u-0126 and baicalein

u-0126 has been researched along with baicalein* in 4 studies

Other Studies

4 other study(ies) available for u-0126 and baicalein

ArticleYear
Baicalein inhibits fibronectin-induced epithelial-mesenchymal transition by decreasing activation and upregulation of calpain-2.
    Cell death & disease, 2019, 04-18, Volume: 10, Issue:5

    The extracellular matrix protein fibronectin (FN) facilitates tumorigenesis and the development of breast cancer. Inhibition of the FN-induced cellular response is a potential strategy for breast cancer treatment. In the present study, we investigated the effects of the flavonoid baicalein on FN-induced epithelial-mesenchymal transition (EMT) in MCF-10A breast epithelial cells and in a transgenic mouse MMTV-polyoma middle T antigen breast cancer model (MMTV-PyMT). Baicalein inhibited FN-induced migration, invasion, and F-actin remodeling. Baicalein also suppressed FN-induced downregulation of the epithelial markers E-cadherin and ZO-1 and upregulation of the mesenchymal markers N-cadherin, vimentin, and Snail. Further investigation revealed that calpain-2 was involved in baicalein suppression of FN-induced EMT. Baicalein significantly decreased FN-enhanced calpain-2 expression and activation by suppressing its plasma membrane localization, substrate cleavage, and degradation of its endogenous inhibitor calpastatin. Overexpression of calpain-2 in MCF-10A cells by gene transfection partially blocked the inhibitory effect of baicalein on FN-induced EMT changes. In addition, baicalein inhibited calpain-2 by decreasing FN-increased intracellular calcium ion levels and extracellular signal-regulated protein kinases activation. Baicalein significantly decreased tumor onset, growth, and pulmonary metastasis in a spontaneous breast cancer MMTV-PyMT mouse model. Baicalein also reduced the expression of FN, calpain-2, and vimentin, but increased E-cadherin expression in MMTV-PyMT mouse tumors. Overall, these results revealed that baicalein markedly inhibited FN-induced EMT by inhibiting calpain-2, thus providing novel insights into the pharmacological action and mechanism of baicalein. Baicalein may therefore possess therapeutic potential for the treatment of breast cancer though interfering with extracellular matrix-cancer cell interactions.

    Topics: Animals; Breast Neoplasms; Butadienes; Cadherins; Calcium; Calpain; Cell Line, Tumor; Epithelial-Mesenchymal Transition; Extracellular Signal-Regulated MAP Kinases; Female; Fibronectins; Flavanones; Humans; Kaplan-Meier Estimate; Mice; Mice, Transgenic; Nitriles; Up-Regulation; Zonula Occludens-1 Protein

2019
The restraining effect of baicalein and U0126 on human cervical cancer cell line HeLa.
    Molecular medicine reports, 2017, Volume: 16, Issue:1

    To explore the restraining effect of baicalein and the mitogen-activation protein kinase kinase inhibitor, U0126, on human cervical cell line HeLa proliferation, apoptosis and migration. HeLa cells were treated by different concentrations of baicalein or U0126. A Cell Counting Kit (CCK)‑8 assay was applied to examine cell viability. Flow cytometry was used to determine cell cycle and apoptosis. A wound healing assay was performed to detect cell migration. A terminal deoxynucleotidyl transferase dUTP nick end labeling assay was adopted to test cell apoptosis. Reverse transcription‑quantitative polymerase chain reaction and western blot analysis was used to detect apoptosis gene and protein expression. CCK‑8 assay demonstrated that baicalein and U0126 suppressed HeLa cell viability by dose dependence. TUNEL, Annexin V‑fluorescein isothiocyanate/propidium iodide, and ratio of Bcl‑2‑associated X protein and B cell lymphoma 2 indicated that baicalein and U0126 induced HeLa cell apoptosis. Flow cytometry revealed that baicalein blocked the cell cycle of HeLa in G0/G1 phase. A wound healing assay demonstrated that baicalein significantly inhibited HeLa cell migration compared with control. Baicalein and U0126 markedly downregulated extracellular signal‑regulated kinase 1/2, matrix metalloproteinase (MMP) 2 and MMP9 levels both in mRNA and protein. In the present study, the authors demonstrated that baicalein and U0126 may be used in cervical cancer treatment by inhibiting cell migration and inducing cell apoptosis.

