LNK suppresses interferon signaling in M202 melanoma cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA525882 | ENA |
REPOSITORIES: ENA
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Project description:LNK attenuates IFN-γ (2,000 U/ml, 24 hours) induced gene expression in M202 melanoma cells.
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Project description:LNK (SH2B3) is a key negative regulator of JAK-STAT signaling which has been extensively studied in malignant hematopoietic diseases. We found that LNK is significantly elevated in cutaneous melanoma; this elevation is correlated with hyperactive signaling of the RAS-RAF-MEK pathway. Elevated LNK enhances cell growth and survival in adverse conditions. Forced expression of LNK inhibits signaling by interferon-STAT1 and suppresses interferon (IFN) induced cell cycle arrest and cell apoptosis. In contrast, silencing LNK expression by either shRNA or CRISPR-Cas9 potentiates the killing effect of IFN. The IFN-LNK signaling is tightly regulated by a negative feedback mechanism; melanoma cells exposed to IFN upregulate expression of LNK to prevent overactivation of this signaling pathway. Our study reveals an unappreciated function of LNK in melanoma and highlights the critical role of the IFN-STAT1-LNK signaling axis in this potentially devastating disease. LNK may be further explored as a potential therapeutic target for melanoma immunotherapy.
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Project description:LNK (SH2B3) is a key negative regulator of JAK-STAT signaling which has been extensively studied in malignant hematopoietic diseases. We found that LNK is significantly elevated in cutaneous melanoma; this elevation is correlated with hyperactive signaling of the RAS-RAF-MEK pathway. Elevated LNK enhances cell growth and survival in adverse conditions. Forced expression of LNK inhibits signaling by interferon-STAT1 and suppresses interferon (IFN) induced cell cycle arrest and cell apoptosis. In contrast, silencing LNK expression by either shRNA or CRISPR-Cas9 potentiates the killing effect of IFN. The IFN-LNK signaling is tightly regulated by a negative feedback mechanism; melanoma cells exposed to IFN upregulate expression of LNK to prevent overactivation of this signaling pathway. Our study reveals an unappreciated function of LNK in melanoma and highlights the critical role of the IFN-STAT1-LNK signaling axis in this potentially devastating disease. LNK may be further explored as a potential therapeutic target for melanoma immunotherapy.
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Project description:Force expression LNK suppresses interferon Gamma signaling
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Project description:An ERF transcription factor, Submergence-1A (Sub1A), dramatically enhances the tolerance to prolonged submergence in rice. For instance, rice accessions which lack Sub1A (e.g. M202) die within 7-10 d of complete submergence. By contrast, genotypes which posses Sub1A (e.g. M202(Sub1)) can endure submergence stress for 14 d. In this study, the two near isogenic lines with and without Sub1A were subjected to microarray analysis using Affymetrix Gene Chip technology. This analysis provided beneficial information to elucidate general response to submergence stress and to estimate Sub1A-dependent defense response to the stress at mRNA accumulation level.
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Project description:Interferon-gamma signaling promotes melanoma progression and metastasis
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Project description:LNK (SH2B3) is a key negative regulator of JAK-STAT signaling which has been extensively studied in malignant hematopoietic diseases. We found that LNK is significantly elevated in cutaneous melanoma; this elevation is correlated with hyperactive signaling of the RAS-RAF-MEK pathway. Elevated LNK enhances cell growth and survival in adverse conditions. Forced expression of LNK inhibits signaling by interferon-STAT1 and suppresses interferon (IFN) induced cell cycle arrest and cell apoptosis. In contrast, silencing LNK expression by either shRNA or CRISPR-Cas9 potentiates the killing effect of IFN. The IFN-LNK signaling is tightly regulated by a negative feedback mechanism; melanoma cells exposed to IFN upregulate expression of LNK to prevent overactivation of this signaling pathway. Our study reveals an unappreciated function of LNK in melanoma and highlights the critical role of the IFN-STAT1-LNK signaling axis in this potentially devastating disease. LNK may be further explored as a potential therapeutic target for melanoma immunotherapy.
| S-EPMC6527565 | biostudies-literature
Project description:An ERF transcription factor, Submergence-1A (Sub1A), dramatically enhances the tolerance to prolonged submergence in rice. For instance, rice accessions which lack Sub1A (e.g. M202) die within 7-10 d of complete submergence. By contrast, genotypes which posses Sub1A (e.g. M202(Sub1)) can endure submergence stress for 14 d. In this study, the two near isogenic lines with and without Sub1A were subjected to microarray analysis using Affymetrix Gene Chip technology. This analysis provided beneficial information to elucidate general response to submergence stress and to estimate Sub1A-dependent defense response to the stress at mRNA accumulation level. Aerial tissue of 14-d-old plants which were submerged for 24 h were subjected to RNA extraction and hybridization on Affymetrix microarrays. Non-submerged plants were used as control. Two independent biological replicates were analyzed for each treatment/genotype.
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