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Article ; Online: Diagnosis: Novel prognostic biomarkers in hepatocellular carcinoma.

Pang, Roberta W C / Poon, Ronnie T P

Nature reviews. Gastroenterology & hepatology

2012 Volume 9, Issue 12, Page(s) 691–692

MeSH term(s)	Antineoplastic Agents/therapeutic use ; Biomarkers, Tumor/metabolism ; C-Reactive Protein/metabolism ; Carcinoma, Hepatocellular/diagnosis ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/metabolism ; Humans ; Interleukin-6/metabolism ; Liver Neoplasms/diagnosis ; Liver Neoplasms/drug therapy ; Liver Neoplasms/metabolism ; Prognosis ; Treatment Outcome
Chemical Substances	Antineoplastic Agents ; Biomarkers, Tumor ; Interleukin-6 ; C-Reactive Protein (9007-41-4)
Language	English
Publishing date	2012-11-13
Publishing country	England
Document type	News ; Research Support, Non-U.S. Gov't
ZDB-ID	2493722-8
ISSN	1759-5053 ; 1759-5045
ISSN (online)	1759-5053
ISSN	1759-5045
DOI	10.1038/nrgastro.2012.208
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Article ; Online: Cancer stem cell as a potential therapeutic target in hepatocellular carcinoma.

Pang, Roberta W C / Poon, Ronnie T P

Current cancer drug targets

2012 Volume 12, Issue 9, Page(s) 1081–1094

Abstract: Hepatocellular carcinoma (HCC) is one of the most common human cancers. HCC is a chemoresistant cancer and the current drug therapy has limited efficacy. As a result, the prognosis of HCC patients is generally poor. Recent studies have demonstrated that ... ...

Abstract	Hepatocellular carcinoma (HCC) is one of the most common human cancers. HCC is a chemoresistant cancer and the current drug therapy has limited efficacy. As a result, the prognosis of HCC patients is generally poor. Recent studies have demonstrated that a subpopulation of cancer cells with stem cell properties, called cancer stem cells (CSCs), are responsible for growth and metastasis of cancer. CSCs characterized by several markers including CD133, CD44, CD90, OV6, Epithelial cell adhesion molecule (EpCAM) and CD13 have been isolated from different human HCC cell lines or specimens. CSCs share many of the signaling pathways found in normal stem cells, such as Wnt, Hedgehog, Notch and Transforming growth factor-beta (TGF-β) pathways. These pathways are involved in self-renewal, differentiation and survival of CSCs. There is evidence of deregulation of these pathways in HCC CSCs. MicroRNAs also play an important role in regulating signaling pathways in HCC, and recent data suggested an important role of microRNA in CSCs of HCC. Therapeutic targeting of CSCs may provide a novel strategy that is more effective than the current drugs targeting the bulk mature cancer cells in treatment of HCC.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Carcinoma, Hepatocellular/prevention & control ; Humans ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Liver Neoplasms/prevention & control ; Neoplastic Stem Cells/drug effects
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2012-06-20
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2064824-8
ISSN	1873-5576 ; 1568-0096
ISSN (online)	1873-5576
ISSN	1568-0096
DOI	10.2174/156800912803987995
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Article ; Online: Suppression of Slit3 induces tumor proliferation and chemoresistance in hepatocellular carcinoma through activation of GSK3β/β-catenin pathway.

Ng, Lui / Chow, Ariel K M / Man, Johnny H W / Yau, Thomas C C / Wan, Timothy M H / Iyer, Deepak N / Kwan, Virginia H T / Poon, Ronnie T P / Pang, Roberta W C / Law, Wai-Lun

BMC cancer

2018 Volume 18, Issue 1, Page(s) 621

Abstract: Background: It is essential to understand the mechanisms responsible for hepatocellular carcinoma (HCC) progression and chemoresistance in order to identify prognostic biomarkers as well as potential therapeutic avenues. Recent findings have shown that ... ...

