ginsenoside-rg3 and Carcinoma--Squamous-Cell

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal).\ \ This article has been retracted at the request of the Editor-in-Chief.\ \ Given the comments regarding this article https://pubpeer.com/publications/917A4D8593F06C8E5ADC7AA0A30136, particularly regarding the background of the Western Blots from Figure 2B, the journal requested the authors to provide the raw data. However, the authors were not able to fulfil this request and therefore the Editor-in-Chief decided to retract the article.

Topics: Apoptosis; Carcinoma, Squamous Cell; Cell Line, Tumor; Cell Proliferation; Down-Regulation; Epithelial-Mesenchymal Transition; Female; Ginsenosides; Humans; Male; MAP Kinase Signaling System; MicroRNAs; Middle Aged; Mouth Neoplasms; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt

The metastatic rate of human cutaneous squamous cell carcinoma (CSCC) has increased in recent years. Despite the current advances in therapies, effective treatments remain lacking. Ginsenoside 20(R)-Rg3 is an effective antitumor monomer extracted from ginseng, but the role of Rg3 in CSCC remains unknown. It has been reported that aberrantly elevated histone deacetylase 3 (HDAC3) is involved in tumor malignancy in multiple malignant tumors. However, the effects of HDAC3 on the regulation of c-Jun acetylation in tumor epithelial-mesenchymal transition (EMT) and migration have not been clearly illuminated. In our research, the immunohistochemistry staining results of skin tissue microarrays showed that HDAC3 staining was increased in CSCC compared with the normal dermal tissue. Then, we found that Rg3 treatment (25 and 50 μg/ml) inhibited CSCC cell (A431 and SCC12 cells) EMT through increasing E-cadherin and decreasing N-cadherin, vimentin, and Snail expression. Wound-healing and transwell assays showed that Rg3 could inhibit migration. Meanwhile, Rg3 significantly downregulated the expression of HDAC3 in CSCC cells as detected by real-time quantitative PCR, western blot, and immunofluorescence. Importantly, c-Jun acetylation was increased by the downregulation of HDAC3 with HDAC3 shRNA, and the downregulation was associated with CSCC cell EMT inhibition. Collectively, our results showed that downregulation of HDAC3 by Rg3 or shHDAC3 treatment resulted in c-Jun acetylation, which in turn inhibited CSCC cell EMT. These results indicate that HDAC3 could potentially serve as a therapeutic target therapeutic target for CSCC. Rg3 is an attractive and efficient agent that has oncotherapeutic effects and requires further investigation.

Topics: Acetylation; Carcinoma, Squamous Cell; Cell Line, Tumor; Cell Movement; Dermis; Down-Regulation; Epithelial-Mesenchymal Transition; Gene Expression Regulation, Neoplastic; Ginsenosides; Histone Deacetylases; Humans; Proto-Oncogene Proteins c-jun; Skin Neoplasms; Up-Regulation

To study the anti-angiogenic effect of ginsenoside Rg3 (Rg3 in abbreviation) in human nasopharyngeal carcinoma HNE-1 cells in vitro.. The tube-like structure (TLS) formation of HNE-1 cells, cultured in medium with different concentrations of Rg3, was determined by in vitro anti-angiogenic test based on preliminary experiment observing the TLSs formed by HNE-1 cells on Matrigel and their structural characteristics. The VEGF expression level in HNE-1 cells was determined by immunohistochemistry (IHC) and Western-blot test after 48-hour cultured in medium with different concentrations of Rg3.. HNE-1 cells could form TLSs and mosaic vessels when mix-cultured with CRL-2480 on Matrigel. Rg3 could inhibit the TLS formation of HNE-1 cells. After 24-hour culture in medium with Rg3 at concentrations of 0, 50, 100 and 200 µg/ml, the number of TLSs were 75.50 ± 6.86, 55.00 ± 11.92, 39.75 ± 7.93 and 24.50 ± 6.25, respectively, which were negatively correlated with the concentrations of Rg3 (r = -0.928; P < 0.01). After 48 hours of culture, the expressions of VEGF significantly declined by IHC test with results as 0.19 ± 0.03, 0.13 ± 0.02, 0.11 ± 0.01, and 0.08 ± 0.01, respectively, which were negatively correlated with the concentrations of Rg3 (r = -0.911; P < 0.01). The expressions of VEGF also gradually decreased as revealed by Western blot test, with corresponding results as 119.49, 111.51, 86.45, and 38.29. All of the tests showed significantly declined results in the group at the concentration of 200 µg/ml Rg3.. Rg3 can inhibit the vasculogenic mimicry of HNE-1 cells, and the possible mechanism might be associated with the down-regulation of VEGF protein expression in HNE-1 cells.

