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Artikel ; Online: TFE3 promotes ferroptosis in melanoma.

Dias, Diogo / Louphrasitthiphol, Pakavarin / Goding, Colin R

2023 Band 37, Heft 2, Seite(n) 286–290

Mesh-Begriff(e)	Humans ; Melanoma/genetics ; Ferroptosis/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
Chemische Substanzen	Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; TFE3 protein, human
Sprache	Englisch
Erscheinungsdatum	2023-11-12
Erscheinungsland	England
Dokumenttyp	Letter
ZDB-ID	2409570-9
ISSN	1755-148X ; 1600-0749 ; 0893-5785 ; 1755-1471
ISSN (online)	1755-148X ; 1600-0749
ISSN	0893-5785 ; 1755-1471
DOI	10.1111/pcmr.13149
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Novel positron emission tomography imaging targeting cell surface glycans for pancreatic cancer:

Kuroda, Yukihito / Oda, Tatsuya / Shimomura, Osamu / Louphrasitthiphol, Pakavarin / Mathis, Bryan J / Tateno, Hiroaki / Hatano, Kentaro

Cancer science

2023 Band 114, Heft 8, Seite(n) 3364–3373

Abstract: Advancement in early detection modalities will greatly improve the overall prognoses of pancreatic ductal adenocarcinoma (PDAC). For this purpose, we report a novel class of tumor-specific probes for positron emission tomography (PET) based on targeting ... ...

Abstract	Advancement in early detection modalities will greatly improve the overall prognoses of pancreatic ductal adenocarcinoma (PDAC). For this purpose, we report a novel class of tumor-specific probes for positron emission tomography (PET) based on targeting cell surface glycans. The PDAC-targeting ability of rBC2LCN lectin, combined with fluorine-18 (
Mesh-Begriff(e)	Humans ; Mice ; Animals ; Mice, Nude ; Cell Line, Tumor ; Positron-Emission Tomography/methods ; Pancreatic Neoplasms/diagnostic imaging ; Carcinoma, Pancreatic Ductal ; Radiopharmaceuticals ; Pancreatic Neoplasms
Chemische Substanzen	Fluorine-18 (GZ5I74KB8G) ; rBC2LCN lectin ; Radiopharmaceuticals
Sprache	Englisch
Erscheinungsdatum	2023-05-19
Erscheinungsland	England
Dokumenttyp	Journal Article
ZDB-ID	2115647-5
ISSN	1349-7006 ; 1349-7006
ISSN (online)	1349-7006
ISSN	1349-7006
DOI	10.1111/cas.15846
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Macrophage Cytoplasmic Transfer in Melanoma Invasion.

Louphrasitthiphol, Pakavarin / Goding, Colin R

Developmental cell

2017 Band 43, Heft 5, Seite(n) 543–544

Abstract: Within tumors, macrophage infiltration can promote cancer cell invasiveness and, consequently, metastatic dissemination. In this issue of Developmental Cell, Roh-Johnson et al. (2017) reveal that cytoplasmic transfer from macrophages to melanoma cells ... ...

Abstract	Within tumors, macrophage infiltration can promote cancer cell invasiveness and, consequently, metastatic dissemination. In this issue of Developmental Cell, Roh-Johnson et al. (2017) reveal that cytoplasmic transfer from macrophages to melanoma cells correlates with melanoma invasion and arises as a result of intimate cell-cell contact.
Mesh-Begriff(e)	Animals ; Cell Line, Tumor ; Cytoplasm/metabolism ; Humans ; Macrophages/pathology ; Melanoma/metabolism ; Neoplasm Invasiveness/pathology
Sprache	Englisch
Erscheinungsdatum	2017--04
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Review ; Comment
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2017.11.012
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: DNA damage remodels the MITF interactome to increase melanoma genomic instability.

