Ginsenoside Rg3 enhances the anticancer effect of 5‑FU in colon cancer cells via the PI3K/AKT pathway

Hong, Shunzhong; Cai, Wenjie; Huang, Zicheng; Wang, Yubin; Mi, Xifeng; Huang, Yisen; Lin, Zhijin; Chen, Xiangbo

doi:10.3892/or.2020.7728

Cited by 21 publications

(18 citation statements)

References 43 publications

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“…Consistently, our data demonstrated that SNORA47 knockdown could result in G1 phase arrest in NSCLC cells through upregulation of p27 Kip1. Meanwhile, CDK2 and Cyclin D1 are known to be cell cycle regulators in NSCLC (21)(22)(23). SNORA78 could induce cell cycle arrest in NSCLC cells via upregulation of CDK2 (7).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of SNORA47 Inhibits the Tumorigenesis of NSCLC via Mediation of PI3K/Akt Signaling Pathway

Tian

Ling

et al. 2021

Front. Oncol.

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BackgroundNon-small cell lung cancer (NSCLC) is a frequently diagnosed aggressive cancer all over the world. Small nucleolar RNAs (snoRNAs) are a group of non-coding mediatory RNAs. A previous report indicated that small nucleolar RNA 47 (SNORA47) is upregulated in NSCLC. However, the role of SNORA47 in NSCLC is unclear.Material and MethodsCell proliferation was measured by immunofluorescence staining. Cell apoptosis and cycle of NSCLC were tested by flow cytometry and the protein expressions were investigated by Western-blot. Meanwhile, cell migration and invasion were detected by transwell assay. Xenograft mice model was established to detect the effect of SNORA47 knockdown on tumor growth of NSLC in vivo.ResultsKnockdown of SNORA47 significantly inhibited the proliferation of NSCLC cells via inducing cell apoptosis. Moreover, migration and invasion of NSCLC cells were notably decreased by SNORA47 shRNA. SNORA47 knockdown significantly induced G1 arrest in NSCLC cells via regulation of p27 Kip1, CDK2, and cyclin D1. Meanwhile, SNORA47 shRNA inhibited EMT process and PI3K/Akt signaling in NSCLC cells. Finally, silencing of SNORA47 significantly inhibited the tumor growth of NSCLC in vivo.ConclusionKnockdown of SNORA47 significantly inhibited the tumorigenesis of NSCLC via inhibition of PI3K/Akt signaling and EMT process. Thereby, our finding might shed a new light on exploring the strategies for the treatment of NSCLC.

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Section: Discussionmentioning

confidence: 99%

Knockdown of SNORA47 Inhibits the Tumorigenesis of NSCLC via Mediation of PI3K/Akt Signaling Pathway

Tian

Ling

et al. 2021

Front. Oncol.

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“…NF-κB activation [57] and IAP protein expression [58] also play important roles in the regulation of cancerous cell apoptosis. Research findings have shown that [9,[59][60][61] compared with chemotherapy alone, Rg3 combined with chemotherapy can significantly enhance the expression of caspase-3/8 and caspase-9, inhibit the overexpression of Bcl-2, and significantly inhibit the expression of IAP protein (IAP-1) and x-chromosome IAP (XIAP). e ratio of Bax/Bcl-2 was significantly increased by inhibiting the activation of NF-κB.…”

Section: Activating Apoptosis Factorsmentioning

confidence: 99%

“…However, existing studies have found that [3][4][5], through the metabolic transformation, the Rg3 monomer still needs to be transformed into 20(s) ginsenoside Rg3 and other isomers in order to play an antitumor role (Figures 1(a)-1(c)). Research on the mechanism of Rg3 has also found that the antitumor effect of Rg3 has been actually realized through multiple levels of gene, protein, and pathway expression [6][7][8][9]. How to collect the antitumor mechanism information of Rg3 and comprehensively evaluate [10] the effect of Shenyi capsule plus chemotherapy on advanced NSCLC has always been a major bottleneck in the study of combined treatment.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Shenyi Capsule on Non-Small-Cell Lung Cancer Combined with Chemotherapy from the Yin-Yang Perspective