Abstract	Background: It is essential to understand the mechanisms responsible for hepatocellular carcinoma (HCC) progression and chemoresistance in order to identify prognostic biomarkers as well as potential therapeutic avenues. Recent findings have shown that SLIT3 appears to function as a novel tumor suppressor gene in various types of cancers, yet its clinical correlation and role in HCC has not been understood clearly. Methods: We determined the transcript levels of Slit3 in tumor and adjacent normal tissues within two cohorts (N = 40 and 25) of HCC patients, and correlated the gene expression with the clinicopathological data. Subsequently, the functional effects and underlying molecular mechanisms of Slit3 overexpression and/or repression were studied using cell-line and mouse models. Results: Our results demonstrated a repression in Slit3 expression in nearly 50% of the HCC patients, while the overall expression of Slit3 inversely correlated with the size of the tumor in both cohorts of patients. Stable down-regulation of Slit3 in HCC cell-lines induced cell proliferation in vitro and tumor growth in vivo, while stable Slit3 overexpression repressed these effects. Molecular investigations showed that the stable Slit3 repression-induced cell proliferation was associated with a higher expression of β-catenin and a repressed GSK3β activity. Moreover, Slit3-repression induced chemoresistance to sorafenib, oxaliplatin and 5-FU through impairment of β-catenin degradation and induction of cyclin D3 and survivin levels. The effects induced by stable Slit3-repression were diminished by transient repression of β-catenin by siRNA approach. Conclusion: This study suggests that Slit3 acts as a tumor suppressor in HCC by repressing the tumor growth and thus tumor progression. Low Slit3 level indicates a poor response of HCC cells to chemotherapy. Restoration or overexpression of Slit3 is a potential therapeutic approach to repress the tumor growth and enhance the efficacy of chemotherapeutic agents.
MeSH term(s)	Adult ; Aged ; Animals ; Carcinoma, Hepatocellular/pathology ; Cell Line, Tumor ; Cell Proliferation/physiology ; Drug Resistance, Neoplasm/physiology ; Female ; Genes, Tumor Suppressor/physiology ; Glycogen Synthase Kinase 3 beta/metabolism ; Heterografts ; Humans ; Liver Neoplasms/pathology ; Male ; Membrane Proteins/metabolism ; Mice ; Mice, Nude ; Middle Aged ; Signal Transduction/physiology ; beta Catenin/metabolism
Chemical Substances	CTNNB1 protein, human ; Membrane Proteins ; SLIT3 protein, human ; beta Catenin ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1)
Language	English
Publishing date	2018-06-01
Publishing country	England
Document type	Journal Article
ISSN	1471-2407
ISSN (online)	1471-2407
DOI	10.1186/s12885-018-4326-5
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Article ; Online: Survivin depletion inhibits tumor growth and enhances chemosensitivity in hepatocellular carcinoma.

Or, Yvonne Y Y / Chow, Ariel K M / Ng, Lui / Fan, Sheung Tat / Yau, Thomas C C / Poon, Ronnie T P / Pang, Roberta W C

Molecular medicine reports

2014 Volume 10, Issue 4, Page(s) 2025–2030

Abstract: Survivin is a member of the inhibitor of apoptosis family, which has been suggested to be crucial in the control of cell division and inhibition of apoptosis. Expression of this protein has been observed in transformed cell lines and human tumor tissues, ...

Abstract	Survivin is a member of the inhibitor of apoptosis family, which has been suggested to be crucial in the control of cell division and inhibition of apoptosis. Expression of this protein has been observed in transformed cell lines and human tumor tissues, including those from colorectal cancer, but not in terminally differentiated adult tissues. Survivin mRNA expression has frequently been detected in hepatocellular carcinoma (HCC) and its protein expression has been demonstrated to be highly correlated with proliferation index rather than apoptotic index. The present study aimed to analyze the effect of survivin on the tumorigenicity and chemosensitivity of HCC via the establishment of an HCC cell line (PLC/PRF/5) with the stable knockdown of the survivin gene (PLC‑k3). This cell line displayed significantly lower rates of survival and proliferation in assays of cell viability and proliferation, respectively, compared with those of the control cell line (PLC‑v). In addition, PLC‑k3 cells were more sensitive to cisplatin treatment, resulting in S phase arrest. These findings were further confirmed by an in vivo experiment. The data of the present study suggest that survivin is critical in promoting cell proliferation but not in inhibition of apoptosis, and enhances the chemosensitivity of HCC. Thus, the suppression of survivin expression in combination with cisplatin may contribute to the development of more effective treatments for HCC.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Antineoplastic Agents/toxicity ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Cell Transformation, Neoplastic/drug effects ; Cisplatin/therapeutic use ; Cisplatin/toxicity ; Humans ; Inhibitor of Apoptosis Proteins/deficiency ; Inhibitor of Apoptosis Proteins/genetics ; Inhibitor of Apoptosis Proteins/metabolism ; Liver Neoplasms/drug therapy ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Oligonucleotides, Antisense/metabolism ; S Phase Cell Cycle Checkpoints/drug effects ; Transplantation, Heterologous
Chemical Substances	Antineoplastic Agents ; BIRC5 protein, human ; Inhibitor of Apoptosis Proteins ; Oligonucleotides, Antisense ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2014-10
Publishing country	Greece
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1791-3004
ISSN (online)	1791-3004
DOI	10.3892/mmr.2014.2413
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Article: Clinical implications of angiogenesis in cancers.

