TABLE 3.
Treatment in cancer.
| Targets | Drugs | Cancer types | Mechanisms |
|---|---|---|---|
| SREBP2 | AtorvastatinL | Breast cancer | Alter the expression of 50 genes with a shared cluster of 37 genes, including the Hippo, Notch, and Wnt signaling pathways, preventing the EMT process (Koohestanimobarhan et al., 2019) |
| Ovastatin | |||
| Simvastatin | |||
| Lovastatin | Breast cancer | Signal through PPARγ and upregulate PTEN at the transcriptional level (Teresi et al., 2006) | |
| Simvastatin | Breast cancer | Contributes to breast cancer cell death by inducing inactivation of PI3K/Akt and MAPK/Erk signaling (Wang et al., 2016) | |
| Cerivastatin | Breast cancer | Inhibits the elevated levels of mevalonate produced by the transcriptional activity of SREBP2 and impedes the nuclear localization and transcription of YAP/TAZ (Piccolo et al., 2014; Sorrentino et al., 2014) | |
| Lovastatin | Osteosarcoma | Reduces the expression of CYR61 via SREBP2/miR-33a, which in turn inhibits osteosarcoma cell invasion (Huang et al., 2018) | |
| Fluvastatin | Thymic carcinoma | Inhibits HMGCR to suppresses cell proliferation, which might be mediated by inhibiting the production of geranylgeranyl-pyrophosphate (Hayashi et al., 2020) | |
| Fluvastatin | Non-small cell lung cancer | Alters Braf/MEK/ERK1/2 and Akt signaling pathways by inhibiting HMGCR, which can inhibit cell growth, induce apoptosis, and inhibit tumorigenesis in non-small cell lung cancer (Zhang et al., 2019) | |
| Simvastatin | Colorectal cancer | Suppresses PD-L1 expression and promotes antitumor immunity by inhibiting lncRNA SNHG29 expression and its mediated YAP activation (Ni et al., 2021) | |
| Simvastatin | Prostate cancer | Reduce cell proliferation and induce apoptosis mediated by phosphorylation downregulation of AKT/FOXO1 signaling pathway (Deng et al., 2019) | |
| Fluvastatin | |||
| Simvastatin | Prostate cancer | Overcome enzalutamide resistance by reducing AR by inhibiting the mTOR signaling pathway (Kong et al., 2018) | |
| Simvastatin | Pancreatic cancer | Inhibit invasion and growth and exhibit synergistic antitumor effects in ORP5-expressing pancreatic cancer cells (Ishikawa et al., 2010) | |
| Tricostatin A | |||
| Fluvastatin | Bladder cancer | Affect cholesterol biosynthesis to enhance archazolid B-induced cell killing (Hamm et al., 2014) | |
| Archazolid B | |||
| Atorvastatin | Cervical cancer | Retain the SCAP-SREBP complex in the ER by stabilizing the INSIG protein (Esquejo et al., 2021) | |
| Dipyridamole | |||
| Fluvastatin | Prostate cancer | Inhibit SREBP2 activation and promotes apoptosis in statin-insensitive prostate cancer cells (Longo et al., 2019) | |
| Dipyridamole | |||
| Simvastatin | Ovarian cancer | Significantly enhance the cytotoxicity and antitumor activity of statins against ovarian cancer cells (Casella et al., 2014) | |
| 25-hydroxycholesterol | |||
| Pitavastatin | Oral and Esophageal Cancer | Suppresses AKT and ERK signaling to inhibit tumor growth alone, and significantly reduces tumor growth in cooperation with capmatinib (Xu et al., 2021b) | |
| Capmatinib | |||
| Simvastatin | Primary leukemia and lymphoma | Enhances the proapoptotic activity of venetoclax (B cell lymphoma-2 inhibitor) in primary leukemia and lymphoma cells but not normal peripheral blood mononuclear cells (Lee et al., 2018) | |
| Venetoclax | |||
| Lovastatin | Renal cell carcinoma | Increases glycolysis levels through regulated HSP90 expression levels, leading to lactate accumulation and acceleration of renal cell carcinoma development. The tumor-promoting effect of lovastatin is reversed by Shikonin (Huang et al., 2021) | |
| Shikonin |