Ganoderiol F purified from <i>Ganoderma leucocontextum</i> retards cell cycle progression by inhibiting CDK4/CDK6

Li, Xiangmin; Xie, Yizhen; Peng, Juanjuan; Hu, Huiping; Wu, Qingping; Yang, Burton B.

doi:10.1080/15384101.2019.1667705

Cited by 17 publications

(8 citation statements)

References 44 publications

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“…Ganoderma leucocontextum is a new species of Ganoderma discovered in southwestern China in 2014 [16]. Several studies have revealed that terpenoids from G. leucocontextum possess potential beneficial effects, including antidiabetic [17], antitumor [18], and neuroprotective activities [19]. However, the structural characteristics and antioxidant activities of polysaccharides from G. leucocontextum remain mostly unknown.…”

Section: Introductionmentioning

confidence: 99%

Purification, Physicochemical Properties, and Antioxidant Activities of Two Low-Molecular-Weight Polysaccharides from Ganoderma leucocontextum Fruiting Bodies

Guan

et al. 2021

Antioxidants

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Two low-molecular-weight polysaccharides (GLP-1 and GLP-2) were purified from Ganoderma leucocontextum fruiting bodies, and their physicochemical properties and antioxidant activities were investigated and compared in this study. The results showed that GLP-1 and GLP-2 were mainly composed of mannose, glucose, galactose, xylose, and arabinose, with weight-average molecular weights of 6.31 and 14.07 kDa, respectively. Additionally, GLP-1 and GLP-2 had a similar chain conformation, crystal structure, and molecular surface morphology. Moreover, GLP-1 exhibited stronger antioxidant activities than GLP-2 in five different assays: 2,2′-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS), hydroxyl radical, superoxide anion radical, ferric reducing antioxidant power (FRAP), and oxygen radical antioxidant capacity (ORAC). The main linkage types of GLP-1 were found to be →4)-α-D-Glcp-(1→, →4)-β-D-Glcp-(1→, →3)-β-D-Glcp-(1→, →6)-β-D-Galp-(1→, →6)-α-D-Glcp-(1→, →4,6)-α-D-Glcp-(1→, and Glcp-(1→ by methylation analysis and nuclear magnetic resonance (NMR) spectroscopy. In addition, GLP-1 could protect NIH3T3 cells against tert-butyl hydroperoxide (tBHP)-induced oxidative damage by increasing catalase (CAT) and glutathione peroxidase (GSH-Px) activities, elevating the glutathione/oxidized glutathione (GSH/GSSG) ratio, and decreasing the malondialdehyde (MDA) level. These findings indicated that GLP-1 could be explored as a potential antioxidant agent for application in functional foods.

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Section: Introductionmentioning

confidence: 99%

Purification, Physicochemical Properties, and Antioxidant Activities of Two Low-Molecular-Weight Polysaccharides from Ganoderma leucocontextum Fruiting Bodies

Guan

et al. 2021

Antioxidants

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“…Cyclin D1 is an essential regulator of the G1-S transition in response to growth factor stimulation in cells [22], CDK4 and CDK6 are also critical factors for G1-S transition. [23] We found that the relative mRNA expression of CDK6 and CYCLIN D1 dramatically decreased with the treatment of JQ1 (Fig. 2d and 2f).…”

Section: Jq1 Arrested Cell Cycle Of Mv-4-11 Cell Lines At G0/g1 Phasementioning

confidence: 76%

JQ1 Inhibits Proliferation and Induces Apoptosis of Leukemia Cells Through BCL-2 Regulated Pathway

Zeng¹,

Liang²,

Xia³

et al. 2021

Preprint

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Objective To explore the mechanism of JQ1 on leukemia cells. Methods This study takes two myeloid leukemia cell lines as a research model. Cells treated with high concentration of JQ1 were collected for quantitative real-time PCR, immunoblot and flow cytometry to verify the effects of JQ1 on myeloid leukemia tumor cells. Combined with mRNA sequencing of cell lines to identify the differences in mRNA expression of different cell lines. Results Two cell lines changed cell morphology under JQ1 treatment. The cell membrane appeared in varying degrees of wrinkled internal subsidence. K562 cell lines can maintain stable proliferation after being induced by a specific concentration of JQ1. However, JQ1 cannot induce the death of the K562 cells. Although the MYC and BCL2 gene expression decreased, JQ1 did not affect the c-Myc targeted genes to affect the cell cycle, nor did it trigger the BCL2-mediated apoptosis pathway. On the contrary, after JQ1 induced the MV-4-11 cells, the MYC-mediated cell cycle significantly slowed down and arrested at the G0/G1 phase. The death of MV-4-11 tumor cells through the apoptosis pathway regulated by BCL-2 family. Conclusion JQ1 has different pharmacological effects on two myeloid leukemia cell lines. For MV-4-11, JQ1 mainly inhibited cell cycle by regulating MYC pathway and induced BCL-2-mediated apoptosis to kill myeloid leukemia tumor cells and thus perform anti-tumor effects. K-562 cells showed drug resistance to JQ1 which confirmed that the K-562 cell line has a feedback mechanism that prevents JQ1-induced apoptosis.

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“…Studies have shown that the overexpression of CDKs could cause the tumor proliferation to go out of control and lead to tumor malignancy and metastasis [ 33 , 34 ]. Inhibiting or downregulating the expression of CDK2 and CDK4 delays or inhibits cell cycle progression and reduces tumor proliferation and metastasis [ 35 – 37 ]. This finding was also consistent with the results of the present research.…”

Section: Discussionmentioning

confidence: 99%

Identification of genes and pathways leading to metastasis and poor prognosis in melanoma

Zhang

Wang

et al. 2021

Aging

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Melanoma causes the highest mortality rate among all skin cancers. However, the underlying molecular mechanisms leading to metastasis and poor prognosis in melanoma have not been fully elucidated. In this study, the differentially expressed genes (DEGs) related to metastasis in melanoma were screened out. The results of gene annotation was combined with The Cancer Genome Atlas (TCGA) database. The microRNA (miRNA) network that regulates key genes and their correlation with BRAF V600E was preliminarily analyzed. Cell and molecular biology experiments were conducted to verify the results of bioinformatics analysis. Results showed that the PI3K-Akt signaling pathway contained the key genes CDK2 , CDK4 , KIT , and Von Willebrand factor . Survival analysis showed that high expression of the four key genes significantly reduced the survival rate of patients with melanoma. Correlation analysis showed that BRAF V600E may regulate the expression of the four key genes, and a total of 240 miRNAs may regulate this expression. Experiments showed that the inactivation of key genes inhibits the proliferation, migration, and invasion of melanoma. In conclusion, the PI3K-Akt signaling pathway and the four key genes promoted the proliferation, migration, and invasion of melanoma, and related to poor prognosis of patients with melanoma.

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Ganoderiol F purified from Ganoderma leucocontextum retards cell cycle progression by inhibiting CDK4/CDK6

Cited by 17 publications

References 44 publications

Purification, Physicochemical Properties, and Antioxidant Activities of Two Low-Molecular-Weight Polysaccharides from Ganoderma leucocontextum Fruiting Bodies

Purification, Physicochemical Properties, and Antioxidant Activities of Two Low-Molecular-Weight Polysaccharides from Ganoderma leucocontextum Fruiting Bodies

JQ1 Inhibits Proliferation and Induces Apoptosis of Leukemia Cells Through BCL-2 Regulated Pathway

Identification of genes and pathways leading to metastasis and poor prognosis in melanoma

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