Pang, Roberta W C / Poon, Ronnie T P

Vascular health and risk management

2007 Volume 2, Issue 2, Page(s) 97–108

Abstract: Angiogenesis plays an important role in the growth and progression of cancer. The regulation of tumor angiogenesis depends on a net balance of angiogenic factors and antiangiogenic factors, which are secreted by both tumor cells and host-infiltrating ... ...

Abstract	Angiogenesis plays an important role in the growth and progression of cancer. The regulation of tumor angiogenesis depends on a net balance of angiogenic factors and antiangiogenic factors, which are secreted by both tumor cells and host-infiltrating cells. Numerous studies have indicated that assessment of angiogenic activity by either microvessel density or expression of angiogenic factors in cancer can provide prognostic information independent of conventional clinicopathological factors such as tumor staging. Some studies also suggested that assessment of tumor angiogenesis may predict cancer response to chemotherapy or radiotherapy. However, the most important clinical implication of tumor angiogenesis is the development of a novel strategy of anticancer therapy targeting tumor vessels instead of cancer cells. Antiangiogenic therapy aims to inhibit the growth of tumor, and current evidence suggests that it works best in combination with conventional cytotoxic chemotherapy. Recently, a monoclonal antibody against vascular endothelial growth factor, which is one of the most potent angiogenic factors, has been approved for clinical use in colorectal cancer patients after a clinical trial confirmed that combining the antibody with standard chemotherapy regimen could prolong patient survival. The clinical implications of angiogenesis in cancer are reviewed in this article.
MeSH term(s)	Angiogenesis Inhibitors/therapeutic use ; Angiogenic Proteins/metabolism ; Angiostatic Proteins ; Animals ; Antineoplastic Agents/therapeutic use ; Biomarkers, Tumor/metabolism ; Humans ; Neoplasms/blood supply ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/pathology ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/pathology ; Prognosis ; Treatment Outcome
Chemical Substances	Angiogenesis Inhibitors ; Angiogenic Proteins ; Angiostatic Proteins ; Antineoplastic Agents ; Biomarkers, Tumor
Language	English
Publishing date	2007-02-23
Publishing country	New Zealand
Document type	Journal Article ; Review
ZDB-ID	2186568-1
ISSN	1178-2048 ; 1176-6344
ISSN (online)	1178-2048
ISSN	1176-6344
DOI	10.2147/vhrm.2006.2.2.97
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Article ; Online: From molecular biology to targeted therapies for hepatocellular carcinoma: the future is now.

Pang, Roberta W C / Poon, Ronnie T P

Oncology

2007 Volume 72 Suppl 1, Page(s) 30–44

Abstract: Hepatocellular carcinoma (HCC) is characterized as a highly chemoresistant cancer with no effective systemic therapy. Despite surgical or locoregional therapies, prognosis remains poor because of high tumor recurrence or tumor progression, and currently ... ...