Binet, Romuald / Lambert, Jean-Philippe / Tomkova, Marketa / Tischfield, Samuel / Baggiolini, Arianna / Picaud, Sarah / Sarkar, Sovan / Louphrasitthiphol, Pakavarin / Dias, Diogo / Carreira, Suzanne / Humphrey, Timothy C / Fillipakopoulos, Panagis / White, Richard / Goding, Colin R

Genes & development

2024 Band 38, Heft 1-2, Seite(n) 70–94

Abstract: Since genome instability can drive cancer initiation and progression, cells have evolved highly effective and ubiquitous DNA damage response (DDR) programs. However, some cells (for example, in skin) are normally exposed to high levels of DNA-damaging ... ...

Abstract	Since genome instability can drive cancer initiation and progression, cells have evolved highly effective and ubiquitous DNA damage response (DDR) programs. However, some cells (for example, in skin) are normally exposed to high levels of DNA-damaging agents. Whether such high-risk cells possess lineage-specific mechanisms that tailor DNA repair to the tissue remains largely unknown. Using melanoma as a model, we show here that the microphthalmia-associated transcription factor MITF, a lineage addition oncogene that coordinates many aspects of melanocyte and melanoma biology, plays a nontranscriptional role in shaping the DDR. On exposure to DNA-damaging agents, MITF is phosphorylated at S325, and its interactome is dramatically remodeled; most transcription cofactors dissociate, and instead MITF interacts with the MRE11-RAD50-NBS1 (MRN) complex. Consequently, cells with high MITF levels accumulate stalled replication forks and display defects in homologous recombination-mediated repair associated with impaired MRN recruitment to DNA damage. In agreement with this, high MITF levels are associated with increased single-nucleotide and copy number variant burdens in melanoma. Significantly, the SUMOylation-defective MITF-E318K melanoma predisposition mutation recapitulates the effects of DNA-PKcs-phosphorylated MITF. Our data suggest that a nontranscriptional function of a lineage-restricted transcription factor contributes to a tissue-specialized modulation of the DDR that can impact cancer initiation.
Mesh-Begriff(e)	Humans ; Melanoma/genetics ; Microphthalmia-Associated Transcription Factor/genetics ; DNA Damage ; Genomic Instability/genetics ; DNA
Chemische Substanzen	Microphthalmia-Associated Transcription Factor ; DNA (9007-49-2) ; MITF protein, human
Sprache	Englisch
Erscheinungsdatum	2024-02-13
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.350740.123
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Hypoxia at 3D organoid establishment selects essential subclones within heterogenous pancreatic cancer.

Kumano, Koichiro / Nakahashi, Hiromitsu / Louphrasitthiphol, Pakavarin / Kuroda, Yukihito / Miyazaki, Yoshihiro / Shimomura, Osamu / Hashimoto, Shinji / Akashi, Yoshimasa / Mathis, Bryan J / Kim, Jaejeong / Owada, Yohei / Goding, Colin R / Oda, Tatsuya

Frontiers in cell and developmental biology

2024 Band 12, Seite(n) 1327772

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is especially hypoxic and composed of heterogeneous cell populations containing hypoxia-adapted cells. Hypoxia as a microenvironment of PDAC is known to cause epithelial-mesenchymal transition (EMT) and resistance ... ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is especially hypoxic and composed of heterogeneous cell populations containing hypoxia-adapted cells. Hypoxia as a microenvironment of PDAC is known to cause epithelial-mesenchymal transition (EMT) and resistance to therapy. Therefore, cells adapted to hypoxia possess malignant traits that should be targeted for therapy. However, current 3D organoid culture systems are usually cultured under normoxia, losing hypoxia-adapted cells due to selectivity bias at the time of organoid establishment. To overcome any potential selection bias, we focused on oxygen concentration during the establishment of 3D organoids. We subjected identical PDAC surgical samples to normoxia (O2 20%) or hypoxia (O2 1%), yielding glandular and solid organoid morphology, respectively. Pancreatic cancer organoids established under hypoxia displayed higher expression of EMT-related proteins, a Moffitt basal-like subtype transcriptome, and higher 5-FU resistance in contrast to organoids established under normoxia. We suggest that hypoxia during organoid establishment efficiently selects for hypoxia-adapted cells possibly responsible for PDAC malignant traits, facilitating a fundamental source for elucidating and developing new treatment strategies against PDAC.
Sprache	Englisch
Erscheinungsdatum	2024-02-05
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2024.1327772
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Phenotype-specific melanoma uptake of fatty acid from human adipocytes activates AXL and CAV1-dependent β-catenin nuclear accumulation.

