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Status |
Public on Aug 24, 2022 |
Title |
Differential gene expression in SMC Ctrl vs TAZ4SA |
Organism |
Mus musculus |
Experiment type |
Expression profiling by high throughput sequencing
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Summary |
Poor prognosis of small cell lung cancer (SCLC) is mainly attributed to its highly metastatic capability. Here we identify the SMC and Non-SMC from Rb1L/L/Trp53 L/L mouse model through FACS with NE and mensenchymal markers. In order to identify functions of these two subpopulations during SCLC malignant progression, we compared their metastatic capability by allograft experiment. In addition, we find that the SMC is progressively transited from the Non-SCLC during mouse SCLC malignant progression. Further investigation reveals that genetic disruption of the SWI/SNF chromatin-remodeling complex, in RP model abrogates SMC phenotype maintenance and SCLC metastasis. In search of important downstream regulators, we find that TAZ, the core transcription cofactor of the Hippo pathway, is epigenetically silenced by SWI/SNF complex during this process. Collectively, our data link phenotypic transition to cancer metastasis and identify TAZ as a critical molecular switch that controls SCLC plasticity.
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Overall design |
SMC were derived from Rb1L/L, Trp53L/L mouse model through FACS. SMC was infected with the Ctrl or TAZ4SA (activated muation) virus. RNA-seq was performed to compare the gene expression profile between SMC with or without TAZ4SA overexpression. Three replicates for each sample were included.
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Contributor(s) |
Jin Y, Ji H |
Citation(s) |
35967587 |
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Submission date |
Sep 21, 2020 |
Last update date |
Aug 24, 2022 |
Contact name |
yujuan jin |
E-mail(s) |
jinyujuan1@163.com
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Organization name |
Shanghai Institutes for Biological Sciences, CAS
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Lab |
Hongbin Ji
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Street address |
Yueyang Road 320#
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City |
Shanghai |
ZIP/Postal code |
200031 |
Country |
China |
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Platforms (1) |
GPL24247 |
Illumina NovaSeq 6000 (Mus musculus) |
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Samples (6)
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Relations |
BioProject |
PRJNA664759 |
SRA |
SRP284254 |