The phenylpropanoid cinnamic acid (CA) is a plant metabolite that can occur under a trans ‐ or cis ‐form. In contrast to the proven bioactivity of the cis ‐form ( c ‐CA), the activity of trans ‐CA ( t ‐CA) is still a matter of debate. We tested both compounds using a submerged rice coleoptile assay and demonstrated that they have opposite effects on cell elongation. Notably, in the tip of rice coleoptile t ‐CA showed an inhibiting and c ‐CA a stimulating activity. By combining transcriptomics and (untargeted) metabolomics with activity assays and genetic and pharmacological experiments, we aimed to explain the underlying mechanistic processes. We propose a model in which c ‐CA treatment activates proton pumps and stimulates acidification of the apoplast, which in turn leads to the loosening of the cell wall, necessary for elongation. We hypothesize that c ‐CA also inactivates auxin efflux transporters, which might cause a local auxin accumulation in the tip of the coleoptile. For t ‐CA, the phenotype can partially be explained by a stimulation of cell wall polysaccharide feruloylation, leading to a more rigid cell wall. Metabolite profiling also demonstrated that salicylic acid (SA) derivatives are increased upon t ‐CA treatment. As SA is a known antagonist of auxin, the shift in SA homeostasis provides an additional explanation of the observed t ‐CA‐mediated restriction on cell growth.