Photodynamic therapy (PDT) is a relatively new and promising modality for the treatment of cancer. PDT involves administering a photosensitizing dye, i.e. photosensitizer, that selectively accumulates in tumors, and shining a light source on the lesion with a wavelength matching the absorption spectrum of the photosensitizer, that exerts a cytotoxic effect after excitation. The reactive oxygen species produced during PDT are responsible for the oxidation of biomolecules, which in turn cause cell death and the necrosis of malignant tissue. PDT is a multi-factorial process that generally involves apoptotic death of the tumor cells, degeneration of the tumor vasculature, stimulation of anti-tumor immune response, and induction of inflammatory reactions in the illuminated lesion. Numerous compounds with photosensitizing activity have been introduced commercially. Although many papers have been published with regard to PDT in the last decade, there has been relatively little focus on natural medicinal plant extracts and compounds derived therefrom. Herbal plants and their extracts are natural substances, and in comparison with synthetic chemicals are considered "green". This review focuses on the different mechanisms of PDT and discusses the role of various plant extracts and natural compounds either alone or in combination for carrying out PDT on different types of cancers.

The lung tissue expresses the cholinergic system including nicotinic acetylcholine receptors (nAChRs) which included in many physiologic and pathologic processes. Mounting evidence revealed that these receptors have important roles in lung carcinogenesis via modulating either stimulatory or inhibitory signaling pathways. Among different members of nicotinic receptors family, alpha7‐subtype of nAChR (α7nAChR) is a critical mediator involved in both inflammatory responses and cancers. Several studies have shown that this receptor is the most powerful regulator of responses that stimulate lung cancer processes such as proliferation, angiogenesis, metastasis, and inhibition of apoptosis. Moreover, aside from its roles in the regulation of cancer pathways, there is growing evidence indicating that α7nAChR has profound impacts on lung inflammation through the cholinergic anti‐inflammatory pathway. Regarding such diverse effects as well as the critical roles of nicotine as an activator of α7nAChR on lung cancer pathogenesis, its modulation has emerged as a promising target for drug developments. In this review, we aim to highlight the detrimental as well as the possible beneficial influences of α7nAChR downstream signaling cascades in the control of lung inflammation and cancer‐associated properties. Consequently, by considering the significant global burden of lung cancer, delineating the complex influences of α7 receptors would be of great interest in designing novel anticancer and anti‐inflammatory strategies for the patients suffering from lung cancer.

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Alpha7 nicotinic acetylcholine receptor (α7nAChR) is one of the main subtypes of nAChRs that modulates various cancer-related properties including proliferative, anti-apoptotic, pro-angiogenic and pro-metastatic activities in most of the cancers. It also plays a crucial role in inflammation control through the cholinergic anti-inflammatory pathway in numerous pathophysiological contexts. Such diverse physiological and pathological functions that initiate from this receptor may have significant impacts in determining the outcome of different cancers. Various tissues of gastrointestinal (GI) cancers such as gastric, colorectal, pancreatic and liver cancers have shown the upregulated expression of α7nAChR as compared to normal adjacent tissues. According to the well-established connection between inflammation and tumorigenesis in the digestive system, there are mounting studies demonstrated either stimulatory or inhibitory effects of α7nAChR signaling in the development of GI cancers. To date, the precise underlying mechanisms related to this receptor in patients with GI cancers have not been fully elucidated. Regarding the paradoxical modulatory effects of this receptor in carcinogenesis, in this review, we aim to summarize the accumulated evidence about the involvement of α7nAChR in inflammation-associated GI cancers. It seems that the complex influences of α7nAChR may be a promising target in designing novel strategies in the treatment of such pathologic conditions.