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Molecules 2020, 25, 4102 9 of 22 5.1. Furanocoumarins The secondary metabolites, furanocoumarins (FC; Figure 3), are mostly present in higher plants. The photoactive furanocoumarins were mainly composed of a linear core, and the biological distribution, photochemistry and phototoxicity mechanisms of FC after PUVA (psoralen and long-wave ultraviolet radiation) irradiation were reported in previous study [92]. In terms of phototherapy, psoralen is activated in the wavelength range of 300–400 nm ultraviolet radiation to treat psoriasis, dermatitis, eczema, and other skin problems [92]. Over a few years, many researchers reported anticancer activity of FCs against various types of cancer such as breast, skin, and leukaemia. FCs modulate several pathways inducing cancer cell death by inhibiting signal transducer and activator of transcription 3 (STAT3), nuclear factor-κB (NF-κB), phosphatidylinositol-3-kinase and AKT protein expression (Figure 4). These pathways play a key role in tumour development through regular activation of several inflammatory genes. Studies show that FC displayed potent activity against breast cancer development by inhibiting STAT3 protein expression [93]. Panno et al. [92,93], demonstrated inhibition of breast cancer cell growth in a dose-dependent manner through activation of p53 and Bax, leading to the cleavage of caspase 9. In contrast, in leukaemia cells, FC inactivated the JAK (Janus-activated kinase), protein c-Src, and STAT3, and downregulated Bcl-xl and Bcl-2 proteins which are responsible for apoptosis [93–96]. The enhanced activity against the malignant melanoma cell line (A375) after UV irradiation of plant extracts containing FC also supported the possible photoactive nature of FCs [93–96]. The linear forms of furanocoumarins like psoralen and its derivatives 5-methoxypsoralen (5-MOP) and 8-methoxypsoralen (8-MOP) are reported to increase the cytotoxicity after irradiation by ultraviolet light in the 320–400 nm wavelength range against cutaneous T-cell lymphoma [97,98], and photoactivated psoralens induce apoptosis by forming adducts with DNA. This leads to the activation of p21waf/Cip and p53 and subsequently leads to cell death by the release of mitochondrial cytochrome c. The photoactivation of psoralen can also cause cell death by blocking oncogenic receptor tyrosine kinase signalling and the PI3K pathway by interfering with efficient recruitment of effector Akt kinase to the activated plasma membrane [92–104]. PUVA treatment was found effectively against B16F10 murine melanoma cells by cell cycle arrest in G2/M phases [93–96].PDF Image | Role of Photoactive Phytocompounds in Photodynamic Therapy of Cancer
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