Dihydromyricetin inhibits cancer cell migration and matrix metalloproteinases‐2 expression in human nasopharyngeal carcinoma through extracellular signal‐regulated kinase signaling pathway

Huang, Cheng−Chen; Su, Chung‐Kuang; Wang, Po-Hui; Lu, Yen‐Ting; Ho, Yu‐Ting; Yang, Shun‐Fa; Hsin, Chung‐Han

doi:10.1002/tox.23480

Cited by 11 publications

(8 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Matrix metalloproteinases, a family of zinc-dependent proteinase, have long been associated with tumor cell invasion and metastasis for its ability in activating cancer cells, modulating immune function, degrading extracellular matrix and basement membrane. [25][26][27][28] In particular, matrix metalloproteinase-9 (MMP-9) has been widely investigated to relate to the pathology of cancer. [29][30][31] TPA (12-O-Tetradecanoylphorbol-13-acetate), a phorbol ester, has been well-documented on cancer metastasis in several cancer types.…”

mentioning

confidence: 99%

EF‐24 inhibits TPA‐induced cellular migration and MMP‐9 expression through the p38 signaling pathway in cervical cancer cells

Lee

Lin

et al. 2022

Environmental Toxicology

Self Cite

View full text Add to dashboard Cite

Diphenyl difluoroketone (EF-24), a synthetic curcumin analog, has enhanced bioavailability over curcumin. EF-24 acts more powerful bioactivity for anti-inflammatory and anti-cancer activity. However, the effects and mechanism of EF-24 on cervical cancer has not been fully investigated. Herein, this study evaluated the effects of EF-24 on TPA-induced cellular migration of cervical cancer. The results showed that EF-24 substantially reduced the cellular migration and cellular invasion of the HeLa and SiHa cells. Moreover, gelatin zymography, western blotting analyses and real-time PCR revealed that EF-24 suppressed Matrix metalloproteinase-9 (MMP-9) activity, protein expression and mRNA levels. Mechanistically, EF-24 inhibited the phosphorylation of the p38 signaling pathway. In conclusion, EF-24 inhibited TPA-induced cellular migration and cellular invasion of cervical cancer cell lines through modulating MMP-9 expression via downregulating signaling p38 pathway and EF-24 may have potential to serve as a chemopreventive agent of cervical cancer.

show abstract

mentioning

confidence: 99%

EF‐24 inhibits TPA‐induced cellular migration and MMP‐9 expression through the p38 signaling pathway in cervical cancer cells

Lee

Lin

et al. 2022

Environmental Toxicology

Self Cite

View full text Add to dashboard Cite

show abstract

“…In an in vivo experiment on mice transplanted with B16 melanoma cells, Zheng et al ( 68 ) reported that mice given DHM at doses of 150, 200 and 250 mg/kg exhibited a significant reduction in the number of metastatic tumours compared with those in the control group, demonstrating the anti-invasive and anti-metastatic effects of DHM on B16 melanoma. Moreover, DHM inhibits the migration and invasion of nasopharyngeal carcinoma cells by suppressing the ERK1/2 signalling pathway and suppressing MMP-2 expression ( 69 ); it also inhibits the proliferation, migration and invasion of CAA HCCC9810 and TFK-1 cells by regulating miR-21 and promoting apoptosis ( 70 ) ( Fig. 3 ).…”

Section: Multiple Molecular and Cellular Mechanisms Of The Antitumour...mentioning

confidence: 99%

Multiple molecular and cellular mechanisms of the antitumour effect of dihydromyricetin (Review)

