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Novel Effects of Statins on Cancer via Autophagy
Daniela Mengual1, Luz Elena Medrano1, Wendy Villamizar-Villamizar2
1Healthcare Pharmacy and Pharmacology Research Group, Faculty of Chemistry and Pharmacy, Universidad del Atlántico, Barranquilla 081008, Colombia.
Abstract:
Cancer is one of the main causes of death globally. Most of the molecular mechanisms underlying cancer are marked by complex aberrations that activate the critical cell-signaling pathways that play a pivotal role in cell metabolism, tumor development, cytoskeletal reorganization, and metastasis. The phosphatidylinositol 3-kinase/protein kinase-B/mammalian target of the rapamycin (PI3K/AKT/mTOR) pathway is one of the main signaling pathways involved in carcinogenesis and metastasis. Autophagy, a cellular pathway that delivers cytoplasmic components to lysosomes for degradation, plays a dual role in cancer, as either a tumor promoter or a tumor suppressor, depending on the stage of the carcinogenesis. Statins are the group of drugs of choice to lower the level of low-density lipoprotein (LDL) cholesterol in the blood. Experimental and clinical data suggest the potential of statins in the treatment of cancer. In vitro and in vivo studies have demonstrated the molecular mechanisms through which statins inhibit the proliferation and metastasis of cancer cells in different types of cancer. The anticancer properties of statins have been shown to result in the suppression of tumor growth, the induction of apoptosis, and autophagy. This literature review shows the dual role of the autophagic process in cancer and the latest scientific evidence related to the inducing effect exerted by statins on autophagy, which could explain their anticancer potential.
Insights
Statins, commonly used for lowering cholesterol, show potential anticancer effects by inhibiting cancer cell proliferation and metastasis. They may exert these effects by inducing autophagy, a cellular process with a dual role in cancer progression.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Cancer remains a leading global cause of death, driven by complex molecular aberrations in cell signaling pathways.
- The phosphatidylinositol 3-kinase/protein kinase-B/mammalian target of the rapamycin (PI3K/AKT/mTOR) pathway is crucial in cancer development and metastasis.
- Autophagy, a cellular degradation process, plays a complex, context-dependent role in cancer, acting as either a tumor promoter or suppressor.
Purpose of the Study:
- To review the dual role of autophagy in cancer.
- To explore the latest scientific evidence on statins' effect on autophagy.
- To elucidate the potential anticancer mechanisms of statins, particularly their role in inducing autophagy.
Main Methods:
- Literature review of experimental and clinical data.
- Analysis of in vitro and in vivo studies on statins' effects on cancer cells.
- Examination of molecular mechanisms underlying statin-induced anticancer effects.
Main Results:
- Statins demonstrate potential in cancer treatment, inhibiting cancer cell proliferation and metastasis.
- Statin administration has been shown to suppress tumor growth, induce apoptosis, and promote autophagy.
- Evidence suggests statins induce autophagy, which may contribute to their observed anticancer properties.
Conclusions:
- Statins exhibit promising anticancer potential through various molecular mechanisms.
- The induction of autophagy by statins is a key mechanism that warrants further investigation for cancer therapy.
- Understanding the interplay between statins, autophagy, and cancer is critical for developing novel therapeutic strategies.
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