Chocarro-Calvo, Ana / Jociles-Ortega, Miguel / García-Martinez, José Manuel / Louphrasitthiphol, Pakavarin / Garcia, Yurena Vivas / Ramírez-Sánchez, Ana / Chauhan, Jagat / Fiuza, M Carmen / Duran, Manuel / García-Jiménez, Custodia / Goding, Colin R

bioRxiv : the preprint server for biology

2024

Abstract: Phenotypic diversity of cancer cells within tumors generated through bi-directional interactions with the tumor microenvironment has emerged as a major driver of disease progression and therapy resistance. Nutrient availability plays a critical role in ... ...

Abstract	Phenotypic diversity of cancer cells within tumors generated through bi-directional interactions with the tumor microenvironment has emerged as a major driver of disease progression and therapy resistance. Nutrient availability plays a critical role in determining phenotype, but whether specific nutrients elicit different responses on distinct phenotypes is poorly understood. Here we show, using melanoma as a model, that only MITF
Sprache	Englisch
Erscheinungsdatum	2024-01-24
Erscheinungsland	United States
Dokumenttyp	Preprint
DOI	10.1101/2024.01.21.576568
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Aberrant Glycosylation in Pancreatic Ductal Adenocarcinoma 3D Organoids Is Mediated by KRAS Mutations.

Nakahashi, Hiromitsu / Oda, Tatsuya / Shimomura, Osamu / Akashi, Yoshimasa / Takahashi, Kazuhiro / Miyazaki, Yoshihiro / Furuta, Tomoaki / Kuroda, Yukihito / Louphrasitthiphol, Pakavarin / Mathis, Bryan J / Tateno, Hiroaki

Journal of oncology

2024 Band 2024, Seite(n) 1529449

Abstract: Aberrant glycosylation in tumor cells is a hallmark during carcinogenesis. KRAS gene mutations are the most well-known oncogenic abnormalities but their association with glycan alterations in pancreatic ductal adenocarcinoma (PDAC) is largely unknown. We ...

Abstract	Aberrant glycosylation in tumor cells is a hallmark during carcinogenesis. KRAS gene mutations are the most well-known oncogenic abnormalities but their association with glycan alterations in pancreatic ductal adenocarcinoma (PDAC) is largely unknown. We employed patient-derived 3D organoids to culture pure live PDAC cells, excluding contamination by fibroblasts and immune cells, to gasp the comprehensive cancer cell surface glycan expression profile using lectin microarray and transcriptomic analyses. Surgical specimens from 24 PDAC patients were digested and embedded into a 3D culture system. Surface-bound glycans of 3D organoids were analyzed by high-density, 96-lectin microarrays. KRAS mutation status and expression of various glycosyltransferases were analyzed by RNA-seq. We successfully established 16 3D organoids: 14 PDAC, 1 intraductal papillary mucinous neoplasm (IPMN), and 1 normal pancreatic duct. KRAS was mutated in 13 (7 G12V, 5 G12D, 1 Q61L) and wild in 3 organoids (1 normal duct, 1 IPMN, 1 PDAC). Lectin reactivity of AAL (
Sprache	Englisch
Erscheinungsdatum	2024-03-18
Erscheinungsland	Egypt
Dokumenttyp	Journal Article
ZDB-ID	2461349-6
ISSN	1687-8469 ; 1687-8450
ISSN (online)	1687-8469
ISSN	1687-8450
DOI	10.1155/2024/1529449
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: ABCB5 is activated by MITF and β-catenin and is associated with melanoma differentiation.