Xia,

Zhu

2024

Biomed Rep

View full text Add to dashboard Cite

Dihydromyricetin (DHM) is a natural flavonoid compound with multiple antitumour effects, including inhibition of proliferation, promotion of apoptosis, inhibition of invasion and migration, clearance of reactive oxygen species (ROS) and induction of autophagy. For example, DHM can effectively block the progression of the tumour cell cycle and inhibit cell proliferation. In different types of cancer cells, DHM can regulate the PI3K/Akt pathway, mTOR, and NF-κB pathway components, such as p53, and endoplasmic reticulum stress can alter the accumulation of ROS or induce autophagy to promote the apoptosis of tumour cells. In addition, when DHM is used in combination with various known chemotherapy drugs, such as paclitaxel, nedaplatin, doxorubicin, oxaliplatin and vinblastine, it can increase the sensitivity of tumour cells to DHM and increase the therapeutic effect of chemotherapy drugs. In the present review, the multiple molecular and cellular mechanisms underlying the antitumour effect of DHM, as well as its ability to increase the effects of various traditional antitumour drugs were summarized. Through the present review, it is expected by the authors to draw attention to the potential of DHM as an antitumour drug and provide valuable references for the clinical translation of DHM research and the development of related treatment strategies.

show abstract

“…DHM can silence the activation of p-IKKβ/α, block the nuclear translocation of NF-κB subunit p65, significantly suppress TNF-α-mediated NF-κB activation in CNE-2 cells, and reduce the expression levels of Bcl-2 and pro-caspase-3, resulting in CNE-2 cell apoptosis [ 105 ]. Moreover, DHM can inhibit the migration and invasion of NPC cells by suppressing the expression of MMP-2 by downregulating the ERK1/2 signaling pathway [ 106 ]. Figure 1 shows the anticancer mechanism of DHM.…”

Section: The Anticancer Potential and Underlying Mechanisms Of Dihydr...mentioning

confidence: 99%

Present Status, Challenges, and Prospects of Dihydromyricetin in the Battle against Cancer

Xiao

Zhu

et al. 2022

Cancers

View full text Add to dashboard Cite

Dihydromyricetin (DHM) is a natural flavonoid compound extracted from Ampelopsis grossedentata that has been used for centuries in traditional Chinese medicine. DHM has attracted intensive attention due to its numerous beneficial activities, such as hepatoprotection, cardioprotection, antioxidant, and anti-inflammation. In addition, DHM inhibits the progression of cancers such as lung cancer, hepatocellular cancer, breast cancer, melanoma, and malignant reproductive systems through multiple mechanisms, including antiangiogenesis, antiproliferation, apoptosis, and inhibition of invasion and migration. Notably, DHM also activates autophagy at different levels, exerting a dual-regulatory effect on cancers. Mechanistically, DHM can effectively regulate mammalian target of rapamycin (mTOR), noncoding RNA-mediated signaling, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway, nuclear factor-κB (NF-κB), p53, and endoplasmic reticulum stress (ER stress)-driven signaling in different types of cancers. DHM has also been shown to have inhibitory effects on various regulators that trigger epithelial–mesenchymal transition (EMT). Furthermore, DHM exhibits a remarkable anticancer reversal ability when used in combination with drugs such as adriamycin, nedaplatin, and other drugs. However, the low bioavailability of DHM limits its potential applications, which are improved through structural modification and the exploration of novel dosage forms. Therefore, DHM may become a promising candidate for treating malignancies alone or combined with conventional anticancer strategies used in clinical practice.

show abstract

Dihydromyricetin inhibits cancer cell migration and matrix metalloproteinases‐2 expression in human nasopharyngeal carcinoma through extracellular signal‐regulated kinase signaling pathway

Cited by 11 publications

References 49 publications

EF‐24 inhibits TPA‐induced cellular migration and MMP‐9 expression through the p38 signaling pathway in cervical cancer cells

EF‐24 inhibits TPA‐induced cellular migration and MMP‐9 expression through the p38 signaling pathway in cervical cancer cells

Multiple molecular and cellular mechanisms of the antitumour effect of dihydromyricetin (Review)

Present Status, Challenges, and Prospects of Dihydromyricetin in the Battle against Cancer

Contact Info

Product

Resources

About