Sinomenine Can Inhibit the Growth and Invasion Ability of Retinoblastoma Cell through Regulating PI3K/AKT Signaling Pathway

Abstract

Sinomenine was found to play anti-cancer functions in different type of cancers, while the mechanisms underlying the anticancer effects of sinomenine in retinoblastoma (RB) remains unclear. The present study was designed to explore the impacts of sinomenine on cell proliferation and invasion ability of RB cells and the related mechanism. Human retinoblastoma cell line WERI-RB-1 and Y79 cells were cultured and treated by different concentration of sinomenine, and then the proliferation ability of the cells was determined via performing the MTT proliferation assay. The cell apoptosis was examined via performing the flow cytometry assay. Then scratch wound healing analysis as well as and transwell invasion analysis have been performed to determine the effect of sinomenine on cell migration ability as well as invasion ability. The proteins level of PI3K/AKT signaling molecules were determined with western blot assay. We found that sinomenine was able to decrease the proliferation and promote the apoptosis of RB cells in a dose-dependent manner; moreover, sinomenine also significantly suppressed the migration as well as invasion ability of WERI-RB-1 and Y79 cells in vitro. Furthermore, sinomenine also deactivated PI3k/AKT signaling in WERI-RB-1 cells via inhibited the phosphorylation of PI3K and AKT proteins. Sinomenine can exert anti-tumor function on RB cells in vitro, therefore sinomenine might be a potential alterative medication for the treatment for RB.

Effect of Eriodictyol on Retinoblastoma via the PI3K/Akt Pathway

“…Currently, some studies have reported that the PI3K/Akt pathway plays an important role in RB [ 21 – 23 ]; however, the anticancer effect of eriodictyol on RB has not been reported. The purpose of this study was to investigate the antitumor effect of eriodictyol on the retinoblastoma Y79 cell line and its potential mechanism of action and to provide a new basis for tumor therapy with the PI3K-Akt signaling pathway as a key molecular target.…”

Sinomenine accelerate wound healing in rats by augmentation of antioxidant, anti-inflammatory, immunuhistochemical pathways

“…These outcomes indicate clear regulator potentials of SN on the immunohistochemical proteins (TGF-β1) associated with wound healing acceleration. Accordingly, Researchers have shown significant potentials of SN in the positive augmentation of immunohistochemically (increasing Bax and decreasing Bcl-2) proteins, regulatory of oxidative stress and inflammation, which were considered as molecular mechanisms behind SN efficacy in the inhibition of growth and migration of retinoblastoma cells in an in vitro experiment [ 56 ]. Similarly, in vitro and in vivo studies have correlated the ameliorative effect of sinomenine on cardiac hypertrophy with its positive regulation of immunohistochemically (Bax/Bcl-2) proteins [ 27 , 57 ].…”

The anti-tumor potential of sinomenine: a narrative review

“…Zhao et al showed that sinomenine hydrochloride not only inhibited the TGF-β/Smad signaling pathway, and depleted p-Smad 2 and p-Smad 3, but also inhibited the EMT-related transcription factors Snail1 and Twist to inhibit EMT ( 26 ). Studies have also shown that sinomenine and its derivatives can inhibit the migration and invasion of cancer cells by inhibiting PI3K/Akt/mTOR activation and MAPK (ERK, p38 and JNK) signalling pathways ( 14 , 16 , 49 ).…”