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dc.creatorHassani, Samira
dc.creatorGhanbari, Fahimeh
dc.creatorLotfi, Marzieh
dc.creatorAlam, Waqas
dc.creatorAschner, Michael
dc.creatorPopović-Djordjević, Jelena
dc.creatorShahcheraghi, Seyed Hossein
dc.creatorKhan, Haroon
dc.date.accessioned2023-11-03T11:28:42Z
dc.date.available2023-11-03T11:28:42Z
dc.date.issued2023
dc.identifier.issn1559-131X
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/pubmed/37755616
dc.identifier.urihttp://aspace.agrif.bg.ac.rs/handle/123456789/6462
dc.description.abstractCancer is one of the deadliest and most heterogeneous diseases. Cancers often develop drug resistance, which can lead to treatment failure or recurrence. Accordingly, anticancer compounds are essential for chemotherapy-resistant cancer cells. Phenolic compounds are of interest in the development of cancer drugs due to their medicinal properties and ability to target different molecular pathways. Gallic acid (GA), as one of the main components of phenol, which is abundantly present in plant compounds such as walnut, sumac, grapes, tea leaves, oak bark, and other plant compounds, has antitumor properties. GA can prevent cancer progression, cell invasion, and metastasis by targeting molecular pathways and is an effective complement to chemotherapy drugs and combating multidrug resistance (MDR). In this review, we discuss various mechanisms related to cancer, the therapeutic potential of GA, the antitumor properties of GA in various cancers, and the targeted delivery of GA with nanocarriers.
dc.languageeng
dc.relation.isversionofpublishedVersion
dc.rightsrestrictedAccess
dc.sourceMedical Oncology (Northwood, London, England)
dc.sourceMedical Oncology (Northwood, London, England)Med Oncol
dc.subjectAntineoplastic Agents
dc.subjectCancer
dc.subjectDrug resistance
dc.subjectDrug Resistance, Neoplasm
dc.subjectGallic acid
dc.subjectGallic Acid
dc.subjectHumans
dc.subjectMolecular pathway
dc.subjectNeoplasms
dc.subjectSignal Transduction
dc.titleHow gallic acid regulates molecular signaling: role in cancer drug resistance
dc.typearticleen
dc.rights.licenseARR
dc.citation.issue11
dc.citation.spage308
dc.citation.volume40
dc.identifier.doi10.1007/s12032-023-02178-4


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