Alternative pre-messenger RNA splicing events (ASE) are regulated as breast cancer cells acquire metastatic features during epithelial mesenchymal transition (EMT). We examined known and exon array-predicted EMT-associated ASE in the PMC42 system of breast cancer EMT, comprising the more mesenchymal parental PMC42-ET (ET) cells and the more epithelial PMC42-LA (LA) subline, each of which are EGF-responsive for EMT. The ASE analysis revealed that the ESRP1/2-related splicing mechanism was active in our system, however, a short variant of LAMA3, which has not been linked to ESRP1/2, was also upregulated during EMT. This encodes the alpha-3 chain of laminin (LM), which together with beta-3 and gamma-2 chains, forms LM-332 (LM-5), an extracellular matrix and basement membrane component implicated in carcinoma progression and metastasis. We examined expression of LAMA3 and other heterotrimeric partners during EGF- and hypoxia-induced EMT, and in other human breast cancer cell lines (MCF-7, MDA-MB-468 and MDA-MB-231) and in MDA-MB-468 xenografts, using alternative variant-specific quantitative PCR and deep sequencing. LAMB1, B2, B3 and LAMC1 were not upregulated, but LAMC2 and the short variant of LAMA3 (V2) were dramatically upregulated during EGF-induced EMT in PMC42-LA cells (p<0.05). Escalating expression of LAMA3V1 and V2 was seen from luminal to basal breast cancer cell lines, with the exception that MDA-MB-231 cells showed a similar low level of LAMA3V2 to MCF-7 cells. In MDA-MB-468 cells, EGF- and hypoxia-induced EMT caused significant elevation of LAMA3V2, LAMB3 and LAMC2, the latter being already constitutively high. In MDA-468 xenografts, the LAMA3V2 was significantly higher than the full length variant LAMA3V1 (p<0.001). These initial observations suggest a role for LM332 in breast cancer EMT.