ERK Activation-Mediated Autophagy Induction Resists Licochalcone A-Induced Anticancer Activities in Lung Cancer Cells in vitro

Luo, Wei; Sun, Ruili; Chen, Xin; Li, Ju; Jiang, Jike; He, Yuxiao; Shi, Shaoqing; Huang, Wen Yao

doi:10.2147/ott.s278268

Cited by 17 publications

(11 citation statements)

References 52 publications

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“…Activated autophagy is associated with the increased ERK signaling in lung cancer 29 . The induction of autophagy mediated by ERK activation can resist anticancer activities in lung cancer cells 30 . Through our research, we found the binding of NCAM1 with ERK.…”

Section: Discussionmentioning

confidence: 59%

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ELF1 suppresses autophagy to reduce cisplatin resistance via the miR‐152‐3p/NCAM1/ERK axis in lung cancer cells

Zhao

Zhang

et al. 2023

Cancer Science

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Resistance to chemotherapeutic drugs limits the efficacy of chemotherapy in non–small cell lung cancer (NSCLC). Autophagy is an essential mechanism which involves in drug resistance. Our previous research has revealed that miR‐152‐3p represses NSCLC progression. However, the mechanism of miR‐152‐3p in autophagy‐mediated chemoresistance in NSCLC remains unclear. Cisplatin‐resistant cell lines (A549/DDP and H446/DDP) were transfected with related vectors and subjected to cisplatin, autophagy inhibitor, activator, or extracellular signal–regulated kinase (ERK) activator. Flow cytometry, CCK8 and colony formation assays were performed for testing apoptosis and cell viability. The related RNAs or proteins were detected by qRT‐PCR or Western blot. Chromatin immunoprecipitation, luciferase reporter assay or RNA immunoprecipitation were used for validating the interaction between miR‐152‐3p and ELF1 or NCAM1. Co‐IP verified the binding between NCAM1 and ERK. The role of miR‐152‐3p in cisplatin resistance of NSCLC was also validated in vivo. The results showed that miR‐152‐3p and ELF1 were decreased in NSCLC tissues. miR‐152‐3p reversed cisplatin resistance by inhibiting autophagy through NCAM1. NCAM1 promoted autophagy through the ERK pathway and facilitated cisplatin resistance. ELF1 positively regulated miR‐152‐3p level by directly interacting with miR‐152‐3p promoter. miR‐152‐3p targeted NCAM1 to regulate NCAM1 level and then affected the binding of NCAM1 to ERK1/2. ELF1 inhibited autophagy and reversed cisplatin resistance through miR‐152‐3p/NCAM1. miR‐152‐3p inhibited autophagy and cisplatin resistance of xenograft tumor in mice. In conclusion, our study revealed that ELF1 inhibited autophagy to attenuate cisplatin resistance through the miR‐152‐3p/NCAM1/ERK pathway in H446/DDP and A549/DDP cells, suggesting a potential novel treatment strategy for NSCLC.

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Section: Discussionmentioning

confidence: 59%

“…29 The induction of autophagy mediated by ERK activation can resist anticancer activities in lung cancer cells. 30 Through our research, we found the binding of NCAM1 with ERK. NCAM1 could activate the ERK signaling pathway, thus promoting autophagy and elevating cisplatin resistance of lung cancer cells with cisplatin-resistance.…”

Section: Discussionmentioning

confidence: 64%

ELF1 suppresses autophagy to reduce cisplatin resistance via the miR‐152‐3p/NCAM1/ERK axis in lung cancer cells

Zhao

Zhang

et al. 2023

Cancer Science

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“…LA significantly activated ERK and p38 in A549 and H460 cells in a time-dependent manner. LA also inhibited the activity of JNK, suppressed the expression of c-IAP1, c-IAP2, XIAP, Survivin, c-FLIPL, and RIP1, and attenuated LA-induced induction of autophagy ( Luo et al, 2021 ). LA also promoted the degradation of EGFR, Met, Her2, and Akt through inactivating EGFR/Met-Akt signaling, resulting in apoptosis of gefitinib-resistant NSCLC cells (H1975) ( Seo, 2013 ).…”

Section: Anticancer Properties Of Lamentioning

confidence: 99%

Role of Licochalcone A in Potential Pharmacological Therapy: A Review

Xie

Jiang

et al. 2022

Front. Pharmacol.