Topics: Angiogenesis Inhibitors; Carcinoma, Squamous Cell; Cell Line; Cell Line, Tumor; Coculture Techniques; Dose-Response Relationship, Drug; Down-Regulation; Endothelial Cells; Ginsenosides; Humans; Nasopharyngeal Neoplasms; Neovascularization, Pathologic; Umbilical Veins; Vascular Endothelial Growth Factor A

To study the mechanism and effect of gensenoside Rg3 on Hep-2 Cell Line during the normoxia and hypoxia.. Hep-2 Human Laryngeal Cancer Cell Line was cultured under anoxic conditions, and set the normal control group and positive control group (DDP). MTT was used to observe the growth inhibition rates of Hep-2 Human Laryngeal Cancer Cell by Rg3; The cell cycle and cell apoptosis analysis were detected by FCM. Then the expression of HIF-1alpha and VEGF protein was detected by immunohistochemistry and FCM; The expression of HIF-1alpha and VEGF mRNA were detected by transcription-polymerase chain reaction (RT-PCR).. Rg3 could significantly inhibit the growth of Hep-2 cells and arrest the cells in G0/G1 phase during normoxia and hypoxia The mRNA and protein expression of HIF-1alpha were dolon-regulated.. Rg3 can inhibit Hep-2 cells growth by delaying the progress of cell cycle and inhibit the expression of HIF-1alpha during hypoxia, this may be the mechanism of its anti-tumor effect.

Topics: Antineoplastic Agents, Phytogenic; Apoptosis; Carcinoma, Squamous Cell; Cell Cycle; Cell Hypoxia; Cell Line, Tumor; Cisplatin; Dose-Response Relationship, Drug; Flow Cytometry; Ginsenosides; Humans; Hypoxia-Inducible Factor 1, alpha Subunit; Immunohistochemistry; Laryngeal Neoplasms; Panax; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger

To investigate the effect of ginsenoside Rg3 on the apoptosis and survivin expression in human lung squamous cell carcinoma cell line SK-MES-1.. SK-MES-1 cells were divided into Rg3 treatment group, blank control group and positive control (arsenic trioxide) group. The apoptotic rate of the cells in each group was determined using flow cytometry, and the expression of survivin protein and mRNA was detected by immunocytochemistry and RT-PCR, respectively.. A 48-h treatment with Ginsenoside Rg3 induced increased apoptotic rate of SK-MES-1 cells in a dose-dependent manner. Ginsenoside Rg3 significantly downregulated the expressions of survivin protein and mRNA as compared with the expression levels in the blank control group (P<0.05).. Ginsenoside Rg3 can induce the apoptosis of SK-MES-1 cells, the mechanism of which may involve inhibited survivin expression.

Topics: Apoptosis; Carcinoma, Squamous Cell; Cell Line, Tumor; Down-Regulation; Ginsenosides; Humans; Inhibitor of Apoptosis Proteins; Lung Neoplasms; Microtubule-Associated Proteins; RNA, Messenger; Survivin

To investigate the inhibitive effects of Ginsenosides Rg3 (GS-Rg3) in the process of tumor angiogenesis and the effects on the expressions of VEGF and its receptor KDR in human lung squamous cancer SK-MES-1 cell line.. Human lung cancer SK-MES-1 cells were cultured in vitro and immunocytochemistry and RT-PCR methods were used to detect the effects of different concentrations of Rg3 on the expressions of VEGF and KDR on SK-MES-1 cells.. The immunocytochemistry results showed that the positive rates of VEGF protein in different group of SK-MES-1 cells were 81.33 +/- 9.04, 61.80 +/- 7.98, 43.80 +/- 5.25, 29.77 +/- 8.04, respectively. The positive rates of KDR protein in different group of SK-MES-1 cells were 65.51 +/- 7.45, 51.73 +/- 9.21, 34.87 +/- 6.15, 22.04 +/- 5.11, respectively. There were significant differences between each group. RT-PCR results suggested that with the increase of the concentration of Rg3, VEGF and KDR amplified bands gradually weakened. There were significant differences between each group.. GS-Rg3 can down-regulate the expressions of KDR and VEGF protein and their mRNA in human lung squamous cancer SK-MES-1 cells. It may be one of the mechanisms in the process of inhibiting tumor angiogenesis.

Topics: Antineoplastic Agents, Phytogenic; Carcinoma, Squamous Cell; Cell Line, Tumor; Dose-Response Relationship, Drug; Ginsenosides; Humans; Immunohistochemistry; Lung Neoplasms; Neovascularization, Pathologic; Panax; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-2