    Topics: Antineoplastic Agents; Apoptosis; Butadienes; Cell Cycle; Cell Line, Tumor; Cell Movement; Cell Proliferation; Cell Survival; Dose-Response Relationship, Drug; Flavanones; HeLa Cells; Humans; MAP Kinase Signaling System; Nitriles

2017
The anti-metastatic effect of baicalein on colorectal cancer.
    Oncology reports, 2017, Volume: 37, Issue:4

    Baicalein, a naturally occurring flavonoid isolated from the roots of Scutellaria baicalensis, is historically and widely used as anti-inflammatory and anticancer therapy. Nevertheless, the anti-metastatic effect and underlying molecular mechanisms of baicalein on colorectal carcinoma (CRC) remain unclear. The aim of the present study was, therefore, to invastigate the anti-metastatic activity of baicalein and related mechanism(s) on CRC cells. In this study, we observed that baicalein treatment inhibited proliferation, as well as migration and invasion of HT-29 and DLD1 cells. Baicalein decreased the expression of the matrix metalloproteinases-2 (MMP-2) and MMP-9 in a dose-dependent manner. Also, baicalein treatment significantly reduced phosphorylation of extracellular signal regulated kinases (ERK). Furthermore, in DLD1 cells, MEK1 overexpression partially blocked the anti-metastatic effects of baicalein. Combined treatment with an ERK inhibitor (U0126) and baicalein led to the synergistic reduction of MMP-2/9 expression; and the invasive capabilities of DLD1 cells were also inhibited markedy. Finally, intragastric administration of baicalein inhibited CRC xenograft growth in vivo and suppressed the phosphorylation of ERK and the expression of MMP-2/9 in tumor tissues. Consequently, baicalein suppresses CRC cell invasion via inhibition of the ERK signaling pathways, indicating that baicalein is a potential agent for CRC treatment.

    Topics: Animals; Butadienes; Cell Line, Tumor; Cell Movement; Cell Proliferation; Colorectal Neoplasms; Dose-Response Relationship, Drug; Drug Synergism; Flavanones; Gene Expression Regulation, Neoplastic; HT29 Cells; Humans; MAP Kinase Signaling System; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; Mice; Neoplasm Invasiveness; Neoplasm Metastasis; Nitriles; Phosphorylation; Xenograft Model Antitumor Assays

2017
[Baicalein promotes the apoptosis of HeLa cells by inhibiting ERK1/2 expression].
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology, 2016, Volume: 32, Issue:11

    Objective To investigate the effects of baicalein and U0126 treatment on the apoptosis of human cervical carcinoma HeLa cells and the potential mechanism. Methods HeLa cells were subjected to (1, 2, 5, 10, 20, 50, 100, 200, 300) μmol/L baicalein or (1, 2, 5, 10, 20, 30) μmol/L U0126 treatment for 24 hours. The optimal concentrations of baicalein and U0126 for HeLa inhibition was determined by a cell counting Kit-8 assay. HeLa cells were then treated with these inhibitory concentrations for 24 hours separately or in combination. The cell cycle and the degree of apoptosis were analyzed by flow cytometry. The cell apoptosis index was evaluated by the TUNEL assay. The expressions of extracellular signal-regulated kinase 1/2 (ERK1/2), Bax, and Bcl-2 at the mRNA and protein levels were examined by real-time PCR and Western blotting, respectively. Results Optimal inhibitory concentrations of baicalein and U0126 for HeLa cells were 200 μmol/L and 10 μmol/L, respectively. Compared with the control group, baicalein treatment increased the growth rate of cells in the G0/G1 phase but decreased the S phase. Combination treatment of 200 μmol/L baicalein and 10 μmol/L U0126 for 24 hours further reduced the S phase growth rate. Treatment with 10 μmol/L U0126 or 200 μmol/L baicalein for 24 hours induced cell apoptosis, and the combination treatment induced more apoptosis. Treatment by baicalein alone or in combination with U0126 for 24 hours significantly decreased ERK1/2 and Bcl-2 mRNA expressions, and upregulated Bax mRNA expression. It also downregulated ERK1/2 phosphorylation and Bcl-2 protein expression, while increasing Bax protein expression. Conclusion Both baicalein and U012 appear to inhibit proliferation, induce apoptosis, and increase the growth rate in the G0/G1 phase but reduce the S phase of HeLa cells. This effect is enhanced when they are used synergistically.

    Topics: Apoptosis; bcl-2-Associated X Protein; Butadienes; Flavanones; Flow Cytometry; HeLa Cells; Humans; Mitogen-Activated Protein Kinase 1; Nitriles; Proto-Oncogene Proteins c-bcl-2

2016