Drug resistance to antibacterial and anticancer drugs is one of the most important global problems in the treatment field that is constantly expanding and hinders the recovery and survival of patients. Therefore, it is necessary to identify compounds that have antibacterial and anticancer properties or increase the effectiveness of existing drugs. One of these approaches is using natural compounds that have few side effects and are effective. Gallic acid (GA) has been identified as one of the most important plant polyphenols that health‐promoting effects in various aspects such as bacterial and viral infections, cancer, inflammatory, neuropsychological, gastrointestinal, and metabolic disease. Various studies have shown that GA inhibits bacterial growth by altering membrane structure, and bacterial metabolism, and inhibits biofilm formation. Also, GA inhibits cancer cell growth by targeting different signaling pathways in apoptosis, increasing reactive oxygen species (ROS) production, targeting the cell cycle, and inhibiting oncogenes and matrix metalloproteinases (MMPs) expression. Due to the powerful function of GA against bacteria and cancer cells. In this review, we describe the latest findings in the field of the sources and chemical properties of GA, its pharmacological properties and bioavailability, the antibacterial and anticancer activities of GA, and its derivatives alone, in combination with other drugs and in the form of nanoformulation. This review can be a comprehensive perspective for scientists to use medicinal compounds containing GA in future research and expand its clinical applications.

Cellular metabolisms produce reactive oxygen species (ROS) which are essential for cellular signaling pathways and physiological functions. Nevertheless, ROS act as “double-edged swords” that have an unstable redox balance between ROS production and removal. A little raise of ROS results in cell proliferation enhancement, survival, and soft immune responses, while a high level of ROS could lead to cellular damage consequently protein, nucleic acid, and lipid damages and finally cell death. ROS play an important role in various pathological circumstances. On the contrary, ROS can show selective toxicity which is used against cancer cells and pathogens. Photodynamic therapy (PDT) is based on three important components including a photosensitizer (PS), oxygen, and light. Upon excitation of the PS at a specific wavelength, the PDT process begins which leads to ROS generation. ROS produced during PDT could induce two different pathways. If PDT produces control and low ROS, it can lead to cell proliferation and differentiation. However, excess production of ROS by PDT causes cellular photo damage which is the main mechanism used in cancer treatment. This review summarizes the functions of ROS in living systems and describes role of PDT in production of controllable ROS and finally a special focus on current ROS-generating therapeutic protocols for regeneration and wound healing.

Background: There are different treatments for breast cancer and melanoma that mostly have some side effects. One of the therapeutic strategies is the use of natural components. Phenol components are a class of antioxidants in plants that have many biological functions like anticancer effects. Gallic acid (GA) is a natural polyhydroxy phenolic compound and commonly found in various foods. In the present study, GA effects alone and in combination with low-level laser irradiation on human dermal fibroblast cell line (HDF), human non-tumorigenic breast epithelial cell line (MCF10A), breast cancer cell line (MDA-MB-231) and melanoma cancer cell line (A375) was under the investigation. Methods: The normal and cancerous cell lines were exposed to 660 nm low-level laser with 3 J/cm² for 90 s. Then, the cells were treated with different concentrations of GA for 24 h. In another study, the cell lines firstly were treated with GA and then exposed to low-level laser irradiation. The effects of GA and low-level laser on cell survival and apoptosis were examined using MTT assay, light microscopy, ROS production assay, fluorescence microscopy (AO/EB double staining) and flow cytometry. Results: The results showed that pre-treatment with low-level laser and then GA reduced the survival of breast cancer cells and melanoma more than the first treatment with GA and then low-level laser irradiation. Our findings showed that ROS production in cells treated with both low-level laser and GA was more than the cells treated with GA alone. The apoptosis and ferroptosis assays confirmed the MTT results which combination treatment with low-level laser and then GA increase the cell death probably via apoptosis and ferroptosis cell death mechanisms compared to GA alone. Conclusions: This study suggests that low-level laser irradiation alone is not able to cause death in human normal and cancerous cells. Preirradiation followed by GA treatment did not change the cell viability in human normal significantly but reduces the cell survival of cancer cells more than GA alone.

At present, after extensive studies in the field of cancer, cancer stem cells (CSCs) have been proposed as a major factor in tumor initiation, progression, metastasis, and recurrence. CSCs are a subpopulation of bulk tumors, with stem cell-like properties and tumorigenic capabilities, having the abilities of self-renewal and differentiation, thereby being able to generate heterogeneous lineages of cancer cells and lead to resistance toward anti-tumor treatments. Highly resistant to conventional chemo- and radiotherapy, CSCs have heterogeneity and can migrate to different organs and metastasize. Recent studies have demonstrated that the population of CSCs and the progression of cancer are increased by the deregulation of different epigenetic pathways having effects on gene expression patterns and key pathways connected with cell proliferation and survival. Further, epigenetic modifications (DNA methylation, histone modifications, and RNA methylations) have been revealed to be key drivers in the formation and maintenance of CSCs. Hence, identifying CSCs and targeting epigenetic pathways therein can offer new insights into the treatment of cancer. In the present review, recent studies are addressed in terms of the characteristics of CSCs, the resistance thereof, and the factors influencing the development thereof, with an emphasis on different types of epigenetic changes in genes and main signaling pathways involved therein. Finally, targeted therapy for CSCs by epigenetic drugs is referred to, which is a new approach in overcoming resistance and recurrence of cancer.