title: Role of Natural Radiosensitizers and Cancer Cell Radioresistance: An Update.
abstract: Cancer originates from genetic mutations accumulation. Cancer stem cells have been depicted as tumorigenic cells that can differentiate and self-renew. Cancer stem cells are thought to be resistant to conventional therapy like chemotherapy and radiation therapy. Radiation therapy and chemotherapy damage carcinomic DNA cells. Because of the ability of cancer stem cells to self-renew and reproduce malignant tumors, they are the subject of intensive research. In this review, CSCs radioresistant mechanisms which include DNA damage response and natural radiosensitizers have been summed up. Reactive oxygen species play an important role in different physiological processes. ROS scavenging is responsible for regulation of reactive oxygen species generation. A researcher has proved that microRNAs regulate tumor radiation resistance. Ionizing radiation does not kill the cancer cells; rather, IR just slows down the signs and symptoms. Ionizing radiation damages DNA directly/indirectly. IR is given mostly in combination with other chemo/radiotherapies. We briefly described here the behavior of cancer stem cells and radioresistance therapies in cancer treatment. To overcome radioresistance in treatment of cancer, strategies like fractionation modification, treatment in combination, inflammation modification, and overcoming hypoxic tumor have been practiced. Natural radiosensitizers, for example, curcumin, genistein, and quercetin, are more beneficial than synthetic compounds.
authors.affiliation: Institute of Molecular Biology and Biotechnology (IMBB), The University of Lahore, Pakistan.
authors.forename: Arif
authors.identifier: 0000-0001-9445-8861
authors.initials: A
authors.lastname: Malik
authors.affiliation: Institute of Molecular Biology and Biotechnology (IMBB), The University of Lahore, Pakistan.
authors.forename: Misbah
authors.initials: M
authors.lastname: Sultana
authors.affiliation: Center for Research in Molecular Medicine (CRiMM), The University of Lahore, Pakistan.
authors.forename: Aamer
authors.initials: A
authors.lastname: Qazi
authors.affiliation: Center for Research in Molecular Medicine (CRiMM), The University of Lahore, Pakistan.
authors.forename: Mahmood Husain
authors.initials: MH
authors.lastname: Qazi
authors.affiliation: Institute of Molecular Biology and Biotechnology (IMBB), The University of Lahore, Pakistan.
authors.forename: Gulshan
authors.initials: G
authors.lastname: Parveen
authors.affiliation: Institute of Molecular Biology and Biotechnology (IMBB), The University of Lahore, Pakistan.
authors.forename: Sulayman
authors.initials: S
authors.lastname: Waquar
authors.affiliation: University College of Medicine and Dentistry, The University of Lahore, Pakistan.
authors.forename: Abdul Basit
authors.initials: AB
authors.lastname: Ashraf
authors.affiliation: Center of Excellence in Genomic Medicine Research (CEGMR), King Abdulaziz University, Jeddah, Saudi Arabia.
authors.forename: Mahmood
authors.initials: M
authors.lastname: Rasool
mesh_terms: D003131:Combined Modality Therapy; D004249:DNA Damage; D006801:Humans; D009369:Neoplasms / Q000235:genetics / Q000378:metabolism / Q000628:therapy*; D014411:Neoplastic Stem Cells / Q000187:drug effects* / Q000378:metabolism / Q000528:radiation effects*; D018384:Oxidative Stress / Q000187:drug effects / Q000528:radiation effects; D011838:Radiation-Sensitizing Agents / Q000627:therapeutic use*; D011878:Radiotherapy / Q000379:methods*; D016896:Treatment Outcome; D059016:Tumor Microenvironment / Q000187:drug effects / Q000235:genetics / Q000528:radiation effects
chemical_list: D011838:Radiation-Sensitizing Agents