How would you separate transcriptional regulation from RNA stability effects?

Why

Suppose a treated cell has twice as much mRNA for a gene. That could be caused by increased transcription, slower turnover, or both. Collect biological replicates over time and consider metabolic RNA labeling such as 4sU pulse and chase to estimate newly made versus pre-existing RNA.

Complement this with nascent-transcript or intronic measurements if appropriate, and verify kinetics using RT-qPCR for selected genes. Transcription-inhibitor chase assays can estimate decay but may perturb cellular physiology, so they require cautious interpretation. Models of RNA half-life also depend on labeling efficiency, sample processing, normalization and assumed steady state.

For example, a sharp rise in nascent signal with unchanged decay is consistent with greater synthesis, whereas stable nascent signal and lengthened half-life implicate stabilization. Avoid claiming causal regulation from steady-state RNA-seq alone.