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Licochalcone A (LA), a useful and valuable flavonoid, is isolated from Glycyrrhiza uralensis Fisch. ex DC. and widely used clinically in traditional Chinese medicine. We systematically updated the latest information on the pharmacology of LA over the past decade from several authoritative internet databases, including Web of Science, Elsevier, Europe PMC, Wiley Online Library, and PubMed. A combination of keywords containing “Licochalcone A,” “Flavonoid,” and “Pharmacological Therapy” was used to help ensure a comprehensive review. Collected information demonstrates a wide range of pharmacological properties for LA, including anticancer, anti-inflammatory, antioxidant, antibacterial, anti-parasitic, bone protection, blood glucose and lipid regulation, neuroprotection, and skin protection. LA activity is mediated through several signaling pathways, such as PI3K/Akt/mTOR, P53, NF-κB, and P38. Caspase-3 apoptosis, MAPK inflammatory, and Nrf2 oxidative stress signaling pathways are also involved with multiple therapeutic targets, such as TNF-α, VEGF, Fas, FasL, PI3K, AKT, and caspases. Recent studies mainly focus on the anticancer properties of LA, which suggests that the pharmacology of other aspects of LA will need additional study. At the end of this review, current challenges and future research directions on LA are discussed. This review is divided into three parts based on the pharmacological effects of LA for the convenience of readers. We anticipate that this review will inspire further research.

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“…Licochalcone A is known to possess a broad spectrum of activities with important pharmacological effects in various cancer cell lines [ 79 ]. Licochalcone A can significantly increase autophagic cytotoxicity (in both A549 and H460 cell lines) and downregulated the expression of c-IAP1, c-IAP2, XIAP, survivin, c-FLIPL, and RIP1, apoptosis-related proteins via inhibiting the activity of phosphorylated extracellular signal-regulated kinase (ERK) and autophagy [ 80 ]. In addition, licochalcone A has been reported to abolish the expression of programmed death ligand-1 (PD-L1) by increasing reactive oxygen species (ROS) levels in a time-dependent manner and interfering with protein translation in cancer cells [ 81 ].…”

Section: Natural Products As Monotherapy For the Treatment Of Lung Cancermentioning

confidence: 99%

Natural Products, Alone or in Combination with FDA-Approved Drugs, to Treat COVID-19 and Lung Cancer

Yang

Wang

2021

Biomedicines

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As a public health emergency of international concern, the highly contagious coronavirus disease 2019 (COVID-19) pandemic has been identified as a severe threat to the lives of billions of individuals. Lung cancer, a malignant tumor with the highest mortality rate, has brought significant challenges to both human health and economic development. Natural products may play a pivotal role in treating lung diseases. We reviewed published studies relating to natural products, used alone or in combination with US Food and Drug Administration-approved drugs, active against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and lung cancer from 1 January 2020 to 31 May 2021. A wide range of natural products can be considered promising anti-COVID-19 or anti-lung cancer agents have gained widespread attention, including natural products as monotherapy for the treatment of SARS-CoV-2 (ginkgolic acid, shiraiachrome A, resveratrol, and baicalein) or lung cancer (daurisoline, graveospene A, deguelin, and erianin) or in combination with FDA-approved anti-SARS-CoV-2 agents (cepharanthine plus nelfinavir, linoleic acid plus remdesivir) and anti-lung cancer agents (curcumin and cisplatin, celastrol and gefitinib). Natural products have demonstrated potential value and with the assistance of nanotechnology, combination drug therapies, and the codrug strategy, this “natural remedy” could serve as a starting point for further drug development in treating these lung diseases.

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ERK Activation-Mediated Autophagy Induction Resists Licochalcone A-Induced Anticancer Activities in Lung Cancer Cells in vitro

Cited by 17 publications

References 52 publications

ELF1 suppresses autophagy to reduce cisplatin resistance via the miR‐152‐3p/NCAM1/ERK axis in lung cancer cells

ELF1 suppresses autophagy to reduce cisplatin resistance via the miR‐152‐3p/NCAM1/ERK axis in lung cancer cells

Role of Licochalcone A in Potential Pharmacological Therapy: A Review

Natural Products, Alone or in Combination with FDA-Approved Drugs, to Treat COVID-19 and Lung Cancer

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