Corilagin Represses Epithelial to Mesenchymal Transition Process Through Modulating Wnt/β-Catenin Signaling Cascade

Abstract

Corilagin (CLG), a major component of several medicinal plants, can exhibit diverse pharmacological properties including those of anti-cancer, anti-inflammatory, and hepatoprotective qualities. However, there are no prior studies on its potential impact on the epithelial-to-mesenchymal transition (EMT) process. EMT can lead to dissemination of tumor cells into other organs and promote cancer progression. Hence, we aimed to investigate the effect of CLG on EMT and its mechanism(s) of action in tumor cells. We noted that CLG reduced the expression of various epithelial markers and up-regulated the expression of Occludin and E-cadherin in both basal and TGFβ-stimulated tumor cells. CLG treatment also abrogated cellular invasion and migration in colon and prostate carcinoma cells. In addition, CLG effectively attenuated the Wnt/β-catenin signaling cascade in TGFβ-stimulated cells. Overall, our study suggests that CLG may function as and effective modulator of EMT and metastasis in neoplastic cells.

Cytoskeletal Dynamics in Epithelial-Mesenchymal Transition: Insights into Therapeutic Targets for Cancer Metastasis

“…The polymerization is associated with the formation of flat, sheet-like membrane protrusions called lamellipodia, or finger-like extensions at the edge of lamellipodia called filopodia [ 19 ]. In lamellipodia, actin filaments are arranged in a loosely organized meshwork, often referred to as dendritic networks [ 20 ], whereas, in filopodia, actin filaments arrange into parallel bundles [ 21 ]. These two different types of organizations rely on the action of specific actin-organizing proteins.…”

“…This is followed by the degradation of the underlying basement membrane and ECM [ 18 , 19 , 20 ]. The ability to degrade the ECM and invade into the surrounding tissue parenchyma is obtained by activating the EMT program, where the epithelial cancer cells transform into a more invasive and motile mesenchymal state [ 21 , 22 ]. During EMT, adherens junctions’ dissolution is stabilized by the cleavage and degradation of E-cadherin at the cell membrane [ 9 ].…”

Small nucleolar RNA host genes promoting epithelial–mesenchymal transition lead cancer progression and metastasis

“…[35][36][37] Moreover, to intricate an already debated and complex process, cancer cells are often reported to display different degrees of EMT phenotypes. [38][39][40][41] As reported above, SNHGs exert multiple roles being able to act as molecular sponges for several miRNAs (Figure 2) or binding proteins modulating in that way multiple biological processes, including the EMT in cancer. 28 The known SNHGs in EMT are resumed in Table 2.…”

“…Indeed, EMT‐induced cells demonstrate enhanced migration, invasion, and frequently express N‐cadherin at the expense of E‐cadherin reducing in this way the intercellular adhesion 35–37 . Moreover, to intricate an already debated and complex process, cancer cells are often reported to display different degrees of EMT phenotypes 38–41 …”

Small in Size, but Large in Action: microRNAs as Potential Modulators of PTEN in Breast and Lung Cancers

“…Interestingly, the proliferation and metastasis of cancer cells are in close relationship with each other and can trigger chemoresistance [ 239 , 240 , 241 ]. It has been reported that TGF-β can induce EMT in mediating chemoresistance [ 242 , 243 , 244 , 245 ]. miRNA-134/487b/655 stimulates TGF-β-mediated EMT in lung cancer cells.…”