S100A11

Case study 1: Mei Zheng, 2023

Hepatocellular carcinoma (HCC) is the most common and malignant liver tumor worldwide, although the treatment approaches for HCC continue to evolve, metastasis is the main reason for high mortality rates. S100A11 is overexpressed in various cells and regulates tumor development and metastasis. However, few studies report the role and underlying regulatory mechanisms of S100A11 in HCC development and metastasis.

This study provided the first demonstration that S100A11 could serve as a novel diagnostic biomarker used in conjunction with AFP for HCC. Using in vitro cell culture model, we demonstrated that S100A11 is overexpressed in metastatic hepatoma cells, knockdown of S100A11 decreases hepatoma cells proliferation, migration, invasion, and epithelial-mesenchymal transition process by inhibiting AKT and ERK signaling pathways.

Fig1. The protein expression level of S100A11 in HepG2, Hep3B, Li-7, and HCCLM3 cells was determined by Western Blot assay.

Fig2. S100A11 activates AKT and ERK signaling pathways. Effects of S100A11 knockdown on the phosphorylation of AKT and ERK in HCCLM3 cells examined by Western Blot.

Case study 2: Youquan Chen, 2021

Tranilast has an ameliorative effect on myocardial fibrosis (MF), but the specific mechanism has not been studied. S100A11 is a key regulator of collagen expression in MF. In this paper, the researchers will study the regulatory roles of Tranilast and S100A11 in MF.

After the introduction of angiotensin II (AngII) to Human cardiac fibroblasts (HCF), Tranilast was administered, CCK-8 kit, Wound Healing assay and Western blot was used to detect cell functions. The expression of S100A11 was detected by qPCR and Western blot, and then S100A11 was overexpressed by cell transfection technology, so as to explore the mechanism by which Tranilast regulated MF. Overexpression of S100A11 reversed the inhibition of Tranilast on AngII-induced over-proliferation, migration, and fibrosis in HCF, accompanied by activation of the TGF-β1/Smad pathway. Overall, Tranilast inhibits angiotensin II-induced myocardial fibrosis through S100A11/TGF-β1/Smad axis.

Fig3. Tranilast down-regulated the expression of S100A11. Western blot detected the expression of S100A11.

Fig4. Overexpression of S100A11 reversed the inhibitory effect of Tranilast on AngII-induced fibrosis of HCF cells. The expression of α-SMA was detected by IF.

Fig1. Schematic presentation of the ambivalent role of S100A11 in growth regulation of normal human keratinocytes (NHK). (Masakiyo Sakaguchi, 2008)

Fig2. Schematic summary of the 'dry-lab discovery/wet-lab validation' approach and key findings. (Bin Zeng, 2023)

S100A11 involved in several pathways and played different roles in them. We selected most pathways S100A11 participated on our site, such as , which may be useful for your reference. Also, other proteins which involved in the same pathway with S100A11 were listed below. Creative BioMart supplied nearly all the proteins listed, you can search them on our site.

S100A11 has several biochemical functions, for example, S100 protein binding, calcium ion binding, calcium-dependent protein binding. Some of the functions are cooperated with other proteins, some of the functions could acted by S100A11 itself. We selected most functions S100A11 had, and list some proteins which have the same functions with S100A11. You can find most of the proteins on our site.

S100A11 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 S100A11 here. Most of them are supplied by our site. Hope this information will be useful for your research of S100A11.

S100B; EPB41; HLA-B; VHL; TRAF6; q5nfd5_fratt; EGFR; ATF2; ATP6V1A; P; GABARAPL1