From: Emerging cellular and molecular mechanisms underlying anticancer indications of chrysin
Health effect | Mechanisms | Refs. |
---|---|---|
Breast cancer | Antiproliferative effect | [79] |
Breast cancer | Downregulated cyclin D1 and hTERT | [78] |
Breast cancer Stem cell | Inhibited EGFR | [84] |
Breast cancer | Apoptosis | [85] |
Breast cancer | Apoptosis | [80] |
Breast cancer | Inhibited angiogenesis, alleviated VEGF expression, Suppressed metastatic growth due to alleviation of activation of STAT3 and hypoxic survival | [30] |
Breast cancer | Inhibited of HDAC8 enzymatic activity | [213] |
Breast cancer | modulated phase I and phase II enzymes | [214] |
Gastric cancer | Altered microRNAs expression | [94] |
Gastric cancer | Blocked AP-1 and suppressed early growth response-1 | |
Buccal pouch carcinoma | mitigated phase-I enzymes (Cyt b5 and Cyt p 450) and increased phase-II enzymes (GSH, GST, GR, and DTD) | [215] |
Colon cancer | Arrested G2/M phase of cell cycle | [112] |
Colorectal cancer | Inhibited cell proliferation, improved antioxidant mineral levels, reduced nitrosative stress | [216] |
Colon cancer | Modulated cryptal cell proliferation activity inhibited apoptosis | [217] |
Hepatocellular carcinoma | Overexpressed hexokinase-2 | [129] |
Hepatocellular carcinoma | attenuated NF-kB p65 levels and COX-2 expression, reduced Bax, Bcl-xL, β-arrestin-2, caspase-3, and p53 regarding apoptosis | [136] |
Hepatocellular carcinoma | Attenuated the canonical Wnt and NF-kB, induced apoptosis | [140] |
Liver cancer | Downregulated the β-catenin expression | [218] |
Renal carcinoma | Ameliorated oxidative stress, hyperproliferation, and inflammation through NF-kB pathway | [143] |
Skin cancer | Attenuated the MSK1/histone H3 signaling | [219] |
Skin cancer | Inhibited tumor growth and neoplastic transformation by targeting CDK2 and CDK4 | [220] |
Melanoma | mitigated the TERT, MMP-2, and MMP-9 genes levels, ameliorated genes expressions of TIMP-1 and TIMP-2 | [192] |
Anaplastic thyroid carcinoma | Induced apoptosis by activating Notch1 signaling related to PARP cleavage | [180] |
Prostate cancer | Inhibited expression of HIF-1α via Akt signaling pathway and abrogated VEGF expression | [153] |
Prostate cancer | Inhibited DNA methyltransferases | [221] |
Leukemia | Enhanced populations of T-and B cells (CD-3, CD-19, and Mac-3), Promoted macrophage phagocytosis and NK cell cytotoxicity | [202] |
Leukemia | reduced cell viability and induced DNA fragmentation regarding apoptotic cell death | [222] |
Leukemia | Induced apoptosis in Bcl-2 overexpressing associated with PLC-Ï’1 degradation, caspase-3 activation, XIAP downregulation, and the Akt inactivation | |
Leukemia | attenuated SCF/c-Kit signaling by abrogation of PI3K pathway | [204] |
Cervical cancer | inhibited proliferation and induced apoptosis | [49] |
Cervical cancer | induced p38 and NF-kB/p65 activation | [224] |
Cervical cancer | Increased caspases-3 and -9, Bax, and cleaved-PARP expression, caused arrest in G2 phase of cell cycle | [22] |
Cervical and ovarian cancer | Antioxidant and anticancer | [54] |
Ovarian cancer | Antioxidant and anticancer | [225] |
NSCLC | Inhibited IL-6-induced AKR1C1/1C2 overexpression | [176] |
Glioma | Antiproliferative and apoptotic activity | [194] |
Glioma | Increased accumulation of arsenic | [226] |
Ehrlich ascites | Enhanced functional activity of macrophages | [212] |