ArticleMolecular oncology2016
Methylisoindigo preferentially kills cancer stem cells by interfering cell metabolism via inhibition of LKB1 and activation of AMPK in PDACs.
Article in Molecular oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Bridging metabolic reprogramming and targeted therapy: the critical role of S-palmitoylation in cancer.Frontiers in cell and developmental biology · 2026Review
- Natural products as inhibitors against pancreatic cancer cell proliferation and invasion: possible mechanisms.American journal of cancer research · 2024Review
- Tumor microenvironment in pancreatic ductal adenocarcinoma: Implications in immunotherapy.World journal of gastroenterology · 2022Review
- Cell fusion enhances energy metabolism of mesenchymal tumor hybrid cells to sustain their proliferation and invasion.BMC cancer · 2021Article
- Article
- The novel interplay between CD44 standard isoform and the caspase-1/IL1B pathway to induce hepatocellular carcinoma progression.Cell death & disease · 2020Article
- Pancreatic ductal adenocarcinoma: Treatment hurdles, tumor microenvironment and immunotherapy.World journal of gastrointestinal oncology · 2020Review
- NHC-gold compounds mediate immune suppression through induction of AHR-TGFβ1 signalling in vitro and in scurfy mice.Communications biology · 2020Article
- Anti-inflammatory Property of AMP-activated Protein Kinase.Anti-inflammatory & anti-allergy agents in medicinal chemistry · 2020Review
- Indirubin 3'-Oxime Inhibits Migration, Invasion, and Metastasis InVivo in Mice Bearing Spontaneously Occurring Pancreatic Cancer via Blocking the RAF/ERK, AKT, and SAPK/JNK Pathways.Translational oncology · 2019Article
- Genetic variants in the liver kinase B1-AMP-activated protein kinase pathway genes and pancreatic cancer risk.Molecular carcinogenesis · 2019Article
- AICAR Induces Apoptosis and Inhibits Migration and Invasion in Prostate Cancer Cells Through an AMPK/mTOR-Dependent Pathway.International journal of molecular sciences · 2019Article
- [The impact of meisoindigo on apoptosis and proliferation of SET2 cell line by JAK-STAT pathway].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2019Article
- Meisoindigo Protects Against Focal Cerebral Ischemia-Reperfusion Injury by Inhibiting NLRP3 Inflammasome Activation and Regulating Microglia/Macrophage Polarization via TLR4/NF-κB Signaling Pathway.Frontiers in cellular neuroscience · 2019Article
- Betulinic acid inhibits stemness and EMT of pancreatic cancer cells via activation of AMPK signaling.International journal of oncology · 2019Article
- Expression of TXNIP in Cancer Cells and Regulation by 1,25(OH)₂D₃: Is It Really the Vitamin D₃ Upregulated Protein?International journal of molecular sciences · 2018Article
- Essential role of mitochondrial Stat3 in p38Scientific reports · 2017Article
- Methylisoindigo and Its Bromo-Derivatives Are Selective Tyrosine Kinase Inhibitors, Repressing Cellular Stat3 Activity, and Target CD133+ Cancer Stem Cells in PDAC.Molecules (Basel, Switzerland) · 2017Article
- The essential role of TAp73 in bortezomib-induced apoptosis in p53-deficient colorectal cancer cells.Scientific reports · 2017Article
- Methylisoindigo preferentially kills cancer stem cells by interfering cell metabolism via inhibition of LKB1 and activation of AMPK in PDACs.Molecular oncology · 2016Article
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16 authors.
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Abstract
Pancreatic ductal adenocarcinoma (PDAC) clinically has a very poor prognosis. No small molecule is available to reliably achieve cures. Meisoindigo is chemically related to the natural product indirubin and showed substantial efficiency in clinical chemotherapy for CML in China. However, its effect on PDAC is still unknown. Our results showed strong anti-proliferation effect of meisoindigo on gemcitabine-resistant PDACs. Using a recently established primary PDAC cell line, called Jopaca-1 with a larger CSCs population as model, we observed a reduction of CD133+ and ESA+/CD44+/CD24+ populations upon treatment and concomitantly a decreased expression of CSC-associated genes, and reduced cellular mobility and sphere formation. Investigating basic cellular metabolic responses, we detected lower oxygen consumption and glucose uptake, while intracellular ROS levels increased. This was effectively neutralized by the addition of antioxidants, indicating an essential role of the cellular redox balance. Further analysis on energy metabolism related signaling revealed that meisoindigo inhibited LKB1, but activated AMPK. Both of them were involved in cellular apoptosis. Additional in situ hybridization in tissue sections of PDAC patients reproducibly demonstrated co-expression and -localization of LKB1 and CD133 in malignant areas. Finally, we detected that CD133+/CD44+ were more vulnerable to meisoindigo, which could be mimicked by LKB1 siRNAs. Our results provide the first evidence, to our knowledge, that LKB1 sustains the CSC population in PDACs and demonstrate a clear benefit of meisoindigo in treatment of gemcitabine-resistant cells. This novel mechanism may provide a promising new treatment option for PDAC.
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