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Table 1 Some of the molecular and cellular mechanisms involved in preventive and therapeutic indications of chrysin

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

[98, 99]

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

[205, 223]

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]