Journal: Oxidative Medicine and Cellular Longevity

Article Title: Zi Shen Decoction Inhibits Growth and Metastasis of Lung Cancer via Regulating the AKT/GSK-3 β / β -Catenin Pathway

doi: 10.1155/2021/6685282

Figure Lengend Snippet: ZSD induced the apoptosis of H1299 cells partially by regulating AKT/GSK-3 β / β -catenin signaling. (a) ZSD induced the apoptosis of H1299 cells after treatment with ZSD (4 mg/mL) for 12 h, 24 h, and 48 h. (b) ZSD induced apoptosis of H1299 cells in a dose-dependent manner. (c) Pathway enrichment analysis of the genes in Human Signal Transduction Pathway Finder PCR Array. (d) The mRNA expression of AKT/GSK-3 β / β -catenin signal cascades in H1299 cells after treatment with ZSD (4 mg/mL). ∗ p < 0.05 and ∗∗ p < 0.01 vs. the control group.

Article Snippet: Antibodies against total AKT and p-AKT, total GSK-3 β and p-GSK-3 β , β -catenin, cleaved caspase-3, and GAPDH were purchased from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Transduction, Expressing

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Zi Shen Decoction Inhibits Growth and Metastasis of Lung Cancer via Regulating the AKT/GSK-3 β / β -Catenin Pathway

doi: 10.1155/2021/6685282

Figure Lengend Snippet: ZSD inhibited the AKT/GSK-3 β / β -catenin pathway in lung cancer cells and tumor tissues. (a) Western blot analysis was used to assess the expression of multiple proteins involved in the AKT/GSK-3 β / β -catenin pathway in lung cancer cells after ZSD treatment for 12 h, 24 h, and 48 h. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the control group. (b) Western blots showing the protein expression of AKT, p-AKT, GSK-3 β , p-GSK-3 β , β -catenin, cleaved caspase-3, and Bax and Bcl-2 in isolated tumor tissues. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the model group.

Article Snippet: Antibodies against total AKT and p-AKT, total GSK-3 β and p-GSK-3 β , β -catenin, cleaved caspase-3, and GAPDH were purchased from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Western Blot, Expressing, Isolation

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Zi Shen Decoction Inhibits Growth and Metastasis of Lung Cancer via Regulating the AKT/GSK-3 β / β -Catenin Pathway

doi: 10.1155/2021/6685282

Figure Lengend Snippet: The AKT/GSK-3 β / β -catenin pathway medicated anticancer effect of ZSD in lung cancer cells. H1299 cells were treated with ZSD and/or SC-79 for 24 h. (a) Representative western blots and quantitative analysis of the AKT/GSK-3 β / β -catenin pathway related proteins. (b) The mobility of H1299 cells was detected by wound-healing assay. (c) The migration and invasion abilities of H1299 cells were detected by transwell assays. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the control group.

Article Snippet: Antibodies against total AKT and p-AKT, total GSK-3 β and p-GSK-3 β , β -catenin, cleaved caspase-3, and GAPDH were purchased from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Western Blot, Wound Healing Assay, Migration

Journal: Evidence-based Complementary and Alternative Medicine : eCAM

Article Title: HRT, Herbal Formula, Induces G 2 /M Cell Cycle Arrest and Apoptosis via Suppressing Akt Signaling Pathway in Human Colon Cancer Cells

doi: 10.1155/2012/871893

Figure Lengend Snippet: HRT inhibited cancer cell proliferation via suppressing Akt signaling. (a) The expression of phosphor-ERK or -Akt was examined in HCT116 cells treated with HRT in a time-dependent manner. HRT induced dephosphorylation of Akt not ERK at 24 h. (b) The effect of HRT on PI3K/Akt signaling pathway. Phosphorylation levels of Akt, mTOR, and GSK3 β were examined in HCT116 cells treated with LY294002 (10 μ M), HRT (300 μ g/mL) or cotreated with LY294002 and HRT for 24 h.

