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Induction of Cancer Cell Death by Apigenin: A Review on Different Cell Death Pathways
Peyman Amini1, Reza Moazamiyanfar2, Mohammad Sedigh Dakkali3
1Medical Technology Research Center, Institute of Health Technology, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Abstract:
Induction of cell death and inhibition of cell proliferation in cancer have been set as some of the main goals in anti-tumor therapy. Cancer cell resistance leads to less efficient cancer therapy, and consequently, to higher doses of anticancer drugs, which may eventually increase the risk of serious side effects in normal tissues. Apigenin, a nature-derived and herbal agent, which has shown anticancer properties in several types of cancer, can induce cell death directly and/or amplify the induction of cell death through other anti-tumor modalities. Although the main mechanism of apigenin in order to induce cell death is apoptosis, other cell death pathways, such as autophagic cell death, senescence, anoikis, necroptosis, and ferroptosis, have been reported to be induced by apigenin. It seems that apigenin enhances apoptosis by inducing anticancer immunity and tumor suppressor genes, like p53 and PTEN, and also by inhibiting STAT3 and NF-κB signaling pathways. Furthermore, it may induce autophagic cell death and ferroptosis by inducing endogenous ROS generation. Stimulation of ROS production and tumor suppressor genes, as well as downregulation of drug-resistance mediators, may induce other mechanisms of cell death, such as senescence, anoikis, and necroptosis. It seems that the induction of each type of cell death is highly dependent on the type of cancer. These modulatory actions of apigenin have been shown to enhance anticancer effects by other agents, such as ionizing radiation and chemotherapy drugs. This review explains how cancer cell death may be induced by apigenin at the cellular and molecular levels.
Insights
Apigenin, a natural compound, effectively induces various cancer cell death pathways, including apoptosis and ferroptosis. It enhances anti-cancer immunity and potentiates treatments like chemotherapy and radiation.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Cancer therapy aims to induce cell death and inhibit proliferation, but drug resistance poses a significant challenge.
- Apigenin, a plant-derived compound, exhibits anticancer properties and can induce cancer cell death through multiple mechanisms.
- Understanding apigenin's molecular actions is crucial for developing more effective anti-tumor strategies.
Approach:
- This review synthesizes current research on apigenin's mechanisms of inducing cancer cell death.
- It explores the various cell death pathways modulated by apigenin, including apoptosis, autophagy, senescence, anoikis, necroptosis, and ferroptosis.
- The review details the molecular targets and signaling pathways affected by apigenin, such as p53, PTEN, STAT3, NF-κB, and ROS generation.
Key Points:
- Apigenin induces apoptosis by enhancing anti-cancer immunity and upregulating tumor suppressor genes (p53, PTEN) while inhibiting pro-survival pathways (STAT3, NF-κB).
- It triggers autophagic cell death and ferroptosis via endogenous reactive oxygen species (ROS) generation.
- Apigenin's ability to induce senescence, anoikis, and necroptosis is linked to ROS production and tumor suppressor gene stimulation.
- The specific cell death pathway induced by apigenin is cancer-type dependent.
- Apigenin potentiates the efficacy of conventional therapies like chemotherapy and ionizing radiation.
Conclusions:
- Apigenin offers a promising therapeutic strategy by inducing diverse cancer cell death mechanisms at the cellular and molecular levels.
- Its ability to overcome drug resistance and enhance other anti-cancer modalities warrants further investigation.
- Apigenin's multifaceted action provides a basis for novel combination therapies in oncology.
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