesis, metastasis, and immunosuppression through communication with inflammatory cytokines and cell adhesion molecules. Notably, infiltrating immune and tumor cells present immunosuppressive molecules, such as programmed death-ligand 1 (PD-L1) and CD80/CD86. Suppression of cytotoxic T cells promotes tumor avoidance of immune surveillance and greater malignancy. Moreover, glycosylation and sialylation of proteins hyperexpressed on the cancer cell surface have been shown to enhance immune escape and metastasis. Cytokine treatments and immune checkpoint inhibitors are widely used in clinical practice. However, the tumor microenvironment is a rapidly changing milieu involving several factors. In this review, we have provided a summary of the interactions of inflammation and cell adhesion molecules between cancer and other cell types, to improve understanding of the tumor microenvironment.
MeSH term(s)	Animals ; Carcinogenesis/metabolism ; Carcinogenesis/pathology ; Cell Adhesion Molecules/metabolism ; Cell Communication ; Gastrointestinal Neoplasms/metabolism ; Gastrointestinal Neoplasms/pathology ; Gastrointestinal Neoplasms/therapy ; Humans ; Inflammation/metabolism ; Tumor Microenvironment
Chemical Substances	Cell Adhesion Molecules
Language	English
Publishing date	2021-01-04
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10010067
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Article ; Online: Evaluation and Application of Drug Resistance by Biomarkers in the Clinical Treatment of Liver Cancer.

Huang, Po-Shuan / Wang, Ling-Yu / Wang, Yi-Wen / Tsai, Ming-Ming / Lin, Tzu-Kang / Liao, Chia-Jung / Yeh, Chau-Ting / Lin, Kwang-Huei

Cells

2023 Volume 12, Issue 6

Abstract: Liver cancer is one of the most lethal cancers in the world, mainly owing to the lack of effective means for early monitoring and treatment. Accordingly, there is considerable research interest in various clinically applicable methods for addressing ... ...

Abstract	Liver cancer is one of the most lethal cancers in the world, mainly owing to the lack of effective means for early monitoring and treatment. Accordingly, there is considerable research interest in various clinically applicable methods for addressing these unmet needs. At present, the most commonly used biomarker for the early diagnosis of liver cancer is alpha-fetoprotein (AFP), but AFP is sensitive to interference from other factors and cannot really be used as the basis for determining liver cancer. Treatment options in addition to liver surgery (resection, transplantation) include radiation therapy, chemotherapy, and targeted therapy. However, even more expensive targeted drug therapies have a limited impact on the clinical outcome of liver cancer. One of the big reasons is the rapid emergence of drug resistance. Therefore, in addition to finding effective biomarkers for early diagnosis, an important focus of current discussions is on how to effectively adjust and select drug strategies and guidelines for the treatment of liver cancer patients. In this review, we bring this thought process to the drug resistance problem faced by different treatment strategies, approaching it from the perspective of gene expression and molecular biology and the possibility of finding effective solutions.
MeSH term(s)	Humans ; alpha-Fetoproteins/metabolism ; Early Detection of Cancer ; Liver Neoplasms/drug therapy ; Liver Neoplasms/genetics ; Liver Neoplasms/diagnosis ; Biomarkers ; Drug Resistance
Chemical Substances	alpha-Fetoproteins ; Biomarkers
Language	English
Publishing date	2023-03-10
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12060869
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