Article Snippet: Primary antibodies against caspase-3, -8, -9, PARP, BID, Akt, phosphor-Akt, ERK, phosphor-ERK, phosphor-GSK3 β , GAPDH, and secondary antibodies were purchased from Cell Signaling (Danver, MA, USA) and cyclin D1, cyclin B1, CDK7, Bcl-2, and β -actin were purchased from Santa Cruz Biotechnology (CA, USA).

Techniques: Expressing, De-Phosphorylation Assay

Journal: Disease Markers

Article Title: Cysteine-Rich Intestinal Protein 1 Served as an Epithelial Ovarian Cancer Marker via Promoting Wnt/ β -Catenin-Mediated EMT and Tumour Metastasis

doi: 10.1155/2021/3566749

Figure Lengend Snippet: The relationship between CRIP1 and EMT indicates that CRIP1 may function in ovarian cancer development via the Wnt/ β -catenin pathway. (a) KEGG pathway enrichment analysis was performed to identify which pathway was significantly enriched in CRIP1-related ovarian cancer progression. (b) The effect of CRIP1 silencing on EMT-related signaling pathways. EMT markers, such as E-cadherin, N-cadherin, and vimentin proteins, were detected by western blot. (c) The effect of CRIP1 silencing on Wnt/ β -catenin signaling pathway. The important molecules of this pathway, including β -catenin, GSK-3 β , p-GSK-3 β , MMP2, and MMP9, were assessed by western blot.

Article Snippet: The antibodies used in this experiment were as follows: β -actin (Cat No. 4970S), β -catenin (Cat No. 8084S), MMP-2 (Cat No. 87809S), and MMP-9 (Cat No. 13667S) were bought from Cell Signaling Technology (Danvers, MA, USA); CRIP1 (Cat No. 15349-1-AP), E-cadherin (Cat No. 20874-1-AP), N-cadherin (Cat No. 22018-1-AP), GSK-3 β (Cat No. 22104-1-AP), and p-GSK-3 β (Cat No. 14850-1-AP) were purchased from Proteintech (Wuhan, China); vimentin (Cat No. bs-8533R) was obtained from Bioss (Beijing, China).

Techniques: Western Blot

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Artemether Activation of AMPK/GSK3 β (ser9)/Nrf2 Signaling Confers Neuroprotection towards β- Amyloid-Induced Neurotoxicity in 3xTg Alzheimer's Mouse Model

doi: 10.1155/2019/1862437

Figure Lengend Snippet: Artemether increased phosphorylation of AMPK/GSK3 β (ser9)in PC12 cell cultures exposed to A β 1-42. (a, c) PC12 cells pretreated for 2 h with different concentrations of Artemether were incubated with 1 μ M A β 1-42 for 24 h .The lysates were submitted for measurements of phosphorylations by western blotting using specific antibodies for AMPK (P-AMPK), total AMPK (T-AMPK), GSK3 β (ser9) (P-GSK3 β ), and total GSK3 β (T-GSK3 β ). GAPDH was used for normalization. Three independent experiments were included. (b, d) Quantitation of phosphorylated kinases. ∗ p < 0.05 and ∗∗ p < 0.01 were considered significantly different.

Article Snippet: Anti-phospho-AMPK, anti-AMPK, anti-phospho-GSK3 β (ser9), anti-GSK3 β , anti-Nrf2, anti-HO-1, anti-phospho-tau, anti-tau, cleaved caspase 3, β -amyloid, anti-GFAP, and anti- β -actin antibodies were purchased from Cell Signaling Technology (Woburn, MA, USA).

Techniques: Incubation, Western Blot, Quantitation Assay

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Artemether Activation of AMPK/GSK3 β (ser9)/Nrf2 Signaling Confers Neuroprotection towards β- Amyloid-Induced Neurotoxicity in 3xTg Alzheimer's Mouse Model

