
-   The expression of Lamc2 were upregulated in aging rat kidneys. Aging is associated with the loss of H3K27m3 and 5mC silencing modifications at the Lamc2 gene. Epigenetic analysis showed that the loss of 5mC at silenced Laminin genes drives their de-repression during aging, contributing to the age-related decline in renal function [PMID: 29846172].
-   LAMC2 gene expression was significantly upregulated in lung adenocarcinoma metastatic cells. Elevated LAMC2 increased traction force, migration, and invasion of lung adenocarcinoma cells accompanied by the induction of epithelial-mesenchymal transition (EMT). LAMC2 knockdown attenuated metastasis in mice. LAMC2 promoted migration and invasion via EMT that was integrin beta1- and ZEB1-dependent. High LAMC2 was significantly correlated with the mesenchymal marker vimentin expression in lung adenocarcinomas, and with higher risk of recurrence or death in patients with lung adenocarcinoma [PMID: 25591736].
-   LAMA3, LAMB3 and LAMC2 are correspond to the alpha3, beta3 and gamma2 chains of laminin 5. Laminin 5 synthesis in human keratinocytes was augmented by inflammatory cytokines and growth factors such as TGF-alpha, TGF-beta1 and TNF-alpha, and lysophospholipids such as S1P, LPA and LPCs, which are supposed to be present in acute wound fluid. The increased laminin 5 protein in the wound area presumably enhances wound repair by stimulating adhesion and migration of keratinocytes on the wound bed and by facilitating basement membrane formation at the dermal-epidermal junction [PMID: 15541073].

## Summary

The Lamc2 gene encodes the gamma 2 chain of laminin, a key component in the basement membrane of epithelial tissues, including the kidneys. This protein is involved in cell adhesion, migration, and signaling, crucial for maintaining tissue integrity and function [CS: 10]. In the kidneys, Lamc2's role is particularly significant in supporting the structure of the glomerular basement membrane and tubular epithelia, essential for efficient filtration and renal function [CS: 9].

In response to kidney disease or toxic events, Lamc2 expression increases, as evidenced by its upregulation in aging kidneys and in conditions like congenital hepatic fibrosis and autosomal recessive polycystic kidney disease (CHF/ARPKD) [CS: 7]. This upregulation likely serves as a compensatory mechanism to counteract damage and maintain kidney function [CS: 8]. For instance, in aging kidneys, the loss of epigenetic silencing at the Lamc2 gene leads to its increased expression, which may help to compensate for the age-related decline in renal function by enhancing tissue repair and maintaining basement membrane integrity [CS: 5]. Similarly, in CHF/ARPKD, the overexpression of Lamc2 could be an attempt to stabilize the epithelial structure in the face of cyst formation and extensive fibrosis, thus preserving kidney function amidst pathological changes [CS: 6].
