Licochalcone C induces apoptosis via B-cell lymphoma 2 family proteins in T24 cells

Wang, Penglong; Xuan, Yue; Wang, Yan; Zhao, Hong; Sun, Xiling; Zheng, Qi

doi:10.3892/mmr.2015.4346

Cited by 19 publications

(16 citation statements)

References 29 publications

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“…Normalized intensity of CHOP, DR5 and DR4 versus actin were presented, and their expression levels were significantly increased. CHOP, C/EBP homologous protein; LCC, licochalcone C; ROS, reactive oxygen species as the PTP1B enzyme inhibitory activity, 32 attenuation of inflammatory response, 7 cardio-protective effect, 7,33 and apoptosis, 10 but their mechanisms of action remain elusive. Therefore, we needed to investigate the unidentified effects of LCC, which is a type of natural phenolic agent isolated from licorice on OSCC cells.…”

Section: Discussionmentioning

confidence: 99%

“…[7][8][9] From LC species, LCC is isolated from Glycyrrhiza inflata and has been reported to be potent against bladder cancer cells. 10 Although LC has many beneficial effects in there are a few reports on LCC.…”

Section: Introductionmentioning

confidence: 99%

“…Among natural products, licochalcone (LC), which is isolated from Licorice, has been widely used as a sweetener in food, tobaccos, and gums, and it is also a medicinal herb having anticancer, anti inflammatory, antibacterial, and antioxidant activities . From LC species, LCC is isolated from Glycyrrhiza inflata and has been reported to be potent against bladder cancer cells . Although LC has many beneficial effects in there are a few reports on LCC.…”

Section: Introductionmentioning

confidence: 99%

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Licochalcone C induced apoptosis in human oral squamous cell carcinoma cells by regulation of the JAK2/STAT3 signaling pathway

Seo

Lee

et al. 2018

J of Cellular Biochemistry

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Oral cancer is of an aggressive malignancy that arises on oral cavity and lip, 90% of cancers histologically originated in the squamous cells. Licochalcone (LC)C has been known as natural phenolic chalconoid substances, and its origin is the root of Glycyrrhiza glabra or Glycyrrhiza inflata. LCC inhibited oral squamous cell carcinoma (OSCC) cell viability, mitochondrial function, and anchorage-independent growth in a dose-dependent manner. To investigate the ability of LCC to target Janus kinase 2 (JAK2), we performed pull-down binding assay, kinase assay, and docking simulation. The molecular docking studies were performed between JAK2 and the potent inhibitor LCC. It was shown that LCC tightly interacted with ATP-binding site of JAK2. In addition, LCC inhibited the JAK2/signal transducer and activator of transcription 3 pathway, upregulated p21, and downregulated Bcl-2, Mcl-1, and Survivin, while it disrupted mitochondrial membrane potential and subsequently caused cytochrome c release with activation of multi-caspase, eventually leading to apoptosis in HN22 and HSC4 cells. LCC elevated the protein levels of Bax, cleaved Bid and PARP, and increased Apaf-1, and this effect was reversed by LCC treatment. Our results demonstrated that treatment of OSCC cells with LCC induced the death receptor (DR)4 and DR5 expression level with the generation of reactive oxygen species and the upregulation of CHOP protein expression. Taken together, these results could provide the basis for clinical application as a new therapeutic strategy in the treatment of oral cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Licochalcone C induced apoptosis in human oral squamous cell carcinoma cells by regulation of the JAK2/STAT3 signaling pathway

Seo

Lee

et al. 2018

J of Cellular Biochemistry

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“…In addition, it attenuated migration, adhesion, and invasion of cancer cells accompanied with the downregulated protein expression of MMP-9 and nuclear translocation of nuclear factor-κB (NF-κB) [115]. Similar to licochalcone B, licochalcones C and D induced apoptosis by altering the expression of Bcl-2 family member genes and activating the caspase-mediated cell death signaling pathway [45,46]. Meanwhile, licochalcone D induced apoptosis through mitochondrial pathway and blocked cell migration and invasion into surrounding tissues by reducing the activity and expression of MMP-2 and MMP-9 [46].…”

