Journal: Theranostics

Article Title: Combinative treatment of β-elemene and cetuximab is sensitive to KRAS mutant colorectal cancer cells by inducing ferroptosis and inhibiting epithelial-mesenchymal transformation

doi: 10.7150/thno.44705

Figure Lengend Snippet: Combinative treatment of β-elemene and cetuximab was sensitive to KRAS mutant CRC cells. (A) The sensitivity of KRAS mutant and wild-type colorectal cancer cells to cetuximab treatment (25 µg/ml) for 24 h was detected by CCK-8 assay. The mean ± s.d. is shown. ** P < 0.01. (B) The inhibitory effects and cytotoxicity of co-treatment with β-elemene (125 µg/ml) and cetuximab (25 µg/ml) in KRAS mutant CRC cells was determined after the treatment for 24 h. (C) Representative cell morphological changes are detected by light microscopy. Scale bar = 100 μm. (D) Representative results of annexin V-FITC/PI staining and quantitative analysis after the treatment (β-elemene 125 µg/ml, cetuximab 25 µg/ml) for 24 h. The mean ± s.d. is shown. ** P < 0.01. (E) Representative results of cell cycle and quantitative analysis after the treatment (β-elemene 125 µg/ml, cetuximab 25 µg/ml) for 24 h. (F) The colony-formation assay was performed and colony numbers are shown (β-elemene 125 µg/ml, cetuximab 25 µg/ml). The mean ± s.d. is shown. ** P < 0.01.

Article Snippet: Cetuximab (#33657) was purchased from MCE.

Techniques: Mutagenesis, CCK-8 Assay, Light Microscopy, Staining, Colony Assay

Journal: Theranostics

Article Title: Combinative treatment of β-elemene and cetuximab is sensitive to KRAS mutant colorectal cancer cells by inducing ferroptosis and inhibiting epithelial-mesenchymal transformation

doi: 10.7150/thno.44705

Figure Lengend Snippet: The effect of co-treatment with β-elemene and cetuximab on several ferroptotic events in KRAS mutant CRC cells. (A) The effect of cetuximab and β-elemene in combination with other cell death inhibitors on the cell viability of KRAS mutant HCT116 and Lovo cells after the treatment for 24 h. The mean ± s.d. is shown. (B) The cellular ROS level after the treatment (β-elemene 125 µg/ml, cetuximab 25 µg/ml) for 24 h was analyzed by a flow cytometer, ** P < 0.01. (C) Intracellular GSH level in KRAS mutant HCT116 and Lovo cells after the treatment (β-elemene 125 µg/ml, cetuximab 25 µg/ml) for 24 h was detected, ** P < 0.01. (D) Intracellular MDA levels in KRAS mutant HCT116 and Lovo cells after the treatment (β-elemene 125 µg/ml, cetuximab 25 µg/ml) for 24 h was detected, ** P < 0.01.

Article Snippet: Cetuximab (#33657) was purchased from MCE.

Techniques: Mutagenesis, Flow Cytometry

Journal: Theranostics

Article Title: Combinative treatment of β-elemene and cetuximab is sensitive to KRAS mutant colorectal cancer cells by inducing ferroptosis and inhibiting epithelial-mesenchymal transformation

doi: 10.7150/thno.44705

Figure Lengend Snippet: The iron ion level and mitochondria staining were detected. (A) The chelatable iron was determined using the fluorescent indicator Phen Green SK (green) after the treatment (β-elemene 125 µg/ml, cetuximab 25 µg/ml) for 24 h. Scale bar = 100 µm. (B) The Mitochondria morphology was assessed with Mito-Tracker Green after the treatment (β-elemene 125 µg/ml, cetuximab 25 µg/ml) for 24 h. Scale bar = 50 µm.

Article Snippet: Cetuximab (#33657) was purchased from MCE.

Techniques: Staining

Journal: Theranostics

Article Title: Combinative treatment of β-elemene and cetuximab is sensitive to KRAS mutant colorectal cancer cells by inducing ferroptosis and inhibiting epithelial-mesenchymal transformation

doi: 10.7150/thno.44705

Figure Lengend Snippet: The effect of co-treatment with β-elemene and cetuximab on ferroptosis-related proteins in KRAS mutant CRC cells. (A) The expression of positive regulatory proteins for ferroptosis (HO-1 and transferrin) and the negative regulatory proteins for ferroptosis (GPX4, SLC7A11, FTH1, glutaminase, and SLC40A1) were detected by western blotting after the treatment (β-elemene 125 µg/ml, cetuximab 25 µg/ml) for 24 h. (B) HCT116 and Lovo cells were treated with cetuximab (25 µg/ml) and β-elemene (125 µg/ml) with or without ferroptosis inhibitors for 24 h and cell viability was assayed. The mean ± s.d. is shown. ** P < 0.01.

Article Snippet: Cetuximab (#33657) was purchased from MCE.

