ArticleAntioxidants (Basel, Switzerland)2023
Licochalcone B Induces ROS-Dependent Apoptosis in Oxaliplatin-Resistant Colorectal Cancer Cells via p38/JNK MAPK Signaling.
Article in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Wool Keratin-Engineered Manganese Nanozyme with Tumor Microenvironment-Adaptive Self-Cascade Capability for Hepatocellular Carcinoma Therapy.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Feilike and Its Constituent Licochalcone B Trigger Caspase-3/GSDME-Mediated Pyroptosis in Triple-Negative Breast Cancer via Modulation of the Mutant p53-Calcium/ER Stress-ROS-MAPK Axis.Antioxidants (Basel, Switzerland) · 2026Article
- Synthesis and Characterization of Sulfonamide-Schiff Bases, and Investigation of Cytotoxic, Antioxidant, HDAC, and Apoptotic Activities in Human Colon Cancer Cells (DLD-1 and HT-29).Archiv der Pharmazie · 2026Article
- A novel quinine derivative as a PIM-1 kinase inhibitor induces apoptosis via mitochondrial depolarization with selective cytotoxicity in acute lymphoblastic leukemia cells.Frontiers in pharmacology · 2026Article
- Phellinus igniarius-derived carbon dots suppress liver cancer through the ROS/MAPK signaling axis.Frontiers in pharmacology · 2026Article
- Programmed cell death in triple-negative breast cancer.Cellular & molecular biology letters · 2025Review
- Gossypin induces apoptosis and autophagy via the MAPK/JNK pathway in HT‑29 human colorectal cancer cells.International journal of molecular medicine · 2025Article
- Natural products modulating MAPK for CRC treatment: a promising strategy.Frontiers in pharmacology · 2025Review
- Synergistic effects of 6-shogaol and hyperthermia on ACHN renal cancer cells: modulation of ROS and heat shock pro-teins in cancer therapy.Frontiers in pharmacology · 2025Article
- TMJ-105, an extract ofHeliyon · 2024Article
- Aldehyde dehydrogenase 2 family member repression promotes colorectal cancer progression by JNK/p38 MAPK pathways-mediated apoptosis and DNA damage.World journal of gastrointestinal oncology · 2024Article
- Knocking Down PIAS3 Reduces HCell biochemistry and biophysics · 2024Article
- GLUD1 inhibits hepatocellular carcinoma progression via ROS-mediated p38/JNK MAPK pathway activation and mitochondrial apoptosis.Discover oncology · 2024Article
- Therapeutic potential and action mechanisms of licochalcone B: a mini review.Frontiers in molecular biosciences · 2024Review
- Polydatin enhances oxaliplatin-induced cell death by activating NOX5-ROS-mediated DNA damage and ER stress in colon cancer cells.Frontiers in pharmacology · 2024Article
- Article
- Acidic Environment-Responsive Metal Organic Framework-Mediated Dihydroartemisinin Delivery for Triggering Production of Reactive Oxygen Species in Drug-Resistant Lung Cancer.International journal of nanomedicine · 2024Article
- Licochalcone D Inhibits Skin Epidermal Cells Transformation through the Regulation of AKT Signaling Pathways.Biomolecules & therapeutics · 2023Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Licochalcone B (LCB) exhibits anticancer activity in oral cancer, lung cancer, and hepatocellular carcinoma cells. However, little is known about its antitumor mechanisms in human oxaliplatin-sensitive and -resistant colorectal cancer (CRC) cells. The purpose of the present study was to investigate the antitumor potential of LCB against human colorectal cancer in vitro and analyze its molecular mechanism of action. The viability of CRC cell lines was evaluated using the MTT assay. Flow cytometric analyses were performed to investigate the effects of LCB on apoptosis, cell cycle distribution, reactive oxygen species (ROS), mitochondrial membrane potential (MMP) dysfunction, and multi-caspase activity in CRC cells. The results demonstrated that LCB induced a reduction in cell viability, apoptosis, G2/M cell cycle arrest, ROS generation, MMP depolarization, activation of multi-caspase, and JNK/p38 MAPK. However, p38 (SB203580) and JNK (SP600125) inhibitors prevented the LCB-induced reduction in cell viability. The ROS scavenger N-acetylcysteine (NAC) inhibited LCB-induced reduction in cell viability, apoptosis, cell cycle arrest, ROS generation, MMP depolarization, and multi-caspase and JNK/p38 MAPK activities. Taken together, LCB has a potential therapeutic effect against CRC cells through the ROS-mediated JNK/p38 MAPK signaling pathway. Therefore, we expect LCB to have promising potential as an anticancer therapeutic and prophylactic agent.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.