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Modifications of Cellular Radiation Damage
Published in Kedar N. Prasad, Handbook of RADIOBIOLOGY, 2020
EGF present after γ-irradiation increased the radiosensitivity of human squamous carcinoma cells (A431 cells derived from vulva); however, the radiation response of silta cells derived for carcinoma of the cervix was unaffected by such treatments.157 The radiosensitization effect of EGF was dependent upon the cell cycle, being highest in the G1 phase. It was reflected in a reduction of the shoulder of the cell survival curve with almost no change in the slope (Figure 5.7). It is unknown whether EGF will increase the radiosensitivity of normal cells in culture.
Functions of Oncogene and Proto-Oncogene Protein Products
Published in Pimentel Enrique, Oncogenes, 2020
A striking structural homology has been observed between the transforming protein of the v-erb-B oncogene of AEV and the EGF receptor protein purified from a human epidermoid carcinoma cell line (line A431) and human normal placenta.41 Amplification (approximately 30-fold), rearrangement, and enhanced expression of the EGF receptor gene occurs in A431 cells.42 Furthermore, both the c-erb-B gene and the EGF receptor gene are located in the same region of human chromosome 7,43,44 which indicates their possible identity.
Disruption of Cellular Growth Control and Signal Transduction Mechanisms as a Target for Cancer Chemotherapy
Published in Robert I. Glazer, Developments in Cancer Chemotherapy, 2019
The next example in Table 1 (A431 cells) represents a different situation. In this case survival following drug exposure has not been measured, but instead growth has been quantified in the continuous presence of the drug by determining the cell number with time. The data show that at low concentration Adriamycin® is not inactive as might be expected, but actually increases the number of viable dividing cells in the cultures when compared to untreated control cells. Table 1 also shows that DNA synthesis, as judged by thymidine incorporation, can be stimulated in A431 cells.
A PD-L1/EGFR bispecific antibody combines immune checkpoint blockade and direct anti-cancer action for an enhanced anti-tumor response
Published in OncoImmunology, 2023
Laura Rubio-Pérez, Rodrigo Lázaro-Gorines, Seandean L. Harwood, Marta Compte, Rocío Navarro, Antonio Tapia-Galisteo, Jaume Bonet, Belén Blanco, Simon Lykkemark, Ángel Ramírez-Fernández, Mariola Ferreras-Gutiérrez, Carmen Domínguez-Alonso, Laura Díez-Alonso, Alejandro Segura-Tudela, Oana Hangiu, Ainhoa Erce-Llamazares, Francisco J. Blanco, Cruz Santos, José L. Rodríguez-Peralto, Laura Sanz, Luis Álvarez-Vallina
A431 cells were seeded in complete DMEM in 96-well plates. After 24 hours, the medium was replaced by DMEM 1% FBS containing equimolar concentrations (0.19–50 nM) of ctx, atz, IgTT-E or IgTT-1E and incubated for 72 hours. Viability was assessed using the CellTiter-Glo luminescent assay (Promega, cat# G7570). For EGFR signaling studies, A431 cells were starved overnight in DMEM 1% FBS and then incubated for 4 hours in serum-free DMEM in the presence of 0.1 µM ctx, atz, IgTT-E or IgTT-1E, followed by 5 min incubation with 25 ng/ml of human EGF (MiltenyiBiotec, cat# 130-093-825). After stimulation, cells were lysed in Laemmli lysis buffer, separated under reducing conditions on 4–12% Tris-glycine gels, transferred to nitrocellulose membrane and incubated with the rabbit anti-human phosphor-EGFR (Tyr1068) mAb (clone D7A5; Cell Signaling Technology, cat# 3777) followed by incubation with an IRDye800CW-conjugated donkey anti-rabbit antibody (LI-COR Biosciences, cat# 925–32213). Simultaneously, anti-β-actin mouse mAb (Abcam, cat# ab8226) was added as a loading control, followed by IRDye680RD-conjugated donkey anti-mouse (LI-COR Biosciences, cat# 925–68072). Visualization and quantitative analysis of protein bands were carried out with the Odyssey system (LI-COR Biosciences).
Trispecific T-cell engagers for dual tumor-targeting of colorectal cancer
Published in OncoImmunology, 2022
Antonio Tapia-Galisteo, Íñigo Sánchez Rodríguez, Oscar Aguilar-Sopeña, Seandean Lykke Harwood, Javier Narbona, Mariola Ferreras Gutierrez, Rocío Navarro, Laura Martín-García, Cesáreo Corbacho, Marta Compte, Javier Lacadena, Francisco J. Blanco, Patrick Chames, Pedro Roda-Navarro, Luis Álvarez-Vallina, Laura Sanz
A431 cells were seeded at 100.000 cells/well in 12-well plates in DMEM supplemented with 10% FBS and incubated for 24 hours. Afterward, cells were starved for 16 h with 1% FBS DMEM. Subsequently, cells were incubated with serum-free DMEM containing serial dilutions of AxOxE TriTE (200–0 nM) or OxE LiTE at 200 nM. Cetuximab was used as positive control. Then, cells were stimulated for 5 min with 25 ng/mL of human EGF and lysed in Laemmli-lysis buffer (Bio-Rad, CA, USA) for 10 min, on ice. Samples were analyzed by SDS-PAGE and Western blot using iBlot Dry Blotting System (Invitrogen Life Technologies). Membranes were incubated ON with a rabbit anti-human phospho EGFR Tyr1068 mAb (clone D7A5, Cell Signaling, Leiden, The Netherlands) and a anti β-actin mouse mAb (clone 8226, Abcam, Cambridge, UK), followed by incubation with an IRDye800-conjugated donkey anti-rabbit antibody (Rockland Immunochemicals, Limerick, PA, USA) and IRDye680-conjugated donkey anti-mouse antibody (Rockland Immunochemicals). Odyssey infrared imaging system (LI-COR Biosciences, Lincoln, NE, USA) was used to visualize and analyzed protein bands.
UHRF1 Knockdown Attenuates Cell Growth, Migration, and Invasion in Cutaneous Squamous Cell Carcinoma
Published in Cancer Investigation, 2021
Qingyan Li, Zhaowei Chu, Songmei Geng
To interrogate UHRF1 impact on migration and invasion, wound healing assay and transwell assay were exploited. From the results of wound healing assays, we observed that the cell healing rate was 90.80 ± 9.65% in NC group of A431 cells (Figure 4(A,C)) and 96.83 ± 3.02% in NC group of Scl-1 cells (Figure 4(B,D)). In UHRF1 knockdown cells of A431, the healing rate was decreased to 46.29 ± 14.40% and 41.04 ± 3.83%. In UHRF1 knockdown cells of Scl-1, the healing rate was decreased to 81.73 ± 2.26% and 82.24 ± 5.74%. These results demonstrated that knockdown of UHRF1 attenuated migration. In addition, transwell assay demonstrated that the invasion rates of knockdown cells of A431 were only 8.22 ± 1.07% and 6.95 ± 1.08% of the A431 cells (Figure 4(E,F)). In knockdown cells of Scl-1, invasion rates were 71.47 ± 5.21% and 59.95 ± 2.52% of the Scl-1 cells (Figure 4(E,G)). These results indicated that knockdown UHRF1 inhibited migration and invasion potential.