Chemoresistance has become a prevalent phenomenon in cancer therapy, which alleviates the effect of chemotherapy and makes it difficult to break the bottleneck of the survival rate of tumor patients. Current approaches for reversing chemoresistance are poorly effective and may cause numerous new problems. Therefore, it is urgent to develop novel and efficient drugs derived from natural non-toxic compounds for the reversal of chemoresistance. Researches and suggest that ginsenosides are undoubtedly low-toxic and effective options for the reversal of chemoresistance. The underlying mechanism of reversal of chemoresistance is correlated with inhibition of drug transporters, induction of apoptosis, and modulation of the tumor microenvironment(TME), as well as the modulation of signaling pathways, such as nuclear factor erythroid-2 related factor 2 (NRF2)/AKT, lncRNA cancer susceptibility candidate 2(CASC2)/ protein tyrosine phosphatase gene (PTEN), AKT/ sirtuin1(SIRT1), epidermal growth factor receptor (EGFR)/ phosphatidylinositol 3-kinase (PI3K)/AKT, PI3K/AKT/ mammalian target of rapamycin(mTOR) and nuclear factor-B (NF-B). Since the effects and the mechanisms of ginsenosides on chemoresistance reversal have not yet been reviewed, this review summarized comprehensively experimental data and to elucidate the functional roles of ginsenosides in chemoresistance reversal and shed light on the future research of ginsenosides.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8719627 | PMC |
http://dx.doi.org/10.3389/fphar.2021.720474 | DOI Listing |
Arab J Gastroenterol
January 2025
Fourth Oncology Department, Anyang Tumor Hospital, Anyang City, Henan Province 455000, China. Electronic address:
Background And Study Aims: Nicotinamide N-methyltransferase (NNMT) is aberrantly expressed in tumors and is implicated in the progression and chemoresistance of cancers. This project attempts to explore the specific molecular mechanism by which NNMT enhances 5-fluorouracil (5-FU) resistance in gastric cancer (GC).
Materials And Methods: By bioinformatics analysis, the expression of NNMT in GC was analyzed and its relationship with patients' prognoses was examined.
Adv Sci (Weinh)
December 2024
Research Center for Tissue Engineering and Regenerative Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
The anti-tumor efficacy of current pharmacotherapy is severely hampered due to the adaptive evolution of tumors, urgently needing effective therapeutic strategies capable of breaking such adaptability. Metabolic reprogramming, as an adaptive survival mechanism, is closely related to therapy resistance of tumors. Colorectal cancer (CRC) cells exhibit a high energy dependency that is sustained by an adaptive metabolic conversion between glucose and glutamine, helping tumor cells to withstand nutrient-deficient microenvironments and various treatments.
View Article and Find Full Text PDFMetaplastic breast cancer (MpBC) is a highly chemoresistant subtype of breast cancer with no standardized therapy options. A clinical study in anthracycline-refractory MpBC patients suggested that nitric oxide synthase (NOS) inhibitor NG-monomethyl-l-arginine (L-NMMA) may augment anti-tumor efficacy of taxane. We report that NOS blockade potentiated response of human MpBC cell lines and tumors to phosphoinositide 3-kinase (PI3K) inhibitor alpelisib and taxane.
View Article and Find Full Text PDFJ Control Release
December 2024
Key Laboratory of Natural Medicine Innovation and Transformation, Henan University, Kaifeng 475000, PR China; State Key Laboratory of Antiviral Drugs, Henan University, Kaifeng 475000, PR China; Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100050, PR China. Electronic address:
Immunogenic cell death (ICD) has recently emerged as a promising strategy in reinforcing anti-PD-L1 blockade immunotherapy of triple-negative breast cancer (TNBC). The CDK4/6 inhibitor palbociclib (PAL), as a clinical star medicine targeting the cell cycle machinery, is an ideal candidate for fabricating a highly efficient ICD inducer for TNBC chemoimmunotherapy. However, the frequently observed chemoresistance and clinical adverse effects, as well as significant antagonistic effects when co-administered with certain chemotherapeutics, have seriously restricted the efficiency of PAL and the feasibility of combination strategies.
View Article and Find Full Text PDFBiochim Biophys Acta Gen Subj
December 2024
Division of Regulatory Glycobiology, Graduate School of Pharmaceutical Sciences, Tohoku Medical and Pharmaceutical University, Japan; Institute of Molecular Biomembrane and Glycobiology, Tohoku Medical and Pharmaceutical University, 4-4-1 Komatsushima, Aoba-ku, Sendai, Miyagi 981-8558, Japan. Electronic address:
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!