Louphrasitthiphol, Pakavarin / Chauhan, Jagat / Goding, Colin R

Pigment cell & melanoma research

2019 Band 33, Heft 1, Seite(n) 112–118

Abstract: Defining markers of different phenotypic states in melanoma is important for understanding disease progression, determining the response to therapy, and defining the molecular mechanisms underpinning phenotype-switching driven by the changing intratumor ... ...

Abstract	Defining markers of different phenotypic states in melanoma is important for understanding disease progression, determining the response to therapy, and defining the molecular mechanisms underpinning phenotype-switching driven by the changing intratumor microenvironment. The ABCB5 transporter is implicated in drug-resistance and has been identified as a marker of melanoma-initiating cells. Indeed ongoing studies are using ABCB5 to define stem cell populations. However, we show here that the ABCB5 is a direct target for the microphthalmia-associated transcription factor MITF and its expression can be induced by β-catenin, a key activator and co-factor for MITF. Consequently, ABCB5 mRNA expression is primarily associated with melanoma cells exhibiting differentiation markers. The results suggest first that ABCB5 is unlikely to represent a marker of de-differentiated melanoma stem cells, and second that ABCB5 may contribute to the non-genetic drug-resistance associated with highly differentiated melanoma cells. To reconcile the apparently conflicting observations in the field, we propose a model in which ABCB5 may mark a slow-cycling differentiated population of melanoma cells.
Mesh-Begriff(e)	ATP Binding Cassette Transporter, Subfamily B/genetics ; ATP Binding Cassette Transporter, Subfamily B/metabolism ; Base Sequence ; Cell Differentiation ; Gene Expression Regulation, Neoplastic ; Humans ; Melanoma/genetics ; Melanoma/metabolism ; Melanoma/pathology ; Microphthalmia-Associated Transcription Factor/metabolism ; Phenotype ; Skin Neoplasms/genetics ; Skin Neoplasms/metabolism ; Skin Neoplasms/pathology ; beta Catenin/metabolism
Chemische Substanzen	ABCB5 protein, human ; ATP Binding Cassette Transporter, Subfamily B ; Microphthalmia-Associated Transcription Factor ; beta Catenin
Sprache	Englisch
Erscheinungsdatum	2019-10-28
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2409570-9
ISSN	1755-148X ; 1600-0749 ; 0893-5785 ; 1755-1471
ISSN (online)	1755-148X ; 1600-0749
ISSN	0893-5785 ; 1755-1471
DOI	10.1111/pcmr.12830
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: DNA damage-induced interaction between a lineage addiction oncogenic transcription factor and the MRN complex shapes a tissue-specific DNA Damage Response and cancer predisposition.

Binet, Romuald / Lambert, Jean-Philippe / Tomkova, Marketa / Tischfield, Samuel / Baggiolini, Arianna / Picaud, Sarah / Sarkar, Sovan / Louphrasitthiphol, Pakavarin / Dias, Diogo / Carreira, Suzanne / Humphrey, Timothy / Fillipakopoulos, Panagis / White, Richard / Goding, Colin R

bioRxiv : the preprint server for biology

2023

Abstract: Since genome instability can drive cancer initiation and progression, cells have evolved highly effective and ubiquitous DNA Damage Response (DDR) programs. However, some cells, in skin for example, are normally exposed to high levels of DNA damaging ... ...

