Ginsenoside Rg3 attenuates the osimertinib resistance by reducing the stemness of non‐small cell lung cancer cells

Tan, Qinquan; Lin, Shunhuan; Zeng, Yihong; Yao, Mantian; Liu, Kejun; Yuan, Haiji; Li, Chun; Jiang, Guanming

doi:10.1002/tox.22899

Cited by 25 publications

(25 citation statements)

References 19 publications

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“…Collectively, Rg3 could sensitize hypoxic lung cancer cells to DDP through preventing NF-κB induced EMT and stemness. Also, Rg3 (Tan et al, 2020) could target CSCs and reverse osimertinib resistance in H1975 and H1975/OR cells by activating the Hippo pathway, which was key cancer signaling in association with cell proliferation, cell death, and cancer metastasis (Kulkarni et al, 2020). Co-treatment of Rg3 and osimertinib could promote expressions of the active components of the Hippo pathway, such as MST1/2 and LATS1/2, and depress the expression of the negative executor or effector.…”

Section: Modulating Tumor Microenvironment (Tme)mentioning

confidence: 99%

Emerging Significance of Ginsenosides as Potentially Reversal Agents of Chemoresistance in Cancer Therapy

Wan

Tang

et al. 2021

Front. Pharmacol.

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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 in vivo and in vitro 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-κB (NF-κB). Since the effects and the mechanisms of ginsenosides on chemoresistance reversal have not yet been reviewed, this review summarized comprehensively experimental data in vivo and in vitro to elucidate the functional roles of ginsenosides in chemoresistance reversal and shed light on the future research of ginsenosides.

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Section: Modulating Tumor Microenvironment (Tme)mentioning

confidence: 99%

Emerging Significance of Ginsenosides as Potentially Reversal Agents of Chemoresistance in Cancer Therapy

Wan

Tang

et al. 2021

Front. Pharmacol.

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“…For example, BST204, a fermented ginseng extract containing high quantities of Rh2 and Rg3, strongly suppressed cancer stemness of embryonic carcinoma cells by downregulating stemness markers and transcription factors at both transcriptional and protein expression levels ( Park et al, 2020 ). Meanwhile, ginsenoside Rg3 was also shown to decrease tumor CSC sphere-forming capacity that led to deregulated expression of stemness-related markers and attenuated CSC tumorigenic activities in several types of cancer ( Wang et al, 2018 ; Phi et al, 2019a ; Oh et al, 2019 ; Tan et al, 2020 ). Moreover, it has been reported that ginsenoside Rd may downregulate levels of genes related to stemness and EMT by binding to epidermal growth factor receptor (EGFR) ( Phi et al, 2019b ).…”

Section: Ginseng Could Inhibit Stemness Of Cancer Stem Cellsmentioning

confidence: 99%

Strategies for Remodeling the Tumor Microenvironment Using Active Ingredients of Ginseng—A Promising Approach for Cancer Therapy

Wang

et al. 2021

Front. Pharmacol.

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The tumor microenvironment (TME) plays a key role in promoting the initiation and progression of tumors, leading to chemoradiotherapy resistance and immunotherapy failure. Targeting of the TME is a novel anti-tumor therapeutic approach and is currently a focus of anti-tumor research. Panax ginseng C. A. Meyer (ginseng), an ingredient of well-known traditional Asia medicines, exerts beneficial anti-tumor effects and can regulate the TME. Here, we present a systematic review that describes the current status of research efforts to elucidate the functions and mechanisms of ginseng active components (including ginsenosides and ginseng polysaccharides) for achieving TME regulation. Ginsenosides have variety effects on TME, such as Rg3, Rd and Rk3 can inhibit tumor angiogenesis; Rg3, Rh2 and M4 can regulate the function of immune cells; Rg3, Rd and Rg5 can restrain the stemness of cancer stem cells. Ginseng polysaccharides (such as red ginseng acidic polysaccharides and polysaccharides extracted from ginseng berry and ginseng leaves) can regulate TME mainly by stimulating immune cells. In addition, we propose a potential mechanistic link between ginseng-associated restoration of gut microbiota and the tumor immune microenvironment. Finally, we describe recent advances for improving ginseng efficacy, including the development of a nano-drug delivery system. Taken together, this review provides novel perspectives on potential applications for ginseng active ingredients as anti-cancer adjuvants that achieve anti-cancer effects by reshaping the tumor microenvironment.

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“…A recent study revealed that osimertinib-resistant NSCLC cells displayed stronger stemness than the parental cells, which conferred to them greater metastatic potential (55). Notably, ginsenoside Rg3 attenuates the stemness of NSCLC cells and the resistance to osimertinib, as evidenced by the decreased expression of stemness markers and decreased spheroid formation ability, which is dependent on the Hippo signaling pathway (56). Furthermore, ginsenosides overcome resistance to chemotherapy drugs such as cisplatin (DDP), which is used for the treatment of NSCLC.…”

Section: Saponinsmentioning

confidence: 99%

Medicinal herbs and bioactive compounds overcome the drug resistance to epidermal growth factor receptor inhibitors in non‑small cell lung cancer (Review)

et al. 2021

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Lung cancer is the leading cause of cancer-related mortality worldwide. Non-small cell lung cancer (NSCLC) accounts for ~85% of all lung cancer cases. Patients harboring epidermal growth factor receptor (EGFR) mutations usually develop resistance to treatment with frontline EGFR-tyrosine kinase inhibitors (EGFR-TKIs). The present review summarizes the current findings and delineates the molecular mechanism of action for the therapeutic effects of herbal extracts and phytochemicals in overcoming EGFR-TKI resistance in NSCLC. Novel molecular targets underlying EGFR-TKI resistance in NSCLC are also discussed. This review provides valuable information for the development of herbal bioactive compounds as alternative treatments for EGFR-TKI-resistant NSCLC.

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Ginsenoside Rg3 attenuates the osimertinib resistance by reducing the stemness of non‐small cell lung cancer cells

Cited by 25 publications

References 19 publications

Emerging Significance of Ginsenosides as Potentially Reversal Agents of Chemoresistance in Cancer Therapy

Emerging Significance of Ginsenosides as Potentially Reversal Agents of Chemoresistance in Cancer Therapy

Strategies for Remodeling the Tumor Microenvironment Using Active Ingredients of Ginseng—A Promising Approach for Cancer Therapy

Medicinal herbs and bioactive compounds overcome the drug resistance to epidermal growth factor receptor inhibitors in non‑small cell lung cancer (Review)

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