Naringenin suppresses TPA-induced tumor invasion by suppressing multiple signal transduction pathways in human hepatocellular carcinoma cells

Yen, Hung-Rong; Liu, Ching-Ju; Yeh, Chia-Chou

doi:10.1016/j.cbi.2015.04.003

Cited by 65 publications

(28 citation statements)

References 44 publications

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“…NRG is considered to have beneficial effects on human health and has been vigorously researched as a potential candidate to protect against various liver diseases[18,19]. Previous studies have shown that NRG could protect against CCl 4 -induced chemical liver injury by reducing the oxidative stress reaction[15].…”

Section: Discussionmentioning

confidence: 99%

Naringenin protects against isoniazid- and rifampicin-induced apoptosis in hepatic injury

Wang¹,

Fan²,

Zhang³

et al. 2016

WJG

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AIMTo explore the protective effects and mechanisms of naringenin (NRG) on hepatic injury induced by isoniazid (INH) and rifampicin (RIF).METHODSMale mice were randomly divided into four groups and treated for 14 d as follows: normal control group was administered intragastrically with normal saline solution alone; model group was administered intragastrically with INH (100 mg/kg) and RIF (100 mg/kg); low- and high-dosage NRG pretreatment groups were administered intragastrically with different doses of NRG (50 or 100 mg/kg) 2 h before INH and RIF challenge. Mice were killed 16 h after the last dose of drug treatment to determine activity of serum transaminases. Oxidative stress was evaluated by measuring hepatic glutathione (GSH) and superoxide dismutase (SOD) and malondialdehyde (MDA) levels. Histopathological changes in hepatic tissue were observed under the optical microscope. Hepatocyte apoptosis was measured by TUNEL assay and caspase-3 activation. Expression of Bcl-2 and Bax in liver was determined by western blot.RESULTSBoth low- and high-dosage NRG pretreatment obviously alleviated serum levels of alanine aminotransferase and aspartate aminotransferase, liver index, hepatic MDA content, and increased hepatic GSH content and SOD activity compared with the INH and RIF-treated group (44.71 ± 8.15 U/L, 38.22 ± 6.64 U/L vs 58.15 ± 10.54 U/L; 98.36 ± 14.78 U/L, 92.41 ± 13.59 U/L vs 133.05 ± 19.36 U/L; 5.34% ± 0.26%, 4.93% ± 0.25% vs 5.71% ± 0.28%; 2.76 ± 0.67 nmol/mgprot, 2.64 ± 0.64 nmol/mgprot vs 4.49 ± 1.12 nmol/mgprot; 5.91 ± 1.31 mg/gprot, 6.42 ± 1.42 mg/gprot vs 3.11 ± 0.73 mg/gprot; 137.31 ± 24.62 U/mgprot, 148.83 ± 26.75 U/mgprot vs 102.34 ± 19.22 U/mgprot; all P < 0.01 or 0.05). Histopathological evaluation showed obvious necrosis and inflammatory cell infiltration in liver of mice administered INH and RIF; however, mice pretreated with NRG showed minor hepatic injury. In addition, INH and RIF resulted in hepatocyte apoptosis, and NRG pretreatment dramatically suppressed INH- and RIF-induced hepatocytes apoptosis. Furthermore, NRG-mediated anti-apoptotic effects seemed to be in connection with its regulation of Bax and Bcl-2 protein expression in hepatic tissue.CONCLUSIONNRG might attenuate INH- and RIF-induced hepatic injury via suppression of oxidative stress and hepatocyte apoptosis.

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Section: Discussionmentioning

confidence: 99%

Naringenin protects against isoniazid- and rifampicin-induced apoptosis in hepatic injury

Wang¹,

Fan²,

Zhang³

et al. 2016

WJG

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“…Another study in colon cancer cells suggested that the pro-apoptotic activity of naringenin was mediated by the p38-dependent pathway [62]. In HCC cells, naringenin could suppress TPA-induced cancer cell invasion by down-regulating multiple signaling pathways, such as the NF-κB pathway, the ERK and c-Jun N-terminal kinase (JNK) signaling pathway [63]. Besides, naringenin treatment to HepG2 liver cancer cells induced mitochondrial-mediated apoptosis and cell cycle arrest through up-regulation of p53 [64].…”

Section: Experimental Studiesmentioning

confidence: 99%

Natural Polyphenols for Prevention and Treatment of Cancer

et al. 2016

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There is much epidemiological evidence that a diet rich in fruits and vegetables could lower the risk of certain cancers. The effect has been attributed, in part, to natural polyphenols. Besides, numerous studies have demonstrated that natural polyphenols could be used for the prevention and treatment of cancer. Potential mechanisms included antioxidant, anti-inflammation as well as the modulation of multiple molecular events involved in carcinogenesis. The current review summarized the anticancer efficacy of major polyphenol classes (flavonoids, phenolic acids, lignans and stilbenes) and discussed the potential mechanisms of action, which were based on epidemiological, in vitro, in vivo and clinical studies within the past five years.

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“…Naringenin (NAR) as a common dietary flavonoid abundantly present in fruits and vegetables is formed from naringin after dietary intake in humans ( Yen et al ., 2015 ). Many studies have shown various pharmacological effects including antioxidant activity ( Pietta, 2000 ), anti-inflammatory activity ( Esmaeili and Alilou, 2014 ) and anti-mutagenic effects ( Ganapathy et al ., 2008 ).…”

Section: Introductionmentioning

confidence: 99%

Naringenin-Mediated ATF3 Expression Contributes to Apoptosis in Human Colon Cancer

Song

Park

Jeong

2016

Biomolecules & Therapeutics

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Naringenin (NAR) as one of the flavonoids observed in grapefruit has been reported to exhibit an anti-cancer activity. Activating transcription factor 3 (ATF3) is associated with apoptosis in human colon cancer cells. This study was performed to investigate the molecular mechanism by which NAR stimulates ATF3 expression and apoptosis in human colon cancer cells. NAR reduced the cell viability and induced an apoptosis in human colon cancer cells. ATF3 overexpression increased NAR-mediated cleaved PARP, while ATF3 knockdown attenuated the cleavage of PARP by NAR. NAR increased ATF3 expression in both protein and mRNA level, and increased the luciferase activity of ATF3 promoter in a dose-dependent manner. The responsible region for ATF3 transcriptional activation by NAR is located between −317 and −148 of ATF3 promoter. p38 inhibition blocked NAR-mediated ATF3 expression, its promoter activation and apoptosis. The results suggest that NAR induces apoptosis through p38-dependent ATF3 activation in human colon cancer cells.

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Naringenin suppresses TPA-induced tumor invasion by suppressing multiple signal transduction pathways in human hepatocellular carcinoma cells

Cited by 65 publications

References 44 publications

Naringenin protects against isoniazid- and rifampicin-induced apoptosis in hepatic injury

Naringenin protects against isoniazid- and rifampicin-induced apoptosis in hepatic injury

Natural Polyphenols for Prevention and Treatment of Cancer

Naringenin-Mediated ATF3 Expression Contributes to Apoptosis in Human Colon Cancer

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