Abstract	Hepatocellular carcinoma (HCC) is characterized as a highly chemoresistant cancer with no effective systemic therapy. Despite surgical or locoregional therapies, prognosis remains poor because of high tumor recurrence or tumor progression, and currently there are no well-established effective adjuvant therapies. The molecular biology of carcinogenesis and tumor progression of HCC has been increasingly understood with intense research in recent years. Several important intracellular signaling pathways such as the Ras/Raf/Mek/Erk pathway and PI3k/Akt/mTOR pathway have been recognized, and the role of several growth factors and angiogenic factors such as EGF and VEGF has been confirmed. Effective agents targeting these molecular abnormalities have been developed and widely tested in preclinical studies of HCC cell lines or xenograft models. Several agents have entered clinical trials in HCC patients, and recent data indicated that a multikinase inhibitor targeting Ras kinase and VEGFR-2, sorafenib, is effective in prolonging survival of patients with advanced HCC. The management of advanced HCC is entering the era of molecular targeting therapy, which is of particular significance for HCC in view of the lack of existing effective systemic therapy for this cancer.
MeSH term(s)	Angiogenesis Inhibitors/pharmacology ; Angiogenic Proteins/metabolism ; Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Carcinoma, Hepatocellular/blood supply ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/metabolism ; Cell Cycle Proteins/metabolism ; Cell Line, Tumor ; Disease Models, Animal ; Glucuronidase/drug effects ; Humans ; Liver Neoplasms/blood supply ; Liver Neoplasms/drug therapy ; Liver Neoplasms/metabolism ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/prevention & control ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Receptor, Epidermal Growth Factor/drug effects ; Receptors, Platelet-Derived Growth Factor/drug effects ; Receptors, Vascular Endothelial Growth Factor/drug effects ; Signal Transduction/drug effects ; TOR Serine-Threonine Kinases ; Transplantation, Heterologous ; Vascular Endothelial Growth Factor A/drug effects ; Wnt Proteins/metabolism ; beta Catenin/metabolism ; raf Kinases/metabolism ; ras Proteins/metabolism
Chemical Substances	Angiogenesis Inhibitors ; Angiogenic Proteins ; Antineoplastic Agents ; Cell Cycle Proteins ; Vascular Endothelial Growth Factor A ; Wnt Proteins ; beta Catenin ; Protein Kinases (EC 2.7.-) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Receptor, Epidermal Growth Factor (EC 2.7.10.1) ; Receptors, Platelet-Derived Growth Factor (EC 2.7.10.1) ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; raf Kinases (EC 2.7.11.1) ; heparanase (EC 3.2.1.-) ; Glucuronidase (EC 3.2.1.31) ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2007
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	250101-6
ISSN	1423-0232 ; 0030-2414
ISSN (online)	1423-0232
ISSN	0030-2414
DOI	10.1159/000111705
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Article ; Online: The Wnt5a Receptor, Receptor Tyrosine Kinase-Like Orphan Receptor 2, Is a Predictive Cell Surface Marker of Human Mesenchymal Stem Cells with an Enhanced Capacity for Chondrogenic Differentiation.

Dickinson, Sally C / Sutton, Catherine A / Brady, Kyla / Salerno, Anna / Katopodi, Theoni / Williams, Rhys L / West, Christopher C / Evseenko, Denis / Wu, Ling / Pang, Suzanna / Ferro de Godoy, Roberta / Goodship, Allen E / Péault, Bruno / Blom, Ashley W / Kafienah, Wael / Hollander, Anthony P

Stem cells (Dayton, Ohio)

2017 Volume 35, Issue 11, Page(s) 2280–2291

Abstract: Multipotent mesenchymal stem cells (MSCs) have enormous potential in tissue engineering and regenerative medicine. However, until now, their development for clinical use has been severely limited as they are a mixed population of cells with varying ... ...

