Licochalcone D directly targets JAK2 to induced apoptosis in human oral squamous cell carcinoma

Seo, Jeong‐Meen; Choi, Hyun Woo; Oh, Han-Mo; Lee, Mee-Hyun; Kim, Eunae; Yoon, Goo; Cho, Seung‐Sik; Park, Seon‐Min; Cho, Young Sik; Chae, Jung‐Il; Shim, Jung‐Hyun

doi:10.1002/jcp.27050

Cited by 24 publications

(14 citation statements)

References 44 publications

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“…Additionally, other lichochalcones including licochalcone H, C, and D have also been described as inhibitors of JAK/STAT signaling in oral squamous cell carcinoma [ 223 , 224 , 225 ].…”

Section: Modulation Of Selected Signaling Pathwaysmentioning

confidence: 99%

Molecular Mechanisms of Antiproliferative Effects of Natural Chalcones

Michalková¹,

Mirossay²,

Gazdova³

et al. 2021

Cancers

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Although great progress has been made in the treatment of cancer, the search for new promising molecules with antitumor activity is still one of the greatest challenges in the fight against cancer due to the increasing number of new cases each year. Chalcones (1,3-diphenyl-2-propen-1-one), the precursors of flavonoid synthesis in higher plants, possess a wide spectrum of biological activities including antimicrobial, anti-inflammatory, antioxidant, and anticancer. A plethora of molecular mechanisms of action have been documented, including induction of apoptosis, autophagy, or other types of cell death, cell cycle changes, and modulation of several signaling pathways associated with cell survival or death. In addition, blockade of several steps of angiogenesis and proteasome inhibition has also been documented. This review summarizes the basic molecular mechanisms related to the antiproliferative effects of chalcones, focusing on research articles from the years January 2015–February 2021.

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“…Additionally, other lichochalcones including licochalcone H, C, and D have also been described as inhibitors of JAK/STAT signaling in oral squamous cell carcinoma [ 223 , 224 , 225 ].…”

Section: Modulation Of Selected Signaling Pathwaysmentioning

confidence: 99%

Molecular Mechanisms of Antiproliferative Effects of Natural Chalcones

Michalková¹,

Mirossay²,

Gazdova³

et al. 2021

Cancers

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“…As shown in Figure 1 A, there were no significant changes in cell viability upon Lico D treatment. However, previous reports highlighted that high concentration of Lico D possesses anti-cancer activity in different cancer cell lines [ 36 , 37 , 38 ]. Therefore, we chose the lowest concentration of Lico D (1 µg/mL) for our further in vitro experiments.…”

Section: Resultsmentioning

confidence: 99%

Licochalcone D Ameliorates Oxidative Stress-Induced Senescence via AMPK Activation

Maharajan

Ganesan

Moon

et al. 2021

IJMS

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Increased oxidative stress is a crucial factor for the progression of cellular senescence and aging. The present study aimed to investigate the effects of licochalcone D (Lico D) on oxidative stress-induced senescence, both in vitro and in vivo, and explore its potential mechanisms. Hydrogen peroxide (200 µM for double time) and D-galactose (D-Gal) (150 mg/kg) were used to induce oxidative stress in human bone marrow-mesenchymal stem cells (hBM-MSCs) and mice, respectively. We performed the SA-β-gal assay and evaluated the senescence markers, activation of AMPK, and autophagy. Lico D potentially reduced oxidative stress-induced senescence by upregulating AMPK-mediated activation of autophagy in hBM-MSCs. D-Gal treatment significantly increased the expression levels of senescence markers, such as p53 and p21, in the heart and hippocampal tissues, while this effect was reversed in the Lico D-treated animals. Furthermore, a significant increase in AMPK activation was observed in both tissues, while the activation of autophagy was only observed in the heart tissue. Interestingly, we found that Lico D significantly reduced the expression levels of the receptors for advanced glycation end products (RAGE) in the hippocampal tissue. Taken together, our findings highlight the antioxidant, anti-senescent, and cardioprotective effects of Lico D and suggest that the activation of AMPK and autophagy ameliorates the oxidative stress-induced senescence.

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“…LB (10–30 μM) can also activate the death receptor pathway (i.e., increased expression of DR 4 and DR5) and induce endoplasmic reticulum stress (i.e., increased CHOP expression) in HN22 and HSC4 cells, which causes mitochondrial membrane depolarization, upregulates the expression of Bax, cleaved PARP, and caspase-3, and downregulates the expression of survivin, Bcl-xL, and Mcl-1 ( Oh et al, 2016 ). By inhibiting the JAK2/STAT3 signaling pathway leading to activation of the death receptor pathway (i.e., increased expression of DR4 and DR5), endoplasmic reticulum stress (i.e., elevated ROS and CHOP levels), and mitochondrial apoptosis pathway (i.e., upregulated expression of p21, Bax, Bid, Apaf-1, and cleaved PARP; downregulated expression of Bcl-2, Mcl-1, and survivin), LC (10–50 μM) and LD (10–30 μM) induced apoptosis in HN22 and HSC4 cells ( Oh et al, 2018 ; Seo et al, 2019 ). LD (12.5–50 μg/mL) induced apoptosis in pharyngeal squamous carcinoma FaDu cells by increasing Fas-L, p53, Bax, Bid, and caspase-3 expression while decreasing the expression of Bcl-2 by activating the death receptor and mitochondrial apoptosis pathways ( Yu et al, 2017 ).…”

Section: Anticancer Effects Of Licochalcones On Tumor Cellsmentioning

confidence: 99%

Anticancer effects of licochalcones: A review of the mechanisms

et al. 2023

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Cancer is a disease with a high fatality rate representing a serious threat to human health. Researchers have tried to identify effective anticancer drugs. Licorice is a widely used traditional Chinese medicine with various pharmacological properties, and licorice-derived flavonoids include licochalcones like licochalcone A, licochalcone B, licochalcone C, licochalcone D, licochalcone E, and licochalcone H. By regulating the expression in multiple signaling pathways such as the EGFR/ERK, PI3K/Akt/mTOR, p38/JNK, JAK2/STAT3, MEK/ERK, Wnt/β-catenin, and MKK4/JNK pathways, and their downstream proteins, licochalcones can activate the mitochondrial apoptosis pathway and death receptor pathway, promote autophagy-related protein expression, inhibit the expression of cell cycle proteins and angiogenesis factors, regulate autophagy and apoptosis, and inhibit the proliferation, migration, and invasion of cancer cells. Among the licochalcones, the largest number of studies examined licochalcone A, far more than other licochalcones. Licochalcone A not only has prominent anticancer effects but also can be used to inhibit the efflux of antineoplastic drugs from cancer cells. Moreover, derivatives of licochalcone A exhibit strong antitumor effects. Currently, most results of the anticancer effects of licochalcones are derived from cell experiments. Thus, more clinical studies are needed to confirm the antineoplastic effects of licochalcones.

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Licochalcone D directly targets JAK2 to induced apoptosis in human oral squamous cell carcinoma

Cited by 24 publications

References 44 publications

Molecular Mechanisms of Antiproliferative Effects of Natural Chalcones

Molecular Mechanisms of Antiproliferative Effects of Natural Chalcones

Licochalcone D Ameliorates Oxidative Stress-Induced Senescence via AMPK Activation

Anticancer effects of licochalcones: A review of the mechanisms

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