P12.09.B Extracellular vesicle derived-miR-146a increases melanoma brain metastasis progression via Notch signalling pathway dysregulation Article Swipe
Emma Rigg
,
Jian Wang
,
Zhiyi Xue
,
Taral R. Lunavat
,
Thomas S. Hoang
,
Himalaya Parajuli
,
Mi-Ryung Han
,
Guangyi Liu
,
Rolf Bjerkvig
,
Petr V. Nazarov
,
Nathalie Nicot
,
Stephanie Kreis
,
C Wurth
,
Hrvoje Miletić
,
Terje Sundstrøm
,
Xiaoxing Li
,
Frits Thorsen
·
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.1093/neuonc/noac174.274
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.1093/neuonc/noac174.274
Background Melanoma has the highest tropism of any cancer to metastasize to the brain, and 40% of late-stage patients develop brain metastasis. Invasion, survival, and progression of tumors is dependent on the support of the surrounding microenvironment; therefore, modulation of neighboring cells is a key factor in metastasis. Extracellular vesicles (EVs) are important in cell-to-cell signalling, shuttling proteins, RNA and DNA to alter the surroundings into a favorable tumor microenvironment. Our aims were to investigate the role of melanoma brain metastasis (MBM) derived EVs in MBM development to find possible contributing mechanisms to cancer progression for eventual therapeutic targeting. Material and Methods MBM-EVs isolated via sequential ultracentrifugation were injected into mice as a pre-treatment prior to intracardial injection of MBM cells. EVs were co-cultured with normal human astrocytes (NHA) to investigate phenotypic changes. MiRNA sequencing was performed on EVs collected from MBM cells and compared to NHA and melanocytes to determine a candidate miRNA for targeting. In situ hybridization was utilized to evaluate the level of miRNA in clinical patient MBM samples. Functional in vivo validation was performed by injecting miRNA knockout MBM cells into mice. Sequencing of NHA in the presence or absence of target miRNA mimic was used to determine downstream targets. Results Mice primed with EVs had a significant increase in MBM tumor burden, compared to non-primed mice. Co-culture with MBM-EVs resulted in NHA activation in vitro, with increased proliferation, invasion, cytokine production, and upregulation of GFAP. MiR-146a was highly upregulated in MBM EVs, and miR-146a mimics activated NHA. Patient samples had a significant increase in miR-146a expression, compared to healthy brain controls. MiR-146a knockdown in MBM mice models reduced MBM burden and prolonged animal survival. Sequencing of NHA determined NUMB, an inhibitor of the Notch signalling pathway, as a target of miR-146a. Numb and other downstream Notch proteins expression was significantly altered in NHA in the presence of both MBM-EVs and miR-146a. Conclusion In conclusion, EVs are important regulators of MBM and establish tumor-supporting reactive astrocytes by delivery of miR-146a. MiR-146a alters Notch signalling in astrocytes via inhibition of the tumor suppressor gene NUMB. Elevated miR-146a levels in patients suggests a potential clinical intervention is possible via miR-146a targeting.
Related Topics
Concepts
Cancer research
Downregulation and upregulation
Tumor microenvironment
Metastasis
Biology
Extracellular vesicle
microRNA
Melanoma
Microvesicles
Tumor progression
Cancer
Gene
Genetics
Biochemistry
Tumor cells
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1093/neuonc/noac174.274
- https://academic.oup.com/neuro-oncology/article-pdf/24/Supplement_2/ii78/45691978/noac174.274.pdf
- OA Status
- bronze
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4294683773
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4294683773Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1093/neuonc/noac174.274Digital Object Identifier
- Title
-
P12.09.B Extracellular vesicle derived-miR-146a increases melanoma brain metastasis progression via Notch signalling pathway dysregulationWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2022Year of publication
- Publication date
-
2022-09-01Full publication date if available
- Authors
-
Emma Rigg, Jian Wang, Zhiyi Xue, Taral R. Lunavat, Thomas S. Hoang, Himalaya Parajuli, Mi-Ryung Han, Guangyi Liu, Rolf Bjerkvig, Petr V. Nazarov, Nathalie Nicot, Stephanie Kreis, C Wurth, Hrvoje Miletić, Terje Sundstrøm, Xiaoxing Li, Frits ThorsenList of authors in order
- Landing page
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https://doi.org/10.1093/neuonc/noac174.274Publisher landing page
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https://academic.oup.com/neuro-oncology/article-pdf/24/Supplement_2/ii78/45691978/noac174.274.pdfDirect link to full text PDF
- Open access
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YesWhether a free full text is available
- OA status
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bronzeOpen access status per OpenAlex
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https://academic.oup.com/neuro-oncology/article-pdf/24/Supplement_2/ii78/45691978/noac174.274.pdfDirect OA link when available
