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Effect of Plant Bioactives and Their Constituents on Human Cell Activity

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (29 November 2024) | Viewed by 1065

Special Issue Editor

Special Issue Information

Dear Colleagues,

Though advanced medical treatments using chemotherapy with synthetic drugs have contributed to human health for years, plants, or herbal mixtures and their compounds used for oriental prescriptions, are becoming increasingly attractive. This is due to their ability to enhance biological effects, such as immune, antithrombotic, and anti-inflammatory properties, as well as other pharmacologic activities, with little or no adverse responses. Hence, this Special Issue covers scientific findings in relation to the impact of plants and herbal mixtures and their compounds, as used for oriental prescriptions, as biological modifiers with strong molecular or pharmacological data in vitro or/and in vivo in the field of evidence-based medicine and molecular research. Furthermore, we invite authors to submit their novel and mechanistic studies for publication in IJMS.

Importantly, the exact active ingredient of the natural origin extract must be reported in the submitted research manuscript, as papers describing the effects of mixed extractions from natural origins do not fall within the scope of this journal.

Prof. Dr. Sung-Hoon Kim
Guest Editor

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Keywords

  • oriental prescriptions
  • herbal extracts
  • natural compounds
  • inflammation
  • cancer
  • immune
  • thrombosis
  • biological activity

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Published Papers (1 paper)

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Research

13 pages, 3706 KiB  
Article
Anti-Warburg Mechanism of Ginsenoside F2 in Human Cervical Cancer Cells via Activation of miR193a-5p and Inhibition of β-Catenin/c-Myc/Hexokinase 2 Signaling Axis
by Nari Shin, Hyo-Jung Lee, Deok Yong Sim, Chi-Hoon Ahn, Su-Yeon Park, Wonil Koh, Jaeho Khil, Bum-Sang Shim, Bonglee Kim and Sung-Hoon Kim
Int. J. Mol. Sci. 2024, 25(17), 9418; https://doi.org/10.3390/ijms25179418 - 30 Aug 2024
Viewed by 844
Abstract
Though Ginsenoside F2 (GF2), a protopanaxadiol saponin from Panax ginseng, is known to have an anticancer effect, its underlying mechanism still remains unclear. In our model, the anti-glycolytic mechanism of GF2 was investigated in human cervical cancer cells in association with miR193a-5p and [...] Read more.
Though Ginsenoside F2 (GF2), a protopanaxadiol saponin from Panax ginseng, is known to have an anticancer effect, its underlying mechanism still remains unclear. In our model, the anti-glycolytic mechanism of GF2 was investigated in human cervical cancer cells in association with miR193a-5p and the β-catenin/c-Myc/Hexokinase 2 (HK2) signaling axis. Here, GF2 exerted significant cytotoxicity and antiproliferation activity, increased sub-G1, and attenuated the expression of pro-Poly (ADPribose) polymerase (pro-PARP) and pro-cysteine aspartyl-specific protease (procaspase3) in HeLa and SiHa cells. Consistently, GF2 attenuated the expression of Wnt, β-catenin, and c-Myc and their downstream target genes such as HK2, pyruvate kinase isozymes M2 (PKM2), and lactate dehydrogenase A (LDHA), along with a decreased production of glucose and lactate in HeLa and SiHa cells. Moreover, GF2 suppressed β-catenin and c-Myc stability in the presence and absence of cycloheximide in HeLa cells, respectively. Additionally, the depletion of β-catenin reduced the expression of c-Myc and HK2 in HeLa cells, while pyruvate treatment reversed the ability of GF2 to inhibit β-catenin, c-Myc, and PKM2 in GF2-treated HeLa cells. Notably, GF2 upregulated the expression of microRNA139a-5p (miR139a-5p) in HeLa cells. Consistently, the miR139a-5p mimic enhanced the suppression of β-catenin, c-Myc, and HK2, while the miR193a-5p inhibitor reversed the ability of GF2 to attenuate the expression of β-catenin, c-Myc, and HK2 in HeLa cells. Overall, these findings suggest that GF2 induces apoptosis via the activation of miR193a-5p and the inhibition of β-catenin/c-Myc/HK signaling in cervical cancer cells. Full article
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