So my answer was deleted because it "didn't answer your question." Except that it did. The article linked here, Gene expression, chromosome position and lamin A/C mutations, is an entire paper devoted to what we knew as of 2011 about lamins and gene expression, with references. Your question was not a simple question, and article details how lamins are involved in gene expression.
I shall quote it here in order to "answer your question", and perhaps the moderators will see fit to not delete the post this time. If said moderators think I should write a review of a review to facilitate your understanding, then I obviously have not understood the meaning for this board.
I don't have enough rep to leave a comment on anything other than my own answer, which seems to have been the appropriate way to link to the paper. I figured an answer to your question would still be useful.
I would recommend reading the entire article as it is very useful in understanding additional indirect hypotheses for lamins controlling gene expression.
The Lamina as a Regulator of Gene Expression
In most cells, a dense heterochromatin network is visualized as electron dense material adjacent to the inner nuclear membrane and the nuclear lamina. The dense network is typically considered to reflect the association of transcriptionally inactive genes with the nuclear lamina. Specifically, this heterochromatin is thought to reflect a repressed gene state and suggests that the nuclear membrane and lamina may play an active role in gene repression.5 Lamin A/C and its binding partners can interact with DNA, histones, transcription factors and chromatin.6 Lamin-associated domains (LADs) are cis-acting sequences thought to range in size from ∼0.1–10 Mb, and these domains are thought to regulate the interaction of chromatin with the nuclear lamina; generally LADs are considered to be transcriptionally repressive.7 The precise sequences that define LADs have been elusive but nonetheless the LAD concept implies that the lamina and the genome interact in a specific manner. Therefore, it follows that one mechanism by which LMNA mutations may confer pathology is by altering the interaction between the lamina and chromatin. Consistent with this, LMNA mutant cells have altered chromosome territories.4 Meaburn and colleagues first examined chromosome localization in proliferating LMNA mutant fibroblasts and found that it resembled the chromosome organization associated with quiescent or senescent fibroblasts. They suggested that mutations in LMNA produced structural disruption to the lamina inducing a chromatin organization that may resemble an inappropriate cell cycle state. The presence of LADs and the fact that mutations in LMNA associate with altered nuclear architecture suggest that the nuclear lamina plays a vital role in both scaffolding chromatin and regulating chromatin organization. In this model, it is possible that distinct LMNA mutations may alter distinct regions of the genome leading to mutation specific profiles of altered gene expression.