- Concepts
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Cancer research, Downregulation and upregulation, Tumor microenvironment, Metastasis, Biology, Extracellular vesicle, microRNA, Melanoma, Microvesicles, Tumor progression, Cancer, Gene, Genetics, Biochemistry, Tumor cellsTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.knockout | 182 |
| abstract_inverted_index.melanoma | 79 |
| abstract_inverted_index.miR-146a | 249, 260, 350, 362 |
| abstract_inverted_index.pathway, | 291 |
| abstract_inverted_index.patients | 19, 353 |
| abstract_inverted_index.possible | 90, 360 |
| abstract_inverted_index.presence | 192, 311 |
| abstract_inverted_index.proteins | 302 |
| abstract_inverted_index.reactive | 329 |
| abstract_inverted_index.resulted | 225 |
| abstract_inverted_index.samples. | 172 |
| abstract_inverted_index.suggests | 354 |
| abstract_inverted_index.targets. | 204 |
| abstract_inverted_index.utilized | 161 |
| abstract_inverted_index.vesicles | 50 |
| abstract_inverted_index.Invasion, | 23 |
| abstract_inverted_index.activated | 251 |
| abstract_inverted_index.candidate | 153 |
| abstract_inverted_index.collected | 140 |
| abstract_inverted_index.controls. | 266 |
| abstract_inverted_index.dependent | 30 |
| abstract_inverted_index.determine | 151, 202 |
| abstract_inverted_index.establish | 327 |
| abstract_inverted_index.favorable | 68 |
| abstract_inverted_index.important | 53, 322 |
| abstract_inverted_index.increased | 232 |
| abstract_inverted_index.inhibitor | 286 |
| abstract_inverted_index.injecting | 180 |
| abstract_inverted_index.injection | 118 |
| abstract_inverted_index.invasion, | 234 |
| abstract_inverted_index.knockdown | 268 |
| abstract_inverted_index.miR-146a. | 296, 316, 334 |
| abstract_inverted_index.performed | 137, 178 |
| abstract_inverted_index.potential | 356 |
| abstract_inverted_index.prolonged | 277 |
| abstract_inverted_index.proteins, | 58 |
| abstract_inverted_index.shuttling | 57 |
| abstract_inverted_index.survival, | 24 |
| abstract_inverted_index.survival. | 279 |
| abstract_inverted_index.Background | 1 |
| abstract_inverted_index.Co-culture | 222 |
| abstract_inverted_index.Conclusion | 317 |
| abstract_inverted_index.Functional | 173 |
| abstract_inverted_index.Sequencing | 187, 280 |
| abstract_inverted_index.activation | 228 |
| abstract_inverted_index.astrocytes | 128, 330, 340 |
| abstract_inverted_index.determined | 283 |
| abstract_inverted_index.downstream | 203, 300 |
| abstract_inverted_index.expression | 303 |
| abstract_inverted_index.inhibition | 342 |
| abstract_inverted_index.late-stage | 18 |
| abstract_inverted_index.mechanisms | 92 |
| abstract_inverted_index.metastasis | 81 |
| abstract_inverted_index.modulation | 39 |
| abstract_inverted_index.non-primed | 220 |
| abstract_inverted_index.phenotypic | 132 |
| abstract_inverted_index.regulators | 323 |
| abstract_inverted_index.sequencing | 135 |
| abstract_inverted_index.sequential | 106 |
| abstract_inverted_index.signalling | 290, 338 |
| abstract_inverted_index.suppressor | 346 |
| abstract_inverted_index.targeting. | 99, 156, 363 |
| abstract_inverted_index.therefore, | 38 |
| abstract_inverted_index.validation | 176 |
| abstract_inverted_index.co-cultured | 124 |
| abstract_inverted_index.conclusion, | 319 |
| abstract_inverted_index.development | 87 |
| abstract_inverted_index.expression, | 261 |
| abstract_inverted_index.investigate | 75, 131 |
| abstract_inverted_index.melanocytes | 149 |
| abstract_inverted_index.metastasis. | 22, 48 |
| abstract_inverted_index.metastasize | 11 |
| abstract_inverted_index.neighboring | 41 |
| abstract_inverted_index.production, | 236 |
| abstract_inverted_index.progression | 26, 95 |
| abstract_inverted_index.signalling, | 56 |
| abstract_inverted_index.significant | 212, 257 |
| abstract_inverted_index.surrounding | 36 |
| abstract_inverted_index.therapeutic | 98 |
| abstract_inverted_index.upregulated | 244 |
| abstract_inverted_index.cell-to-cell | 55 |
| abstract_inverted_index.contributing | 91 |
| abstract_inverted_index.intervention | 358 |
| abstract_inverted_index.intracardial | 117 |
| abstract_inverted_index.surroundings | 65 |
| abstract_inverted_index.upregulation | 238 |
| abstract_inverted_index.Extracellular | 49 |
| abstract_inverted_index.hybridization | 159 |
| abstract_inverted_index.pre-treatment | 114 |
| abstract_inverted_index.significantly | 305 |
| abstract_inverted_index.proliferation, | 233 |
| abstract_inverted_index.tumor-supporting | 328 |
| abstract_inverted_index.microenvironment. | 70 |
| abstract_inverted_index.microenvironment; | 37 |
| abstract_inverted_index.ultracentrifugation | 107 |
| cited_by_percentile_year | |
| countries_distinct_count | 3 |
| institutions_distinct_count | 17 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.7699999809265137 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.10680269 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |