GEO series
Spatiotemporal control of SMARCA5 by a MAPK-RUNX1 axis distinguishes mutant KRAS-driven pancreatic malignancy from tissue regeneration (ATAC-Seq)
GSE248942
Homo sapiens; Mus musculus
Genome binding/occupancy profiling by high throughput sequencing
123 samples
Submitted 2025/07/01
Platform GPL28330Platform GPL29480Platform GPL24247
Summary
De-differentiation or trans-differentiation is a common response to injury in many tissues, and the processes predispose cells to cancer. Acute pancreatitis-induced acinar-to-ductal metaplasia (ADM) is similar to pancreatic ductal adenocarcinoma (PDAC) at both the chromatin level and gene expression level. Mutant KRAS induces chromatin remodeling activities required for both regeneration and tumorigenesis at the peak of ADM, and it blocks regeneration. We show that chromatin remodeler SMARCA5 (SNF2H) can promotes the regeneration defects caused by mutant KRAS by maintaining chromatin accessibility at regions specifically required for malignancy. Mechanistically, regeneration-related chromatin remodeling activities are shared between wild-type and mutant KRAS and they occur very early upon pancreatitis, while the malignancy-related chromatin regions become accessible much later. The activity of SMARCA5 is controlled spatiotemporally by transcription factor RUNX1, which is only accumulated at sufficient levels at late ADM lock-in stage. Finally, we show that the malignancy regulation activity of SMARCA5 is different from its general function in CTCF recruitment. In summary, we have identified a specific function of a general chromatin remodeler that is precisely controlled during acinar cell trans-differentiation to separate malignancy from tissue regeneration.
This dataset
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Direct links to NCBI, no account and no request form: the whole study as GSE248942_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 123 samples. Raw sequencing reads are also available from ENA.
Also filed as BioProject PRJNA1046488 and SRA study SRP475027. Searching any of these in the dataset finder brings you back here.
Study design
16 conditions, mostly in duplicate
ATAC_KCa_24h_Rosa ×5
ATAC_Ca_8h_Rosa ×3
ATAC_Ca_8h_Smarca5 ×3
ATAC_Ca_D2_Smarca5 ×3
ATAC_Ca_D5_Rosa ×3
ATAC_Ca_D5_Smarca5 ×3
ATAC_Ca_0h_Rosa ×2
ATAC_Ca_0h_Smarca5 ×2
+8 more
Supports a between-group comparison across 40 samples.
16 replicated groups read from the first 40 of 123 sample titles; they account for 40 of them. Check it against the sample list below before relying on it.
Samples in this study
0 selected
- GSM7923345 ATAC_Ca_0h_Rosa_58
- GSM7923346 ATAC_Ca_0h_Rosa_60
- GSM7923347 ATAC_Ca_0h_Smarca5_69
- GSM7923348 ATAC_Ca_0h_Smarca5_70
- GSM7923349 ATAC_Ca_8h_Rosa_435
- GSM7923350 ATAC_Ca_8h_Rosa_452
- GSM7923351 ATAC_Ca_8h_Rosa_453
- GSM7923352 ATAC_Ca_8h_Smarca5_438
- GSM7923353 ATAC_Ca_8h_Smarca5_454
- GSM7923354 ATAC_Ca_8h_Smarca5_455
- GSM7923355 ATAC_Ca_D2_Rosa_456
- GSM7923356 ATAC_Ca_D2_Rosa_457
- GSM7923357 ATAC_Ca_D2_Smarca5_459
- GSM7923358 ATAC_Ca_D2_Smarca5_470
- GSM7923359 ATAC_Ca_D2_Smarca5_472
- GSM7923360 ATAC_Ca_D5_Rosa_422
- GSM7923361 ATAC_Ca_D5_Rosa_423
- GSM7923362 ATAC_Ca_D5_Rosa_433
- GSM7923363 ATAC_Ca_D5_Smarca5_428
- GSM7923364 ATAC_Ca_D5_Smarca5_429
- GSM7923365 ATAC_Ca_D5_Smarca5_434
- GSM7923366 ATAC_Ca_D7_Rosa_474
- GSM7923367 ATAC_Ca_D7_Rosa_476
- GSM7923368 ATAC_Ca_D7_Smarca5_475
- GSM7923369 ATAC_Ca_D7_Smarca5_480
- GSM7923370 ATAC_KCa_0h_Rosa_211
- GSM7923371 ATAC_KCa_0h_Rosa_212
- GSM7923372 ATAC_KCa_0h_Smarca5_213
- GSM7923373 ATAC_KCa_0h_Smarca5_218
- GSM7923374 ATAC_KCa_8h_Rosa_236
- GSM7923375 ATAC_KCa_8h_Rosa_261
- GSM7923376 ATAC_KCa_8h_Smarca5_250
- GSM7923377 ATAC_KCa_8h_Smarca5_262
- GSM7923378 ATAC_KCa_24h_Rosa_72
- GSM7923379 ATAC_KCa_24h_Rosa_133
- GSM7923380 ATAC_KCa_24h_Rosa_247
- GSM7923381 ATAC_KCa_24h_Rosa_266
- GSM7923382 ATAC_KCa_24h_Rosa_372
- GSM7923383 ATAC_KCa_24h_Smarca5_73
- GSM7923384 ATAC_KCa_24h_Smarca5_274
+ 83 more — browse all 123 samples with per-sample file links →
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