Ginsenoside Rh2 represses autophagy to promote cervical cancer cell apoptosis during starvation

Wang, Jiawen; Bian, Shuai; Wang, Siming; Song, Yang; Zhang, Wanying; Zhao, Daqing; Liu, Meichen; Bai, Xueyuan

doi:10.1186/s13020-020-00396-w

Cited by 16 publications

(4 citation statements)

References 35 publications

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“…The specific mechanism is to impair mitochondrial function through increased ROS, leading to defective/impaired lysosomal acidification/function and, ultimately, HGC-27 cell death ( Han et al, 2020 ). The conclusion that Rh2 inhibits autophagy in cervical cancer cells was also drawn by Wang et al in cervical cancer cells ( Wang J. et al, 2020 ). Furthermore, by the preapplication of N-acetyl- l -cysteine (NAC) to esophageal cancer cells, Bian et al identified that ginsenoside Ro-induced elevated expression of autophagy-associated proteins, such as LC3B-II, was significantly reversed, precisely through the modulation of the ESR2-NCF1-ROS axis.…”

Section: Mechanism Of Ginsenoside Inhibition Of Cancer Development Th...supporting

confidence: 53%

Anticancer therapeutic effect of ginsenosides through mediating reactive oxygen species

Li¹,

Cao²,

Sun³

et al. 2023

Front. Pharmacol.

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Dysregulation of reactive oxygen species (ROS) production and ROS-regulated pathways in cancer cells leads to abnormal accumulation of reactive oxygen species, displaying a double-edged role in cancer progression, either supporting transformation/proliferation and stimulating tumorigenesis or inducing cell death. Cancer cells can accommodate reactive oxygen species by regulating them at levels that allow the activation of pro-cancer signaling pathways without inducing cell death via modulation of the antioxidant defense system. Therefore, targeting reactive oxygen species is a promising approach for cancer treatment. Ginsenosides, their derivatives, and related drug carriers are well-positioned to modulate multiple signaling pathways by regulating oxidative stress-mediated cellular and molecular targets to induce apoptosis; regulate cell cycle arrest and autophagy, invasion, and metastasis; and enhance the sensitivity of drug-resistant cells to chemotherapeutic agents of different cancers depending on the type, level, and source of reactive oxygen species, and the type and stage of the cancer. Our review focuses on the pro- and anticancer effects of reactive oxygen species, and summarizes the mechanisms and recent advances in different ginsenosides that bring about anticancer effects by targeting reactive oxygen species, providing new ideas for designing further anticancer studies or conducting more preclinical and clinical studies.

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Section: Mechanism Of Ginsenoside Inhibition Of Cancer Development Th...supporting

confidence: 53%

Anticancer therapeutic effect of ginsenosides through mediating reactive oxygen species

Li¹,

Cao²,

Sun³

et al. 2023

Front. Pharmacol.

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“…In previous studies, Rh2 has also been found to modulate the oxidative stress response of nerve tissue and the autophagy capacity of cells [ 25 , 26 ], which may also be the mechanism by which Rh2 influences AMI. Hence, it is worthwhile to carry out more in vitro experiments to confirm.…”

Section: Discussionmentioning

confidence: 99%

Influence of Ginsenoside Rh2 on Cardiomyocyte Pyroptosis in Rats with Acute Myocardial Infarction

