Mai multe produse naturale s-au dovedit a fi surse puternice de medicamente împotriva cancerului, deoarece cancerul este una dintre principalele cauze de deces la nivel mondial.
Ca urmare a explorării continue a medicinei tradiționale chineze, plantele medicinale au apărut ca o strategie unică de tratament pentru cancer, în primul rând datorită accesibilității, toxicității scăzute și naturii bine tolerate.
Compușii naturali bioactivi, în special flavonoidele, au un impact semnificativ asupra tratamentului cancerului. Taxifolinul prezintă o activitate anticanceroasă semnificativă și există efecte secundare ușoare sau deloc asupra celulelor normale sănătoase
Taxifolinul reglează genele asociate cu cancerul, inclusiv cele implicate în detoxifierea hepatică, antioxidare, ciclul celular și creșterea celulelo. Micromatricele ADN din cancer sunt utilizate pentru a demonstra această asociere.
Rezultatele au arătat că taxifolina a inhibat semnificativ supraviețuirea, proliferarea, migrarea, invazia și creșterea tumorii cancerului gastric.
Deocamdata nu se știe cum contribuie taxifolinul la tratamentul cancerului de sân extrem de agresiv și care sunt mecanismele de bază. Dar taxifolina inhibă proliferarea, migrarea și invazia celulelor agresive de cancer de sân. Mai mult, taxifolina a inhibat semnificativ creșterea tumorilor primare și a redus metastazele pulmonare ale cancerului de sân.
Taxifolinul este de așteptat să fie utilizat ca un medicament promițător pentru tratamentul clinic al cancerului de sân extrem de agresiv.
Taxifolinul are potențialul de a deveni un nou medicament pentru tratamentul cancerului hepatic.
Sursa
https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2023.1173855/full
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Therapeutic effects of taxifolin on cancers
Several natural products have proved to be potent sources of anti-cancer drugs, as cancer is one of the leading causes of death worldwide (Butler, 2004; Ghosh et al., 2014). As a result of the continuous exploration of traditional Chinese medicine, medicinal plants have emerged as a unique treatment strategy for cancer, primarily due to their accessibility, low toxicity, and well tolerated nature (Takebe et al., 2011; Thakor et al., 2016). Natural bioactive compounds, especially flavonoids, have a significant impact on the treatment of cancer. Taxifolin exhibits significant anticancer activity, and there are mild or no side effects on normal healthy cells (Das et al., 2021). Taxifolin regulates genes associated with cancer, including those involved in hepatic detoxification, antioxidation, cell cycle, and cell growth, according to Lee et al. DNA microarrays from cancer DNA microarrays are used to demonstrate this association (Lee et al., 2007). Taxifolin is an antagonist of epidermal growth factor receptors and PI3K receptors. It has demonstrated many chemotherapeutic activities in cancer model systems, including antiproliferative, antiangiogenic, stemness and EMT regulation, among others.
It is pertinent to note, however, that taxifolin’s anticancer activity is not universally positive, and there are ambiguous and even conflicting results. ZEB2 protein is a transcription factor that plays an instrumental role in the epithelial/mesenchymal transition (EMT) (Vandewalle et al., 2009; Gonzalez and Medici, 2014). After treatment with taxifolin, the ZEB2 protein was upregulated in a dose-dependent manner. However, this regulation did not lead to an epithelial/mesenchymal transition. By inhibiting Akt phosphorylation, taxifolin reduced ZEB2 signaling, which could trigger cancer. Due to non-specific effects on cells, Z et al. suggest that taxifolin’s biological activity may have vague or even contradictory results (Z et al., 2021).
Taxifolin has not been shown to have an anti-tumor effect on gastric cancer in the studies conducted to date. To investigate the effect and mechanism of taxifolin on gastric cancer, Xie et al. treated AGS and NCI N87 cells with taxifolin. Viability and proliferation of cells are determined using Cell Counting Kit 8 and colony formation assays, migration and invasion capacity are determined by wound healing and Transwell assays, and protein expression is assessed using Western blots in vitro and in vivo. The results showed that taxifolin significantly inhibited the survival, proliferation, migration, invasion and tumor growth of gastric cancer through the aryl hydrocarbon receptor (AhR)/cytochrome P450 1A1 (CYP1A1) signaling pathway. Taxifolin may prove to be a potential treatment strategy for stomach cancer (Xie et al., 2021).
It is also unknown how taxifolin contributes to the treatment of highly aggressive breast cancer and what the underlying mechanisms are. According to Li et al., taxifolin inhibits proliferation, migration, and invasion of aggressive breast cancer cells and exhibits dose dependence. Furthermore, taxifolin significantly inhibited the growth of primary tumors and reduced lung metastases of breast cancer in a 4T1 xenograft mouse model. However, excessive expression of adenovirus to β-catenin diminishes these beneficial effects of taxifolin. Taxifolin is expected to be used as a promising drug for the clinical treatment of highly aggressive breast cancer (Li et al., 2019).
The expression of SOS1, a key regulator of the Ras pathway, is highly elevated in African American (AA) breast cancer patients. Taxifolin inhibited signal transduction of SOS1 by blocking the interaction between SOS1 and Grb2, demonstrating that taxifolin could be effective in combating SOS1-driven tumor progression, demonstrating the potential utility of the compound as a treatment for patients with AA-type breast cancer (Xing et al., 2021).
Taxifolin has the potential to become a new drug for the treatment of liver cancer. Liver cancer is the result of structural abnormalities in the blood vessels of the liver, and this angiogenesis is driven by the overexpression of hypoxia-inducible factor 1-α (Hif1-α) and vascular endothelial growth factor (VEGF), in addition, protein kinase B (Akt) are also compromised in liver cancer. A et al. confirmed that taxifolin showed positive docking scores with Hif1-α, VEGF and Akt through molecular docking experiments, and taxifolin could also directly affect the expression levels of the three. In vitro experiments showed that treatment with taxifolin could induce apoptosis in HepG2 and Huh7 cell lines. The potential of taxifolin in the treatment of liver cancer has been confirmed, but further verification in animal model experiments is still required (Butt et al., 2021).