Techniques: Mutagenesis, Expressing, Western Blot

Journal: Theranostics

Article Title: Combinative treatment of β-elemene and cetuximab is sensitive to KRAS mutant colorectal cancer cells by inducing ferroptosis and inhibiting epithelial-mesenchymal transformation

doi: 10.7150/thno.44705

Figure Lengend Snippet: Combinative treatment of β-elemene and cetuximab suppressed the migration of KRAS mutant CRC cells by inhibiting EMT. (A) Representative results of wound healing after the treatment (β-elemene 125 µg/ml, cetuximab 25 µg/ml, DFO 20 nM) for 24 h. The mean ± s.d. is shown. ** P < 0.01. (B) Transwell invasion assay was performed by the 24-transwell system and quantitative analysis. The pictures were taken 24 h after seeding (original magnification: × 100). The mean ± s.d. is shown. ** P < 0.01. (C) The expression of several key EMT markers Vimentin, E-Cadherin, N-Cadherin, Slug, Snail and MMP-9 were detected after the treatment (β-elemene 125 µg/ml, cetuximab 25 µg/ml) for 24 h by western blotting.

Article Snippet: Cetuximab (#33657) was purchased from MCE.

Techniques: Migration, Mutagenesis, Transwell Invasion Assay, Expressing, Western Blot

Journal: Theranostics

Article Title: Combinative treatment of β-elemene and cetuximab is sensitive to KRAS mutant colorectal cancer cells by inducing ferroptosis and inhibiting epithelial-mesenchymal transformation

doi: 10.7150/thno.44705

Figure Lengend Snippet: The antitumor efficacy of co-treatment with β-elemene and cetuximab in vivo . (A) The scheme of tumor inoculation and systemic injection. (B) Bioluminescent imaging for HCT116-luc orthotopic xenograft colon tumors at different time points post treatment (β-elemene 50 mg/kg, cetuximab 50 mg/kg) and representative image of metastatic lymph nodes. (C) Fold change in average radiance per mouse at experimental endpoint (day 18) was analyzed for each treatment group. Data are expressed as the mean ± s.d. (D) The survival curves of mice in each group were assessed.

Article Snippet: Cetuximab (#33657) was purchased from MCE.

Techniques: In Vivo, Injection, Imaging

Journal: Frontiers in Oncology

Article Title: Intrinsic Differences in Spatiotemporal Organization and Stromal Cell Interactions Between Isogenic Lung Cancer Cells of Epithelial and Mesenchymal Phenotypes Revealed by High-Dimensional Single-Cell Analysis of Heterotypic 3D Spheroid Models

doi: 10.3389/fonc.2022.818437

Figure Lengend Snippet: List of IMC antibodies.

Article Snippet: 142 Nd , EGFR , D38B1 , 3142013D , Fluidigm , 1:50.

Techniques:

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: Naringenin suppresses epithelial ovarian cancer by inhibiting proliferation and modulating gut microbiota.

doi: 10.1016/j.phymed.2022.154401

Figure Lengend Snippet: Fig. 4. Naringenin suppressed EOC through the PI3K signaling pathway in vitro. Western blotting analysis of lysates (40 μg) of EOC cells treated with naringenin at the indicated concentrations for 24 h (a, b, i, j). Membranes were incubated with antibodies against EGFR (c, f), PI3K (d, g), CCND1 (e, h) and p-PI3K (k, l). All data are expressed as the mean ± SD of values from experiments performed in triplicate. * p < 0.05; ** p < 0.01; *** p < 0.001 compared to ctrl groups.

Article Snippet: Tissues were stained with primary antibodies against EGFR (1:50, A00023-2, Boster, Wuhan, China), PI3K (1:50, bs-4160R, Bioss, Beijing, China) and CCND1 (1:50, BM4272, Boster, Wuhan, China) for immunohistochemical analysis.

Techniques: In Vitro, Western Blot, Incubation

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: Naringenin suppresses epithelial ovarian cancer by inhibiting proliferation and modulating gut microbiota.

doi: 10.1016/j.phymed.2022.154401

Figure Lengend Snippet: Fig. 6. Naringenin suppressed EOC through the PI3K signaling pathway in vivo. HE staining (a) and IHC staining for EGFR (b, f), PI3K (c, g) and CCND1 (d, h) in tumors and quantification (n=5) (Nar p.o. means Nar p.o., per os; ns means not statistically significant, * p < 0.05; ** p < 0.01; *** p < 0.001 compared to untreated; # p < 0.05 Nar p.o., per os compared to Nar i.p.).

Article Snippet: Tissues were stained with primary antibodies against EGFR (1:50, A00023-2, Boster, Wuhan, China), PI3K (1:50, bs-4160R, Bioss, Beijing, China) and CCND1 (1:50, BM4272, Boster, Wuhan, China) for immunohistochemical analysis.

Techniques: In Vivo, Staining, Immunohistochemistry