Abstract
TRPV4 activity modulates cell activities including receptor trafficking and transcriptional or translational regulations. We tested its CRISPR/Cas9 scissor efficacy in HepG2 (HEK293) cell noticed that it worked well in both cell lines to eliminate TRPV4 genome sequences. To confirm TRPV4 functions in the cell morphology maintenance and cell growth (beyond Ca2+ channel), we compared its wound healing, cell surface area, survival property and soft agar growth ability after deletion of TRPV4 gene in the cells with its CRISPR/Cas9 system. With these experiments, we confirmed that TRPV4 is required not only to function as Ca2+ channel but also to maintain its proper cell morphology as a corner stone protein on the cell adhesion junction.
Highlights
The TRPV4 channel, a member of the transient receptor potential (TRP) vanilloid subfamily, is expressed in a broad range of tissues where it involves the generation of a Ca2+ signal and/or depolarization of membrane potential [1] [2] [3] [4]
We suggest here that the novel role for TRPV4 has been established as a suppressor protein in HepG2 cell to inhibit metastasis or the epithelial-mesenchymal transition (EMT)
HepG2 morphology change by TRPV4 scissor treatment: Previously we demonstrated that the interaction of TRPV4 with actin is differentially regulated by its 824 serine phosphorylation of TRPV4 [28]
Summary
The TRPV4 channel, a member of the transient receptor potential (TRP) vanilloid subfamily, is expressed in a broad range of tissues where it involves the generation of a Ca2+ signal and/or depolarization of membrane potential [1] [2] [3] [4]. This human TRPV4 gene is found in chromosome, at q24.1. C and D: the mRNA consists of 3229 bases, whereas the TRPV4 protein, contains 839 amino [11] [12].
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