Section: Anticancer Activitymentioning

confidence: 99%

Natural Chalcones in Chinese Materia Medica: Licorice

Wang

Liang

Zhang

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Licorice is an important Chinese materia medica frequently used in clinical practice, which contains more than 20 triterpenoids and 300 flavonoids. Chalcone, one of the major classes of flavonoid, has a variety of biological activities and is widely distributed in nature. To date, about 42 chalcones have been isolated and identified from licorice. These chalcones play a pivotal role when licorice exerts its pharmacological effects. According to the research reports, these compounds have a wide range of biological activities, containing anticancer, anti-inflammatory, antimicrobial, antioxidative, antiviral, antidiabetic, antidepressive, hepatoprotective activities, and so on. This review aims to summarize structures and biological activities of chalcones from licorice. We hope that this work can provide a theoretical basis for the further studies of chalcones from licorice.

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“…Numerous flavonoids in traditional Chinese herbs may be promising candidates for the development of novel anticancer drugs ( 3 ). Previously, we found that Licochalcone C induced apoptosis via B-cell lymphoma 2 family proteins in T24 cells ( 4 ). Licochalcone A induced T24 bladder cancer cell apoptosis by increasing intracellular calcium levels ( 5 ).…”

Section: Introductionmentioning

confidence: 98%

Licochalconeï¿½D induces apoptosis and inhibits migration and invasion in human melanoma A375 cells

Yan

et al. 2018

Oncol Rep

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The aim of the present study was to determine the effects of Licochalcone D (LD) on the apoptosis and migration and invasion in human melanoma A375 cells. Cell proliferation was determined by sulforhodamine B assay. Apoptosis was assessed by Hoechst 33258 and Annexin V-FITC/PI staining and JC-1 assay. Total intracellular reactive oxygen species (ROS) was examined by DCFH-DA. Wound healing and Transwell assays were used to detect migration and invasion of the cells. The activities of matrix metalloproteinase (MMP-2 and MMP-9) were assessed via gelatin zymography. Tumor growth in vivo was evaluated in C57BL/6 mice. RT-PCR, qPCR, ELISA and western blot analysis were utilized to measure the mRNA and protein levels. Our results showed that LD inhibited the proliferation of A375 and SK-MEL-5 cells in a concentration-dependent manner. After treatment with LD, A375 cells displayed obvious apoptotic characteristics, and the number of apoptotic cells was significantly increased. Pro-apoptotic protein Bax, caspase-9 and caspase-3 were upregulated, while anti-apoptotic protein Bcl-2 was downregulated in the LD-treated cells. Meanwhile, LD induced the loss of mitochondrial membrane potential (ΔΨm) and increased the level of ROS. ROS production was inhibited by the co-treatment of LD and free radical scavenger N-acetyl-cysteine (NAC). Furthermore, LD also blocked A375 cell migration and invasion in vitro which was associated with the downregulation of MMP-9 and MMP-2. Finally, intragastric administration of LD suppressed tumor growth in the mouse xenograft model of murine melanoma B16F0 cells. These results suggest that LD may be a potential drug for human melanoma treatment by inhibiting proliferation, inducing apoptosis via the mitochondrial pathway and blocking cell migration and invasion.

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Licochalcone C induces apoptosis via B-cell lymphoma 2 family proteins in T24 cells

Cited by 19 publications

References 29 publications

Licochalcone C induced apoptosis in human oral squamous cell carcinoma cells by regulation of the JAK2/STAT3 signaling pathway

Licochalcone C induced apoptosis in human oral squamous cell carcinoma cells by regulation of the JAK2/STAT3 signaling pathway

Natural Chalcones in Chinese Materia Medica: Licorice

Licochalconeï¿½D induces apoptosis and inhibits migration and invasion in human melanoma A375 cells

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