GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE336nnn/GSE336415/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE336415GEOGSEfalseZFP36L2 orchestrates stress-adaptive plasticity in intestinal regeneration and colorectal cancer metastasis (ActDseq)Actinomycin D pulse-chase RNA sequencing (ActD-seq) was used to measure ZFP36L2-dependent mRNA decay rates in two patient-derived colorectal cancer (CRC) liver metastasis organoid lines (MSK107Li and OKG146Li). Organoids expressing a doxycycline-inducible short hairpin RNA targeting ZFP36L2 (shZFP36L2) or a non-targeting control (shCtrl) were cultured for 5 days with 2 μg/mL doxycycline, then treated with or without 5 μg/mL Actinomycin D (ActD) for 5 hours to block de novo transcription. Total RNA was extracted using the RNeasy Mini Kit (Qiagen), and strand-specific mRNA libraries were prepared using the TruSeq Stranded mRNA Kit and sequenced on the Illumina NovaSeq 6000 (PE100). Decay rates were quantified by comparing transcript abundance between ActD-treated and untreated conditions within each knockdown condition; ZFP36L2-dependent decay was calculated as the differential decay rate between shZFP36L2 and shCtrl. ZFP36L2 knockdown significantly stabilized stress-associated transcripts, consistent with ZFP36L2 promoting post-transcriptional decay of AU-rich stress-response mRNAs.2026/07/20GSE336415GSM9834832GSM9834821GSM9834833GSM9834822GSM9834830GSM9834820GSM9834831GSM9834836GSM9834814GSM9834825GSM9834826GSM9834815GSM9834834GSM9834823GSM9834813GSM9834824GSM9834835GSM9834829GSM9834818GSM9834819GSM9834816GSM9834827GSM9834817GSM983482824676336415Homo sapiens