Ampelopsin targets in cellular processes of cancer: Recent trends and advances

Abstract

Cancer is being considered as a serious threat to human health globally due to limited availability and efficacy of therapeutics. In addition, existing chemotherapeutic drugs possess a diverse range of toxic side effects. Therefore, more research is welcomed to investigate the chemo-preventive action of plant-based metabolites. Ampelopsin (dihydromyricetin) is one among the biologically active plant-based chemicals with promising anti-cancer actions. It modulates the expression of various cellular molecules that are involved in cancer progressions. For instance, ampelopsin enhances the expression of apoptosis inducing proteins. It regulates the expression of angiogenic and metastatic proteins to inhibit tumor growth. Expression of inflammatory markers has also been found to be suppressed by ampelopsin in cancer cells. The present review article describes various anti-tumor cellular targets of ampelopsin at a single podium which will help the researchers to understand mechanistic insight of this phytochemical.

Keywords: Ampelopsin; Angiogenesis inhibition; Anti-inflammation; Anti-proliferation; Apoptotic; Cell cycle arrest.

Graphical abstract

Fig. 1

Chemical structure of Ampelopsin.

Fig. 2

: Schematic representations of two novel 5-fluorouracil-substituted ampelopsin derivatives.

Fig. 3

: Apoptotic mechanisms of action of ampelopsin in cancer. It initiates intrinsic (mitochondrial) as well extrinsic (Death receptor medicated) mechanisms of apoptosis induction.

Fig. 4

: Anti-angiogenic and anti-metastatic action of ampelopsin via modulation of VEGF and MMPs expression.

Fig. 5

: Anti-inflammatory mechanisms governed by ampelopsin. It mainly regulates PI3K/Akt/NF-κB and STATs signaling to inhibit inflammation in tumor microenvironment.

Fig. 6

: Ampelopsin incorporation into the cancer cells attenuates the oncogenic effect of miR-21 and tumor-suppressive effect of miR-455–3p through PTEN and PI3K pathway, which results in the activation of protein kinase B (p-Akt), which leads to the sequestration of mesenchymal markers and anti-apoptotic genes and enrichment of epithelial markers and pro-apoptotic genes.