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CLDN6

Official Full Name
claudin 6
Organism
Homo sapiens
GeneID
9074
Background
Tight junctions represent one mode of cell-to-cell adhesion in epithelial or endothelial cell sheets, forming continuous seals around cells and serving as a physical barrier to prevent solutes and water from passing freely through the paracellular space. These junctions are comprised of sets of continuous networking strands in the outwardly facing cytoplasmic leaflet, with complementary grooves in the inwardly facing extracytoplasmic leaflet. This gene encodes a component of tight junction strands, which is a member of the claudin family. The protein is an integral membrane protein and is one of the entry cofactors for hepatitis C virus. The gene methylation may be involved in esophageal tumorigenesis. This gene is adjacent to another family member CLDN9 on chromosome 16.[provided by RefSeq, Aug 2010]
Synonyms
CLDN6; claudin 6; claudin-6; skullin;
Protein Sequence
MASAGMQILGVVLTLLGWVNGLVSCALPMWKVTAFIGNSIVVAQVVWEGLWMSCVVQSTGQMQCKVYDSLLALPQDLQAARALCVIALLVALFGLLVYLAGAKCTTCVEEKDSKARLVLTSGIVFVISGVLTLIPVCWTAHAIIRDFYNPLVAEAQKRELGASLYLGWAASGLLLLGGGLLCCTCPSGGSQGPSHYMARYSTSAPAISRGPSEYPTKNYV
Open
Disease
Solid tumour/cancer
Approved Drug
0
Clinical Trial Drug
1 +
Discontinued Drug
0

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Detailed Information

The CLDN6 gene, which is part of the Claudin protein family, is located on chromosome 16 at position 16p3.3. Every member of the Claudin family has four parts that cross the cell membrane, two loops outside the cell, and two tails inside the cell, so they share similar structures. Tight junctions between cells are mainly made of proteins that create a barrier to prevent substances and water from easily passing between the cells. CLDN6 is important for maintaining the shape and function of epithelial and vascular cells because it affects tight junctions.

The protein structure of CLDN6 includes a C-terminal PDZ-binding motif, allowing it to interact with various intracellular proteins. This interaction plays a key role in cellular signal transduction, the formation of epithelial barriers, and intercellular material exchange. CLDN6 works together with other tight junction proteins, such as ZO-1, to maintain cell polarity and stable intercellular connections.

Figure 1 illustrates the structural and molecular diagrams of CLDN6, showcasing its transmembrane domains, extracellular loops, and termini, alongside its AlphaFold-predicted chemical structure.Figure 1. Schematic presentation and molecular diagram of CLDN6. (Qu H, et al., 2021)

Biological Functions of CLDN6

As a component of tight junctions, CLDN6 plays an important barrier role. Tight junctions are a crucial adhesive method between epithelial cells, forming continuous sealing belts that prevent unordered solute and water flow. By acting as this physical barrier, CLDN6 not only maintains cellular structural integrity under normal physiological conditions but also exhibits varied functions under pathological conditions such as tumors, infections, and inflammation.

One key function of CLDN6 is its involvement in the invasion mechanism of hepatitis C virus (HCV). HCV uses CLDN6 as a receptor to enter liver cells, leading to infection. This characteristic highlights CLDN6's importance in virology research and its significance in the diagnosis and treatment of liver diseases.

Moreover, CLDN6 expression is closely related to the development of various tumors. Studies have shown abnormal CLDN6 expression in several malignancies, including breast, ovarian, cervical, and gastric cancers. Disruption of intercellular structures and the loss of tight junction function are often precursors to tumor cell invasion and metastasis. Dysfunctional CLDN6 may lead to the proliferation and migration of tumor cells and affect the efficacy of antitumor drugs, making tumors more challenging to treat.

Relationship Between CLDN6 and Cancer

CLDN6 exhibits varying roles and mechanisms in different types of tumors. In ovarian cancer, overexpression of CLDN6 has been linked to increased tumor proliferation and invasiveness. Additionally, altering CLDN6 expression can change tumor cell growth patterns, providing new therapeutic avenues. For example, studies have shown that antibodies or small molecules that elevate CLDN6 expression can effectively inhibit the proliferation of ovarian cancer cells, reducing their invasiveness.

In breast cancer, low CLDN6 expression is typically associated with enhanced tumor cell invasiveness. Overexpression of CLDN6 can restore tight junction function, inhibiting tumor cell motility and invasiveness. Similar studies have shown that CLDN6 can promote apoptosis of cancer cells through specific signaling pathways (e.g., ASK1/P38 pathway), thereby inhibiting tumor growth.

CLDN6's role in other tumors has also garnered attention. For instance, in cervical cancer, overexpression of CLDN6 can modulate apoptosis-related proteins, further suppressing tumor growth. Overall, abnormal expression of CLDN6 in various cancers indicates its significant potential in tumor development, progression, and treatment.

CLDN6 Signaling Pathways and Regulatory Mechanisms

CLDN6's roles are not limited to being a tight junction molecule; it also participates in the regulation of various intracellular signaling pathways. Research indicates that CLDN6 interacts with multiple intracellular proteins via its PDZ-binding motif, regulating signaling pathways such as Ras, Raf, ERK, and PI3K. These pathways are closely linked to processes like cell proliferation, differentiation, and apoptosis.

For example, in cervical cancer cells, CLDN6 recruits AF-6 protein through its PDZ domain and inhibits the binding of Ras and Raf, thereby controlling downstream ERK and PI3K pathways. This process significantly impacts tumor cell biological behavior, highlighting CLDN6's precise regulation of cell function through signal transduction pathways.

In other cancers, such as breast and ovarian cancer, CLDN6 overexpression shows similar roles by activating specific MAPK pathways or regulating the PTEN/AKT pathway through interaction with ZO-1, inhibiting tumor growth and metastasis. These studies suggest that CLDN6 not only stabilizes intercellular structures but may also influence tumor occurrence and progression by regulating intracellular signaling networks.

Clinical Applications of CLDN6

More research on CLDN6 as a potential therapy choice is being conducted as our knowledge of what it does increases. Treatments aiming targeting CLDN6 have made some advancement in clinical trials right present. Early investigations and clinical trials have showed promising outcomes for antibodies, bispecific antibodies, and CAR-T cell therapy aiming targeting CLDN6.

For instance, Astellas Pharma's antibody IMAB-027, developed in Japan, has progressed to phase II clinical trials to target testicular and ovarian tumors. Early phase I clinical trials on Amgen's AMG 704 bispecific antibody are in progress. It shows encouraging success treating non-small cell lung cancer and ovarian cancer. Working on a CAR-T cell treatment for malignancies linked to CLDN6, Germany's BioNTech Early findings reveal that this medication successfully fights cancers positive for CLDN6-positive tolerance is well-tolerated.

These findings of research indicate that CLDN6 may be a fresh target for immune system-based cancer therapy, therefore offering fresh hope to cancer sufferers.

References:

  1. Qu H, Jin Q, Quan C. CLDN6: From Traditional Barrier Function to Emerging Roles in Cancers. Int J Mol Sci. 2021 Dec 14;22(24):13416.
  2. Du H, Yang X, Fan J, Du X. Claudin 6: Therapeutic prospects for tumors, and mechanisms of expression and regulation (Review). Mol Med Rep. 2021 Sep;24(3):677.
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