CDC42

Case Study 1: Hui Cao, 2023

Cell division control protein 42 (CDC42) modulates insulin secretion and angiogenesis to participate in the pathology of diabetic complications and retinal vascular-associated diseases. This study intended to explore the role of CDC42 in the progression of diabetic retinopathy, and the underlying mechanism. Human retinal microvascular endothelial cells (hRMECs) were cultured in 5.5 mM glucose (normal glucose) or 25 mM glucose (high glucose; HG) medium, respectively. CDC42 overexpression plasmid and small interference RNA (oe-CDC42 and si-CDC42) or corresponding negative controls (oe-NC and si-NC) were transfected into hRMECs under HG. Then, platelet-activating factor C-16 (C16-PAF) (MEK/ERK pathway activator) was added to si-CDC42 or si-NC transfected hRMECs under HG. HG increased CDC42 mRNA and protein, cell viability, invasive cell count, branch points, and tube length but reduced cell apoptosis in hRMECs. CDC42 upregulation enhanced cell viability, invasive cell count, branch points, tube length, p-MEK, and p-ERK, but attenuated cell apoptosis. Downregulation of CDC42 exhibited opposite trends. In addition, C16-PAF also increased cell viability, invasive cell count, branch points, and tube length, p-MEK, and p-ERK, but retarded cell apoptosis.

Fig1. Representative images of CDC42 protein by immunoblotting.

Fig2. Representative images of MEK and ERK by immunoblotting.

Case Study 2: Li-Li Ma, 2020

Microscopic indications of malignancy and hallmark molecules of cancer are pivotal to determining cancer patient prognosis and subsequent medical intervention. Here, the researchers found that compared to apical expression of Cdc42, which indicated that basal expression of Cdc42 occurred at the migrating cell front, glandular basal expression of Cdc42 (cell division cycle 42) in tissues indicated poorer prognoses for colorectal cancer (CRC) patients. The current study shows that activated Cdc42 was rapidly recruited to the migrating CRC cell front after VEGF stimulation through engagement of membrane-anchored neuropilin-1 (NRP1). When VEGF signalling was blocked with NRP1 knockdown or ATWLPPR (A7R, antagonist of VEGF/NRP1 interaction), Cdc42 activation and relocation to the cell front was attenuated, and filopodia and invadopodia formation was inhibited. The VEGF/NRP1 axis regulates directional migration, invasion, and metastasis through Cdc42 activation and relocation resulting from actin filament polymerisation of the extensions of membrane protrusions.

Fig3. Cell membrane fractions were isolated and probed for Cdc42.

Fig4. LS174T and SW480 cells were transfected with NC or shCdc42 in the first column.

Fig1. Downstream effector/adaptor proteins of Cdc42. (Xing-Hua Xiao, 2018)

Fig2. Schematic of Cdc42 expression predicting the prognosis of colorectal cancer. (Li-Li Ma, 2020)

CDC42 involved in several pathways and played different roles in them. We selected most pathways CDC42 participated on our site, such as MAPK signaling pathway, Ras signaling pathway, Rap signaling pathway, which may be useful for your reference. Also, other proteins which involved in the same pathway with CDC42 were listed below. Creative BioMart supplied nearly all the proteins listed, you can search them on our site.

CDC42 has several biochemical functions, for example, GTP binding, GTP-dependent protein binding, GTPase activity. Some of the functions are cooperated with other proteins, some of the functions could acted by CDC42 itself. We selected most functions CDC42 had, and list some proteins which have the same functions with CDC42. You can find most of the proteins on our site.

CDC42 has direct interactions with proteins and molecules. Those interactions were detected by several methods such as yeast two hybrid, co-IP, pull-down and so on. We selected proteins and molecules interacted with CDC42 here. Most of them are supplied by our site. Hope this information will be useful for your research of CDC42.

PAK1; WAS