Song¹,

Dai²,

Dai³

2022

Evidence-Based Complementary and Alternative Medicine

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Objective. This paper intends to verify through in vivo experiments whether ginsenoside Rh2 (G-Rh2) can play an anti-inflammatory role by modulating cardiomyocyte (CM) pyroptosis in rats with acute myocardial infarction (AMI), thereby alleviating myocardial injury. Methods. Twenty SD rats were randomized into control, L-Rh2, M-Rh2, and H-Rh2 groups, among which the latter three groups were modeled for AMI and given an intraperitoneal injection of G-Rh2 (L-Rh2: 2 mg/kg; M-Rh2: 4 mg/kg; H-Rh2: 8 mg/kg), while the control group was only treated with thoracotomy and sodium chloride injection. Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), and left ventricular end-diastolic pressure (LVEDP) were recorded by ultrasonic diagnosis. Rats were killed under anesthesia, and the morphological characteristics of ventricular tissue were observed by electron microscope. Additionally, cardiac blood and ventricular tissues were collected to quantify the contents of myocardial injury markers (creatine phosphate kinase (CK), creatine phosphokinase-MB isoenzyme (CK-MB), and lactate dehydrogenase (LDH) by ELISA, as well as the expression of pyroptosis-related genes cysteinyl aspartate specific proteinase 1 (Caspase-1), gasdermin D (GSDMD), interleukin (IL)-1β, and NOD-like receptor thermal protein domain associated protein 3 (NLRP3) by qRT-PCR and Western blot). Results. Ultrasonic examination identified lower HR, SBP, DBP, MAP, and LVSP in the three Rh2 injection groups compared with the control group ( P < 0.05); and in comparison with M- and H-Rh2 groups, HR, SBP, DBP, MAP, and LVSP were all lower in L-Rh2 group, while LVEDP was higher ( P < 0.05). Microscopically, CMs and organelles in the L-RH2, M-RH2, and H-RH2 groups were damaged to varying degrees compared with the control group, with those in the L-RH2 group being the most serious. CK, CK-MB, and LDH were also the highest in the L-Rh2 group and the lowest in the control group, while their levels were obviously reduced in M- and H-Rh2 groups ( P < 0.05). Finally, GSDMD, IL-1β, NLRP3, and Caspase-1 were found to be reduced in the control group, while pyroptosis-related gene expression in the M-Rh2 group was improved markedly ( P < 0.05). Conclusion. G-Rh2 can inhibit the pathological development of AMI by relieving the focal death of CM and inhibiting the release of proinflammatory factors in the body, and the effect is significantly related to the dosage, which is expected to become a new treatment option for AMI in the future.

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“…The tumor-suppressive effects of ginsenoside Rh2 have been reported in cancers such as breast cancer [ 5 ], colon cancer [ 4 ], lung cancer [ 27 ] and prostate cancer [ 28 ]. It induces epigenetic silencing of some tumor-associated genes, such as long non-coding RNA C3orf67-AS1 [ 6 ] and CASP1 , INSL5 , and OR52A1 [ 5 ] via promoter hypermethylation.…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rh2 reduces m6A RNA methylation in cancer via the KIF26B-SRF positive feedback loop

Yang²,

Wang

et al. 2021

Journal of Ginseng Research

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Background The underlying mechanisms of the potential tumor-suppressive effects of ginsenoside Rh2 are complex. N 6-methyladenosine (m6A) RNA methylation is usually dysregulated in cancer. This study explored the regulatory effect of ginsenoside Rh2 on m6A RNA methylation in cancer. Methods: m6A RNA quantification and gene-specific m6A RIP-qPCR assays were applied to assess total and gene-specific m6A RNA levels. Co-immunoprecipitation, fractionation western blotting, and immunofluorescence staining were performed to detect protein interactions and distribution. QRT-PCR, dual-luciferase, and ChIP-qPCR assays were conducted to check the transcriptional regulation. Results Ginsenoside Rh2 reduces m6A RNA methylation and KIF26B expression in a dose-dependent manner in some cancers. KIF26B interacts with ZC3H13 and CBLL1 in the cytoplasm of cancer cells and enhances their nuclear distribution. KIF26B inhibition reduces m6A RNA methylation level in cancer cells. SRF bound to the KIF26B promoter and activated its transcription. SRF mRNA m6A abundance significantly decreased upon KIF26B silencing. SRF knockdown suppressed cancer cell proliferation and growth both in vitro and in vivo , the effect of which was partly rescued by KIF26B overexpression. Conclusion: ginsenoside Rh2 reduces m6A RNA methylation via downregulating KIF26B expression in some cancer cells. KIF26B elevates m6A RNA methylation via enhancing ZC3H13/CBLL1 nuclear localization. KIF26B-SRF forms a positive feedback loop facilitating tumor growth.

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Ginsenoside Rh2 represses autophagy to promote cervical cancer cell apoptosis during starvation

Cited by 16 publications

References 35 publications

Anticancer therapeutic effect of ginsenosides through mediating reactive oxygen species

Anticancer therapeutic effect of ginsenosides through mediating reactive oxygen species

Influence of Ginsenoside Rh2 on Cardiomyocyte Pyroptosis in Rats with Acute Myocardial Infarction

Ginsenoside Rh2 reduces m6A RNA methylation in cancer via the KIF26B-SRF positive feedback loop

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