Cai

Teng

Chen

2021

Evidence-Based Complementary and Alternative Medicine

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As an example of Shenyi capsule on non-small-cell lung cancer combined with chemotherapy, this review discusses the synergistic effect and mechanism of natural drugs in oncotherapy from the yin-yang perspective in ancient Chinese philosophy, so as to reflect the therapeutic principle of natural drugs for tumor more comprehensively. The major focuses of this review are on the philosophical thinking of yin-yang as a tool which can not only explain the effect of Shenyi capsule in NSCLC combined with chemotherapy but also explore the mechanism of Shenyi capsule at the cellular and molecular level. Learning from the “yin-yang” thinking of ancient Chinese philosophy will bring more enlightenment to the research and development of traditional Chinese drugs in the future.

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“…Moreover, Ginsenoside Rg3 is a component obtained from puffed ginseng and presented anti-tumor activity in breast cancer [ 20 , 21 ]. Rg3 can induce an inhibitory effect on cancer development by affecting different processes and pathways, such as metastasis, DNA damage, epigenetic modification, cancer stemness, drug resistance, PI3K/AKT signaling [ 22 – 27 ], but its correlation with PD-L1 is poorly understood. Meanwhile, it has been identified that two other gradients of ginsenoside, termed Rb1 and Rg1, can be carried by CNTs and induce an inhibitory effect on cancer development [ 28 ].…”

Section: Introductionmentioning

confidence: 99%

Carbon nanotubes (CNT)-loaded ginsenosides Rb3 suppresses the PD-1/PD-L1 pathway in triple-negative breast cancer

Luo

Wang

2021

Aging

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Carbon nanotubes (CNTs), as advanced nanotechnology with specific properties and structures, have presented practical drug delivery properties. Ginsenoside Rg3 is a component of puffed ginseng and demonstrates anti-cancer activities. To explore the effect of CNTs-loaded Rg3 (Rg3-CNT) on the PD-1/PD-L1 signaling and the development of triple-negative breast cancer (TNBC). Our data revealed that Rg3 inhibited the cell viability of TNBC cells, in which Rg3-CNT further enhanced this effect in the system. Similarly, the colony formation of TNBC cells was decreased by Rg3, while Rg3-CNT could reinforce its effect in the cells. Besides, the treatment of Rg3 induced apoptosis of TNBC cells, in which Rg3-CNT treatment further increased the phenotype in the cells. Remarkably, Rg3-CNT, but not Rg3, attenuated PD-L1 expression in TNBC cells. Rg3-CNT decreased the PD-L1 upregulation induced by interferon-γ (IFN-γ) in breast cancer cells. Importantly, Rg3-CNT was able to reduce PD-1 expression in activated T cells. Specifically, Rg3-CNT reduced the PD-1/PD-L1 axis in a T cell/triple-negative TNBC cell co-culture system. Moreover, the levels of IFN-γ, interleukins-2 (IL-2), interleukins-9 (IL-9), interleukins-10 (IL-10), interleukins-22 (IL-22), and interleukins-23 (IL-23) were significantly stimulated in the activated T cells, while the treatment of Rg3-CNT could reverse these phenotypes in the cells. Rg3-CNT attenuated the TNBC cell growth in vivo. The Rg3-CNT improved the anti-cancer effect of Rg3 toward TNBC by inhibiting the PD-1/PD-L1 axis. Our finding provides new insights into the mechanism by which Rg3-CNT attenuates the development of TNBC. Rg3-CNT may be applied as the potential therapeutic strategy for immunotherapy of TNBC.

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Ginsenoside Rg3 enhances the anticancer effect of 5‑FU in colon cancer cells via the PI3K/AKT pathway

Cited by 21 publications

References 43 publications

Knockdown of SNORA47 Inhibits the Tumorigenesis of NSCLC via Mediation of PI3K/Akt Signaling Pathway

Knockdown of SNORA47 Inhibits the Tumorigenesis of NSCLC via Mediation of PI3K/Akt Signaling Pathway

The Effect of Shenyi Capsule on Non-Small-Cell Lung Cancer Combined with Chemotherapy from the Yin-Yang Perspective

Carbon nanotubes (CNT)-loaded ginsenosides Rb3 suppresses the PD-1/PD-L1 pathway in triple-negative breast cancer

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