TRPV Related Drug Discovery Products

TRPV channels can act as Ca²⁺ entry pathways in the plasma membrane, regulate the expression and activity of cell-surface glycoproteins, control the binding, trafficking, and functional activity of several growth factors, interact with specific G protein-coupled receptors (GPCRs) at the plasma membrane, and/or indirectly regulate cancer cell proliferation, apoptosis, angiogenesis, migration, and invasion during tumor progression.

Fig.1 Hypothetical role of TRPV channels in cancer.^1,2

Creative Biolabs provides professional TRPV in vitro assays and related products to facilitate our customers' research and development of membrane protein drugs:

• TRPV Assays
• Ion Channel Cell Lines
• Ion Channel Membranes
• Membrane Protein Tools

Overview of TRPV

• TRPV1

While TRPV1 expression is largely absent in invasive carcinoma, it is substantially and specifically expressed in both premalignant (leukoplasia) and low-grade papillary skin cancer. Because of its capacity to reduce the expression of the EGFR, TRPV1 has been reported to have tumor-suppressive effects on the development of skin cancer in mice. TRPV1 helps EGFR be ubiquitinated by Cbl and then degraded via the lysosomal pathway by interacting with EGFR through its terminal cytosolic domain.

• TRPV2

TRPV2 is also referred to as a "growth receptor channel" (GRC) since growth factor signaling controls it. A cross-talk between TRPV2 and the IGF-I receptor in particular has been described. Through encouraging Ca²⁺'s translocation from intracellular pools to the plasma membrane, IGF-I can increase Ca²⁺ influx in TRPV2-transfected cells. Along with IGF-I and its receptor, TRPV2 is also overexpressed in urothelial cancer cells. Additionally, higher levels of IGF-I were linked to increased proliferation and survival of human bladder smooth-muscle cells brought on by mechanical stress. Consequently, it can be assumed that TRPV2 exerts significant control over urothelial cancer cell growth and progression through altering the IGF-1/IGF-1R pathway.

• TRPV3

The tongue, nasal epithelium, and epidermal keratinocytes all express TRPV3, a calcium-permeable temperature-sensitive cation channel. TRPV3 has recently been found to be abundantly and specifically expressed, both at the mRNA and protein levels, in the superficial enterocytes of the distal colon. Here, it plays a role in a number of cellular processes, including immune defense, cell volume regulation, cell proliferation and mitogenesis, apoptosis, and epithelial ion and water transport in neighboring cells.

• TRPV4

Both Ca²⁺ inflow and Ca²⁺ release channels are controlled by the TRPV4 channel. The activation of TRPV4 and TRPV1 channels by HGF/SF has also been proposed as the initial step of a signaling cascade that gives rise to cell locomotion and migratory phenotype by the reorganization of actin cytoskeleton, based on the evidence that HGF/SF enhanced Ca²⁺ entry via TRPV1 activation and that its action was restricted to migrating cells.

• TRPV5

TRPV5 is the apical calcium channels. TRPV5 and TRPV6, which work as apical calcium entry mechanisms in absortive and secretory tissues, are noteworthy Ca²⁺-selective channels, in contrast to the other four members of the TRPV family (TRPV1-4), which are non-selective cation channels. The distal convoluted and connected tubules of the kidney exhibit the highest levels of TRPV5.

• TRPV6

The TRPV6 channel, which is under the control of androgens, appears to be essential for the emergence of prostate cancer. In normal, benign human prostate tissues, TRPV6 expression is incredibly low or even undetectable, but as the disease progresses and metastasis increases, it becomes more pronounced.

References

1. Kärki, Tytti, and Sari Tojkander. "Trpv protein family—From mechanosensing to cancer invasion." Biomolecules 11.7 (2021): 1019.
2. Image retrieved from Figure 1 "Hypothetical role of TRPV channels in cancer progression. " Kärki, et al. 2021, used under CC BY 4.0. The original image was modified by extracting and the title was changed to " Hypothetical role of TRPV channels in cancer.".