ArticleCell & bioscience2016
Hedgehog pathway is involved in nitidine chloride induced inhibition of epithelial-mesenchymal transition and cancer stem cells-like properties in breast cancer cells.
Article in Cell & bioscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 69 citations in OpenAlex.
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- Hepatocellular carcinoma stem cells: the current state of small molecule-based inhibitors.Cell death & disease · 2025Review
- Probing the biological efficacy and mechanistic pathways of natural compounds in breast cancer therapy via the Hedgehog signaling pathway.Journal of pharmaceutical analysis · 2025Review
- The natural alkaloid nitidine chloride targets RNA polymerase I to inhibit ribosome biogenesis and repress cancer cell growth.Cell death discovery · 2025Article
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- Role of EMT in drug resistance of breast cancer: molecular mechanisms and therapeutic strategies.Frontiers in oncology · 2025Review
- Interactions between hedgehog signaling pathway and the complex tumor microenvironment in breast cancer: current knowledge and therapeutic promises.Cell communication and signaling : CCS · 2024Review
- Dual mass spectrometry imaging and spatial metabolomics to investigate the metabolism and nephrotoxicity of nitidine chloride.Journal of pharmaceutical analysis · 2024Article
- Modulation of hypoxia-inducible factor-1 signaling pathways in cancer angiogenesis, invasion, and metastasis by natural compounds: a comprehensive and critical review.Cancer metastasis reviews · 2024Review
- Exploring the dynamic interplay between cancer stem cells and the tumor microenvironment: implications for novel therapeutic strategies.Journal of translational medicine · 2023Review
- Insights on Antitumor Activity and Mechanism of Natural Benzophenanthridine Alkaloids.Molecules (Basel, Switzerland) · 2023Review
- Review
- Signaling pathways governing the maintenance of breast cancer stem cells and their therapeutic implications.Frontiers in cell and developmental biology · 2023Review
- Nitidine Chloride Triggers Autophagy and Apoptosis of Ovarian Cancer Cells through Akt/mTOR Signaling Pathway.Current pharmaceutical design · 2023Article
- Selectively Targeting Breast Cancer Stem Cells by 8-Quinolinol and Niclosamide.International journal of molecular sciences · 2022Article
- Nitidine chloride, a benzophenanthridine alkaloid fromFrontiers in pharmacology · 2022Review
- Natural products targeting cancer cell dependency.The Journal of antibiotics · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe complications of clinical metastatic disease are responsible for the majority of breast cancer related deaths, and fewer therapies substantially prolong survival. Nitidine chloride (NC), a natural polyphenolic compound, has been shown to exhibit potent anticancer effects in many cancer types, including breast cancer. The epithelial-mesenchymal transition (EMT) and the acquisition of cancer stem cells (CSCs)-like properties emerge as critical steps in the metastasis of human cancers. However, the effects of NC on the EMT and the CSCs-like properties in breast cancer cells, and the underlying molecular mechanisms are not fully understood.
resultsIn the present study, MDA-MB-468 and MCF-7 cancer cells were treated with NC. Scratch and Transwell assays were performed to determine whether NC could attenuate the migratory and invasive capability of cancer cells; Mammosphere formation and flow cytometry analysis were performed to confirm that NC decreased CSCs-like phenotype; RT-PCR and western blot analysis were used to examine the expression level of EMT and CSC related markers in both cells. Mechanistically, NC could inhibit the components of Hedgehog pathway (smoothened, patched, Gli1 and Gli2), subsequently inhibited the expression of Snail, Slug and Zeb1, which were correlated with the significant changes of the expression of EMT related markers (N-cadherin, E-cadherin, and Vimentin) to reverse EMT. On the other hand, NC could also inhibit the expression of CSCs related factors such as Nanog, Nestin, Oct-4 and CD44 via Hedgehog pathway. Furthermore, transforming growth factor-β1 (TGF-β1)-induced increment of EMT and CSCs properties could be reversed by NC.
conclusionsTaken together, these data indicated that NC suppressed breast cancer EMT and CSCs-like properties through inhibiting Hedgehog signaling pathway. Our study suggested that NC may be a potential anticancer agent for breast cancer.
Identifiers
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Registered trials
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.