Eriocitrin, a dietary flavonoid suppressed cell proliferation, induced apoptosis through modulation of JAK2/STAT3 and JNK/p38 MAPKs signaling pathway in MCF‐7 cells

Yuan, Chengliang; Chen, Guoping; Jing, Chengbao; Liu, Mengxue; Liang, Bo; Gong, Guojin; Yu, Mei

doi:10.1002/jbt.22943

Cited by 17 publications

(15 citation statements)

References 38 publications

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“…Wang Z et al founded that eriocitrin could stimulate liver carcinoma cells apoptosis by activating mitochondrial-mediated apoptotic singling pathway [ 19 ]. Apart from that, recent study showed that eriocitrin strongly promotes ROS generation and thus to induce breast cancer cells apoptosis via STAT3 pathway [ 20 ]. However, little is known about its role in LUAD.…”

Section: Introductionmentioning

confidence: 99%

Eriocitrin inhibits epithelial-mesenchymal transformation (EMT) in lung adenocarcinoma cells via triggering ferroptosis

Gao,

Lai,

Deng

et al. 2023

Aging

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Introduction: Lung adenocarcinoma (LUAD) is the most prevalent pathological subtype of non-small cell lung cancer (NSCLC), characterized by a high propensity for relapse and metastasis due to epithelial-mesenchymal transition (EMT) of cancer cells. Ferroptosis, a newly discovered regulated cell death modality, is interconnected with the EMT process in certain cancers. Eriocitrin, a natural flavonoid compound, exerts anti-inflammatory and anticancer effects. Objectives: The aim of this study is to investigate the potential inhibitory effect of eriocitrin on lung adenocarcinoma metastasis and explore whether its underlying mechanism involves ferroptosis induction in cancer cells. Methods: The CCK8 assay and wound healing assay and transwell were conducted to determine the cell viability and migration ability of A549 and H1299 cells, respectively. EMT process was assessed by western blot and RT-PCR to detect protein and mRNA levels of EMT markers. ROS and cell iron were measured to determine ferroptosis level. Results: Eriocitrin treatment significantly inhibited cell viability and migration ability in a concentration-dependent manner. Furthermore, eriocitrin administration for 24 hours resulted in enhanced expression of E-cadherin, while downregulating vimentin, N-cadherin and snail expression, indicating marked repression of the EMT process. Additionally, eriocitrin significantly induced ferroptosis in A549 and H1299 cells, as evidenced by increased ROS levels, downregulation of Nrf-2, SLC7A11 and GPX4 expression, and enhanced cellular iron accumulation. Moreover, pretreatment with the ferroptosis inhibitor ferrostatin-1 effectively abrogated the inhibitory effects of eriocitrin on EMT. Conclusions: Our findings further support the anti-cancer properties of eriocitrin, as evidenced by its ability to inhibit the EMT process in LUAD cells, which is partially mediated through induction of ferroptosis in cancer cells.

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Section: Introductionmentioning

confidence: 99%

Eriocitrin inhibits epithelial-mesenchymal transformation (EMT) in lung adenocarcinoma cells via triggering ferroptosis

Gao,

Lai,

Deng

et al. 2023

Aging

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“…Flavonoids ( Figure 1 ) can modulate proliferation [ 5 , 39 , 41 , 42 , 43 , 44 ], invasion [ 45 , 46 ], and inflammatory signals through a variety of pathways associated with their qualities as antioxidants [ 24 , 47 ], estrogen agonists, or CYP1 (Cytochrome P450) inhibitors [ 39 ]. Flavonoids have also been found to influence inflammatory signaling via systems such as NF-кB (nuclear factor B), which regulates cell proliferation and survival [ 21 , 23 ].…”

Section: Flavonoid and Anti-cancer Effectmentioning

confidence: 99%

“…Many flavonoids have been shown to have anticancer properties. In human breast cancer cells, certain flavonoids (isorhamnetin, genkwanin, acacetin, silymarin, eriocitrin, icariin, kaempferol, silibinin, apigenin, and luteolin) suppress cell growth and induce apoptosis, autophagy, or cell cycle arrest [ 5 , 20 , 38 , 43 , 44 , 48 , 49 ]. Table 1 shows the anticancer properties of introduced flavonoids.…”

Section: Flavonoid and Anti-cancer Effectmentioning

confidence: 99%

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Function and Application of Flavonoids in the Breast Cancer

Park

Kim

et al. 2022

IJMS

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Breast cancer is one of the top causes of death, particularly among women, and it affects many women. Cancer can also be caused by various factors, including acquiring genetic alteration. Doctors use radiation to detect and treat breast cancer. As a result, breast cancer becomes radiation-resistant, necessitating a new strategy for its treatment. The approach discovered by the researchers is a flavonoid, which is being researched to see if it might help treat radiation-resistant breast cancer more safely than an approved medicine already being used in the field. As a result, this study focuses on the role of flavonoids in breast cancer suppression, breast cancer gene anomalies, and the resulting apoptotic mechanism.

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“…This kinase can phosphorylate IRS1 on serine residues to trigger insulin resistance [ 10 ]. Additionally, the phosphorylation of signal transducer and activator of transcription 3 (STAT3) can increase p38 mitogen-activated protein kinase (p38-MAPK), and in turn activates JNK [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Chronic Central Leptin Infusion Promotes an Anti-Inflammatory Cytokine Profile Related to the Activation of Insulin Signaling in the Gastrocnemius of Male Rats

et al. 2022

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Leptin is involved in the modulation of insulin signaling in peripheral tissues, being closely associated with changes in lipid metabolism. This adipokine modifies inflammatory pathways that can interact with insulin targets in peripheral organs; however, the mechanisms remain unclear. Inflammatory and insulin signaling targets, cytokines, adiponectin, irisin and non-esterified fatty acid (NEFA) levels and enzymes of fatty acid anabolism were studied in the gastrocnemius of chronic centrally infused leptin (L), pair-fed and control rats. The phosphorylation of signal transducer and activator of transcription 3 (STAT3) and c-Jun N-terminal kinase (JNK) was reduced in L rats (59% and 58%, respectively). The phosphorylation of the insulin receptor and Akt and adiponectin and irisin content was increased in L rats (154%, 157%, 308% and 329%, respectively). The levels of glucose-6-phosphate dehydrogenase, the mRNA content of acetyl Co-A carboxylase and NEFA concentrations were diminished in the muscles of L rats (59%, 50% and 61%, respectively). The activation of JNK correlated positively with STAT3 phosphorylation, tumoral necrosis factor-α and NEFA and negatively with irisin and Akt phosphorylation. These data suggest that the activation of insulin signaling targets and a decrease in NEFA content are associated with a reduction in muscle inflammation parameters, suggesting that leptin may integrate these pathways.

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Eriocitrin, a dietary flavonoid suppressed cell proliferation, induced apoptosis through modulation of JAK2/STAT3 and JNK/p38 MAPKs signaling pathway in MCF‐7 cells

Cited by 17 publications

References 38 publications

Eriocitrin inhibits epithelial-mesenchymal transformation (EMT) in lung adenocarcinoma cells via triggering ferroptosis

Eriocitrin inhibits epithelial-mesenchymal transformation (EMT) in lung adenocarcinoma cells via triggering ferroptosis

Function and Application of Flavonoids in the Breast Cancer

Chronic Central Leptin Infusion Promotes an Anti-Inflammatory Cytokine Profile Related to the Activation of Insulin Signaling in the Gastrocnemius of Male Rats

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