Abstract	Multipotent mesenchymal stem cells (MSCs) have enormous potential in tissue engineering and regenerative medicine. However, until now, their development for clinical use has been severely limited as they are a mixed population of cells with varying capacities for lineage differentiation and tissue formation. Here, we identify receptor tyrosine kinase-like orphan receptor 2 (ROR2) as a cell surface marker expressed by those MSCs with an enhanced capacity for cartilage formation. We generated clonal human MSC populations with varying capacities for chondrogenesis. ROR2 was identified through screening for upregulated genes in the most chondrogenic clones. When isolated from uncloned populations, ROR2+ve MSCs were significantly more chondrogenic than either ROR2-ve or unfractionated MSCs. In a sheep cartilage-repair model, they produced significantly more defect filling with no loss of cartilage quality compared with controls. ROR2+ve MSCs/perivascular cells were present in developing human cartilage, adult bone marrow, and adipose tissue. Their frequency in bone marrow was significantly lower in patients with osteoarthritis (OA) than in controls. However, after isolation of these cells and their initial expansion in vitro, there was greater ROR2 expression in the population derived from OA patients compared with controls. Furthermore, osteoarthritis-derived MSCs were better able to form cartilage than MSCs from control patients in a tissue engineering assay. We conclude that MSCs expressing high levels of ROR2 provide a defined population capable of predictably enhanced cartilage production. Stem Cells 2017;35:2280-2291.
MeSH term(s)	Animals ; Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Chondrogenesis/genetics ; Humans ; Mesenchymal Stem Cells/metabolism ; Receptor Tyrosine Kinase-like Orphan Receptors/genetics ; Receptor Tyrosine Kinase-like Orphan Receptors/metabolism ; Sheep ; Tissue Engineering ; Wnt-5a Protein/genetics ; Wnt-5a Protein/metabolism
Chemical Substances	WNT5A protein, human ; Wnt-5a Protein ; Receptor Tyrosine Kinase-like Orphan Receptors (EC 2.7.10.1)
Language	English
Publishing date	2017-08-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	1143556-2
ISSN	1549-4918 ; 1066-5099
ISSN (online)	1549-4918
ISSN	1066-5099
DOI	10.1002/stem.2691
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Article ; Online: Replication of type 5 adenovirus promotes middle ear infection by Streptococcus pneumoniae in the chinchilla model of otitis media.

Murrah, Kyle A / Turner, Roberta L / Pang, Bing / Perez, Antonia C / Reimche, Jennifer L / King, Lauren B / Wren, John / Gandhi, Uma / Swords, W Edward / Ornelles, David A

Pathogens and disease

2015 Volume 73, Issue 2, Page(s) 1–8

Abstract: Adenoviral infection is a major risk factor for otitis media. We hypothesized that adenovirus promotes bacterial ascension into the middle ear through the disruption of normal function in the Eustachian tubes due to inflammation-induced changes. An ... ...

Abstract	Adenoviral infection is a major risk factor for otitis media. We hypothesized that adenovirus promotes bacterial ascension into the middle ear through the disruption of normal function in the Eustachian tubes due to inflammation-induced changes. An intranasal infection model of the chinchilla was used to test the ability of type 5 adenovirus to promote middle ear infection by Streptococcus pneumoniae. The hyperinflammatory adenovirus mutant dl327 and the nonreplicating adenovirus mutant H5wt300ΔpTP were used to test the role of inflammation and viral replication, respectively, in promotion of pneumococcal middle ear infection. Precedent infection with adenovirus resulted in a significantly greater incidence of middle ear disease by S. pneumoniae as compared to nonadenovirus infected animals. Infection with the adenovirus mutant dl327 induced a comparable degree of bacterial ascension into the middle ear as did infection with the wild-type virus. By contrast, infection with the nonreplicating adenovirus mutant H5wt300ΔpTP resulted in less extensive middle ear infection compared to the wild-type adenovirus. We conclude that viral replication is necessary for adenoviral-induced pneumococcal middle ear disease.
MeSH term(s)	Adenoviridae/physiology ; Adenoviridae Infections/pathology ; Adenoviridae Infections/virology ; Animals ; Coinfection/microbiology ; Coinfection/pathology ; Coinfection/virology ; Disease Models, Animal ; Ear, Middle/microbiology ; Ear, Middle/pathology ; Ear, Middle/virology ; Otitis Media/microbiology ; Otitis Media/pathology ; Otitis Media/virology ; Pneumococcal Infections/microbiology ; Pneumococcal Infections/pathology ; Rabbits ; Streptococcus pneumoniae/growth & development ; Virus Replication
Language	English
Publishing date	2015-02-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2049-632X
ISSN (online)	2049-632X
DOI	10.1111/2049-632X.12216
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Article ; Online: Preclinical analysis of the anti-tumor and anti-metastatic effects of Raf265 on colon cancer cells and CD26(+) cancer stem cells in colorectal carcinoma.