Abstract	Since genome instability can drive cancer initiation and progression, cells have evolved highly effective and ubiquitous DNA Damage Response (DDR) programs. However, some cells, in skin for example, are normally exposed to high levels of DNA damaging agents. Whether such high-risk cells possess lineage-specific mechanisms that tailor DNA repair to the tissue remains largely unknown. Here we show, using melanoma as a model, that the microphthalmia-associated transcription factor MITF, a lineage addition oncogene that coordinates many aspects of melanocyte and melanoma biology, plays a non-transcriptional role in shaping the DDR. On exposure to DNA damaging agents, MITF is phosphorylated by ATM/DNA-PKcs, and unexpectedly its interactome is dramatically remodelled; most transcription (co)factors dissociate, and instead MITF interacts with the MRE11-RAD50-NBS1 (MRN) complex. Consequently, cells with high MITF levels accumulate stalled replication forks, and display defects in homologous recombination-mediated repair associated with impaired MRN recruitment to DNA damage. In agreement, high MITF levels are associated with increased SNV burden in melanoma. Significantly, the SUMOylation-defective MITF-E318K melanoma predisposition mutation recapitulates the effects of ATM/DNA-PKcs-phosphorylated MITF. Our data suggest that a non-transcriptional function of a lineage-restricted transcription factor contributes to a tissue-specialised modulation of the DDR that can impact cancer initiation.
Sprache	Englisch
Erscheinungsdatum	2023-04-21
Erscheinungsland	United States
Dokumenttyp	Preprint
DOI	10.1101/2023.04.21.537819
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Single-cell profiling of MC1R-inhibited melanocytes.

Berns, H Matthew / Watkins-Chow, Dawn E / Lu, Sizhu / Louphrasitthiphol, Pakavarin / Zhang, Tongwu / Brown, Kevin M / Moura-Alves, Pedro / Goding, Colin R / Pavan, William J

Pigment cell & melanoma research

2023 Band 37, Heft 2, Seite(n) 291–308

Abstract: The human red hair color (RHC) trait is caused by increased pheomelanin (red-yellow) and reduced eumelanin (black-brown) pigment in skin and hair due to diminished melanocortin 1 receptor (MC1R) function. In addition, individuals harboring the RHC trait ... ...

Abstract	The human red hair color (RHC) trait is caused by increased pheomelanin (red-yellow) and reduced eumelanin (black-brown) pigment in skin and hair due to diminished melanocortin 1 receptor (MC1R) function. In addition, individuals harboring the RHC trait are predisposed to melanoma development. While MC1R variants have been established as causative of RHC and are a well-defined risk factor for melanoma, it remains unclear mechanistically why decreased MC1R signaling alters pigmentation and increases melanoma susceptibility. Here, we use single-cell RNA sequencing (scRNA-seq) of melanocytes isolated from RHC mouse models to define a MC1R-inhibited Gene Signature (MiGS) comprising a large set of previously unidentified genes which may be implicated in melanogenesis and oncogenic transformation. We show that one of the candidate MiGS genes, TBX3, a well-known anti-senescence transcription factor implicated in melanoma progression, binds both E-box and T-box elements to regulate genes associated with melanogenesis and senescence bypass. Our results provide key insights into further mechanisms by which melanocytes with reduced MC1R signaling may regulate pigmentation and offer new candidates of study toward understanding how individuals with the RHC phenotype are predisposed to melanoma.
Mesh-Begriff(e)	Mice ; Animals ; Humans ; Melanoma/metabolism ; Receptor, Melanocortin, Type 1/genetics ; Receptor, Melanocortin, Type 1/metabolism ; Melanocytes/metabolism ; Pigmentation/genetics ; Gene Expression Regulation ; Hair Color
Chemische Substanzen	Receptor, Melanocortin, Type 1
Sprache	Englisch
Erscheinungsdatum	2023-11-16
Erscheinungsland	England
Dokumenttyp	Journal Article
ZDB-ID	2409570-9
ISSN	1755-148X ; 1600-0749 ; 0893-5785 ; 1755-1471
ISSN (online)	1755-148X ; 1600-0749
ISSN	0893-5785 ; 1755-1471
DOI	10.1111/pcmr.13141
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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