Background: Lamins are the major component of nuclear lamina. Alternative splicing of the 12 exons comprising lamin A/C gene creates five known transcript variants, lamin A, lamin C, lamin A\mathrm{\Delta }10, lamin A\mathrm{\Delta }50, and lamin C2. The main objective for this study was to examine the association of critical pathways, networks, molecular and cellular functions regulated by each Lamin A/C transcript variants. Methods: Ion AmpliSeq Transcriptome Human Gene Expression analysis was performed on MCF7 cells stably transfected with lamin A/C transcript variants. Results: Lamin A or lamin A\mathrm{\Delta }50 upregulation was associated with activation of cell death and inactivation of carcinogenesis while both lamin C or lamin A\mathrm{\Delta }10 upregulation activated carcinogenesis and cell death. Conclusions: Data suggest anti-apoptotic and anti-senescence effects of lamin C and lamin A\mathrm{\Delta }10 as several functions, including apoptosis and necrosis functions are inactivated following lamin C or lamin A\mathrm{\Delta }10 upregulation. However, lamin A\mathrm{\Delta }10 upregulation is associated with a more carcinogenic and aggressive tumor phenotype. Lamin A or lamin A\mathrm{\Delta }50 upregulation is associated with a predicted activation of increased cell death and inactivation of carcinogenesis. Thus, different signaling pathways, networks, molecular and cellular functions are activated/inactivated by lamin A/C transcript variants resulting in a large number of laminopathies.