LIN28A is an RNA-binding protein and stem cell marker, and its overexpression was described in rare malignant brain tumours of early childhood. CTNNB1 is an effector of the WNT pathway which plays important roles during development and activating mutations have been reported in malignant brain tumours. In order to investigate the interplay of these oncogenic proteins during embryonal brain development, we overexpressed both in murine neural progenitor cells in vivo.The sole overexpression of either LIN28A, stabilized Ctnnb1 or the combination of both in hGFAP-positive forebrain precursor cells did not lead to brain tumour formation but resulted in distinct phenotypes in the cerebral cortex during embryonal development. The cortical layering in hGFAP-cre::Ctnnb1Δex3fl/+ (GB) and hGFAP-cre::Ctnnb1Δex3fl/+::IsI-Lin28A (GBL) mice was highly disturbed and revealed impaired migration in the cerebral cortex. Immunostainings with the pial marker LAMININ and dendritic marker MAP2C revealed a porous pia mater and aggregations of neurons above the pial border in the GBL model at embryonal day 14 (E14.5). At later embryonal stage (E18.5), the GBL model showed large blood vessels located in deeper cortical layers. Whereas the GB phenotype is reminiscent of human lissencephaly type I, GBL brain morphology showed similarities to neuronal overmigration observed in the human Cobblestone (Type II) Lissencephaly. We applied spatially resolved proteome analysis of the cortices in the respective genotypes. We show characteristic CTRL layer signatures which were altered in the other genotypes. Moreover, we show proteins with different rate of change over layers across the genotypes related to migration disorder.