doi: 10.1155/2019/1862437

Figure Lengend Snippet: Direct relationship between Artemether effects on AMPK/GSK3 β (ser9) phosphorylation and neuroprotection towards A β 1-42 -induced apoptotic cell death in PC12 cells. PC12 cells pretreated with 5 μ M compound C (AMPK inhibitor) for 30 min, followed by incubation with 1 μ M A β 1-42 in the presence or absence of different concentrations of Artemether. (a) Cell viability was measured by MTT assay. ∗ p < 0.05 and ∗∗∗ p < 0.001 were considered significantly different. (b) Apoptosis was determined by flow cytometry. (c) Quantitation of the percentage of cell apoptosis. ∗∗∗ p < 0.001 was considered significantly different. (d) Phosphorylation activities of AMPK/GSK3 β (ser9). GAPDH was used for normalization. (e, f) Quantitation of phosphorylation activities of AMPK/GSK3 β . All results are presented as mean ± SEM ( n = 3); ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 were considered significantly different.

Article Snippet: Anti-phospho-AMPK, anti-AMPK, anti-phospho-GSK3 β (ser9), anti-GSK3 β , anti-Nrf2, anti-HO-1, anti-phospho-tau, anti-tau, cleaved caspase 3, β -amyloid, anti-GFAP, and anti- β -actin antibodies were purchased from Cell Signaling Technology (Woburn, MA, USA).

Techniques: Incubation, MTT Assay, Flow Cytometry, Quantitation Assay

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Artemether Activation of AMPK/GSK3 β (ser9)/Nrf2 Signaling Confers Neuroprotection towards β- Amyloid-Induced Neurotoxicity in 3xTg Alzheimer's Mouse Model

doi: 10.1155/2019/1862437

Figure Lengend Snippet: Artemether stimulated the phosphorylation of AMPK/GSK3 β (ser9) and increased the expression levels of Nrf2 and heme oxygenase-1 (HO-1) in the brain cortex of 3xTg-AD mice. Artemether was administered to mice by intraperitoneal injection, once a day, at low doses of 5 mg/kg and high doses of 20 mg/kg for 4 weeks. Thereafter, the brain cortex extracts of wild-type (WT) compared to 3xTg-AD mice treated with either a low (Arte low) or high dose (Arte high) of Artemether or untreated (3xTg) were submitted for analyses. (a) Phosphorylations of AMPK/GSK3 β (ser9) and protein expression levels of Nrf2 and heme oxygenase-1 (HO-1); three mice per treatment group were used for western blot. (b–e) Quantitation of western blotting results of the different experimental groups. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 were considered significantly different.

Article Snippet: Anti-phospho-AMPK, anti-AMPK, anti-phospho-GSK3 β (ser9), anti-GSK3 β , anti-Nrf2, anti-HO-1, anti-phospho-tau, anti-tau, cleaved caspase 3, β -amyloid, anti-GFAP, and anti- β -actin antibodies were purchased from Cell Signaling Technology (Woburn, MA, USA).

Techniques: Expressing, Injection, Western Blot, Quantitation Assay

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Artemether Activation of AMPK/GSK3 β (ser9)/Nrf2 Signaling Confers Neuroprotection towards β- Amyloid-Induced Neurotoxicity in 3xTg Alzheimer's Mouse Model

doi: 10.1155/2019/1862437

Figure Lengend Snippet: A schematic diagram of Artemether-induced AMPK/GSK3 β (ser9)/Nrf2 activation towards reduction of amyloid- β -evoked oxidative stress to confer neuroprotection. Artemether stimulated AMPK/GSK3 β (ser9) phosphorylation output in neuronal cells and animal brain cortex to increase the nuclear expression of Nrf2 with induction of the phase II antioxidant enzymes and anti-inflammatory genes containing ARE. This process (dotted line) caused attenuation of APP-derived and A β -induced ROS production, reduction of oxidative stress, correction of mitochondrial dysfunction, reduction of inflammation, and conferring neuroprotection.

Article Snippet: Anti-phospho-AMPK, anti-AMPK, anti-phospho-GSK3 β (ser9), anti-GSK3 β , anti-Nrf2, anti-HO-1, anti-phospho-tau, anti-tau, cleaved caspase 3, β -amyloid, anti-GFAP, and anti- β -actin antibodies were purchased from Cell Signaling Technology (Woburn, MA, USA).

Techniques: Activation Assay, Expressing, Derivative Assay