Table 1 Homologous CAMs

Desmosome

Cadherin (calcium-dependent)

Desmoglein 1, Desmoglein 2, Desmoglein 3, Desmoglein 4

DSG1 DSG2, DSG3, DSG4

Play important roles in cell adhesion, ensuring that cells within tissues are bound together. Cadherins behave as both receptors and ligands.

Desmocollin 1, Desmocollin 2, Desmocollin 3, Desmocollin 4

DSC1 DSC2 DSC3

Catenin

Junction plakoglobin ( JUP)

JUP

JUP can bind to the desmoglein I.

Tight junctions

Claudins

Claudin 1

CLDN1

The main component of the tight junctions

Occludins

Occludin

OCLN

The main component of the tight junctions

Cadherin

E-cadherin

CDH1

Loss of E-cadherin function or expression has been implicated in cancer progression and metastasis. E-cadherin downregulation decreases the strength of cellular adhesion within a tissue, resulting in an increase of cellular motility. This in turn may allow cancer cells to cross the basement membrane and invade surrounding tissues[21].

F11 receptor (JCAM)

JAM-1

The ligand for the integrin LFA1, a platelet receptor

Catenins

α-(E, N,T), β-, δ-catenins, γ-catenin (or Junction plakoglobin, JUP)

CTNNA1 (CAP102), CTNNA2 (CAPR), CTNNA3 (VR22), CTNNB1, CTNND1, CTNND2, JUP

Catenins belong to a family of proteins found in complexes with cadherin cell adhesion molecules. The primary mechanical role of catenins is connecting cadherins to actin filaments, specifically in these adhesion junctions of epithelial cells[22]. β-catenin may play a role in telling the cell to stop proliferating, as there is no room for more cells in the area.

The role of catenin in EMT has also received a lot of recent attention for its contributions to cancer development. It has been shown that HIF-1α can induce the EMT pathway, as well as the Wnt/β-catenin signaling pathway, thus enhancing the invasive potential of LNCaP cells (human prostate cancer cells)[23]. As a result, it is possible that the EMT associated with upregulated HIF-1α is controlled by signals from this Wnt/β-catenin pathway[23]. Catenin and EMT interactions may also play a role in hepatocellular carcinoma. VEGF-B treatment of hepatoma carcinoma cells can cause α-catenin to move from its normal location on the membrane into the nucleus and E-cadherin expression to decrease, thus promoting EMT and tumor invasiveness[24].

JUP protein is the only known constituent common to submembranous plaques of both desmosomes and intermediate junctions. JUP also associates with classical cadherins such as E-cadherin; in that context. Plakoglobin is O-glycosylated.

Cingulin

Cingulin

CGN

Cingulin is specifically localized at tight junctions in epithelial cells, unlike ZO-1, which is also detected at adherens-type junctions in non-epithelial cells. Cingulin interacts with ZO-1 and several other tight junction proteins, in addition to interacting with actin and myosin[25, 26].

Actin

α-, β-, γ-actins

ACTA1, ACTA2, ACTB, ACTG1, ACTG2

Participates in many important cellular processes, including cell motility, cell division and cytokinesis, vesicle and organelle movement, cell signalling, and the establishment and maintenance of cell junctions and cell shape.

Gap junctions

Connexin (or hemichannel)

Connexins

GJA1, GJC1, GJB4 etc.

Connexins are assembled in groups of six to form hemichannels, or connexons, and two hemichannels then combine to form a gap junction. The connexin gene family is diverse, with 21 identified members in the sequenced human genome.