Chow, Ariel K M / Cheng, Nathan S M / Lam, Colin S C / Ng, Lui / Wong, Sunny K M / Wan, Timothy M H / Man, Johnny H W / Cheung, Alvin H K / Yau, Thomas C C / Poon, Jensen T C / Law, Wai-Lun / Pang, Roberta W C

Molecular cancer

2015 Volume 14, Page(s) 80

Abstract: Background: In colorectal carcinoma (CRC), activation of the Raf/MEK/ERK signaling pathway is commonly observed. In addition, the commonly used 5FU-based chemotherapy in patients with metastatic CRC was found to enrich a subpopulation of CD26(+) cancer ... ...

Abstract	Background: In colorectal carcinoma (CRC), activation of the Raf/MEK/ERK signaling pathway is commonly observed. In addition, the commonly used 5FU-based chemotherapy in patients with metastatic CRC was found to enrich a subpopulation of CD26(+) cancer stem cells (CSCs). As activation of the Raf/MEK/ERK signaling pathway was also found in the CD26(+) CSCs and therefore, we hypothesized that an ATP-competitive pan-Raf inhibitor, Raf265, is effective in eliminating the cancer cells and the CD26(+) CSCs in CRC patients. Methods: HT29 and HCT116 cells were treated with various concentrations of Raf265 to study the anti-proliferative and apoptotic effects of Raf265. Anti-tumor effect was also demonstrated using a xenograft model. Cells were also treated with Raf265 in combination with 5FU to demonstrate the anti-migratory and invasive effects by targeting on the CD26(+) CSCs and the anti-metastatic effect of the combined treatment was shown in an orthotopic CRC model. Results: Raf265 was found to be highly effective in inhibiting cell proliferation and tumor growth through the inhibition of the RAF/MEK/ERK signaling pathway. In addition, anti-migratory and invasive effect was found with Raf265 treatment in combination with 5FU by targeting on the CD26(+) cells. Finally, the anti-tumor and anti-metastatic effect of Raf265 in combination with 5FU was also demonstrated. Conclusions: This preclinical study demonstrates the anti-tumor and anti-metastatic activity of Raf265 in CRC, providing the basis for exploiting its potential use and combination therapy with 5FU in the clinical treatment of CRC.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Cell Self Renewal ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Drug Evaluation, Preclinical ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Fluorouracil/pharmacology ; HCT116 Cells ; HT29 Cells ; Humans ; Imidazoles/pharmacology ; Mice ; Mitogen-Activated Protein Kinases/metabolism ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/metabolism ; Proto-Oncogene Proteins B-raf/metabolism ; Pyridines/pharmacology ; Signal Transduction/drug effects
Chemical Substances	Antineoplastic Agents ; Imidazoles ; Pyridines ; RAF265 (927880-90-8) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Fluorouracil (U3P01618RT)
Language	English
Publishing date	2015-04-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1476-4598
ISSN (online)	1476-4598
DOI	10.1186/s12943-015-0352-y
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Article ; Online: Comparative evaluation of biased agonists Sarcosine

Noto, Natalia M / Restrepo, Yazmin M / Pang, Hong W / Stoyell-Conti, Filipe / West, Crystal A / Speth, Robert C

Pharmacology research & perspectives

2023 Volume 11, Issue 1, Page(s) e01053

Abstract: Angiotensin II analogue and β-arrestin biased agonist TRV027 ( ... ...

Abstract	Angiotensin II analogue and β-arrestin biased agonist TRV027 (Sarcosine
MeSH term(s)	Animals ; Female ; Male ; Rats ; Alanine/metabolism ; Angiotensin II/pharmacology ; beta-Arrestins/metabolism ; Isoleucine/metabolism ; Liver/metabolism ; Sarcosine/metabolism ; Receptor, Angiotensin, Type 1/metabolism
Chemical Substances	Alanine (OF5P57N2ZX) ; Angiotensin II (11128-99-7) ; beta-Arrestins ; Isoleucine (04Y7590D77) ; Sarcosine (Z711V88R5F) ; Receptor, Angiotensin, Type 1
Language	English
Publishing date	2023-01-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2740389-0
ISSN	2052-1707 ; 2052-1707
ISSN (online)	2052-1707
ISSN	2052-1707
DOI	10.1002/prp2.1053
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