Journal: British Journal of Cancer

Article Title: Molecular disruption of NBS1 with targeted gene delivery enhances chemosensitisation in head and neck cancer

doi: 10.1038/sj.bjc.6605980

Figure Lengend Snippet: Transgene expression of mutant NBS1 interacts with MRN after Ad-NBS1 gene transfer and significantly reduces the expression of wild-type RAD50 and NBS1. ( A ) Anti-MRE11 antibody Co-IP wild-type NBS1 in all cells. It indicated direct interaction between MRE11 and wild-type NBS1 (lanes 2, 4, 6 and 8). Mutant NBS1 was Co-IP in Ad-NBS1-infected cells, indicated direct interaction between MRE11 and mutant NBS1 (lane 8). A significant downregulation of wild-type NBS1 protein was observed in cells infected with Ad-NBS1 (lane 8) relative to non-infected cells (lanes 2, 4 and 6). All lanes shown were run simultaneously on a single gel as contiguous lanes. Lane 1: control cells; lane 2: control cells after Co-IP with MRE11 antibody; lane 3: cells treated with cisplatin (0.3 μ g ml −1 ); lane 4: cisplatin-treated cells after Co-IP with MRE11antibody; lane 5: Ad-GFP-infected cells; lane 6: Ad-GFP-infected cells after Co-IP; lane 7: Ad-NBS1-infected cells and lane 8: Ad-NBS1-infected cells after Co-IP with MRE11 antibody. ( B – D ) Wild-type MRE11 was not downregulated after infection of JHU006 cells with Ad-NBS1 relative to non-infected controls or Ad-GFP controls ( B ). Downregulation of wild-type RAD50 ( P <0.05; C ) and NBS1 proteins ( P <0.01; D ) is seen after infection with Ad-NBS1 when compared with non-infected controls or Ad-GFP controls.

Article Snippet: The human HNSCC cell line JHU006 (originally derived at the Johns Hopkins University Head and Neck Laboratories, Baltimore, MD, USA) was used in all experiments.

Techniques: Expressing, Mutagenesis, Co-Immunoprecipitation Assay, Infection, Control

Journal: Analytical Cellular Pathology (Amsterdam)

Article Title: FAP Serves as a Prognostic Biomarker in Head and Neck Squamous Cell Carcinoma

doi: 10.1155/2024/8810804

Figure Lengend Snippet: Regulatory role of FAP in cellular proliferation and apoptosis in HNSCC. (a) Western blot analysis across diverse HNSCC cell lines unveils elevated FAP expression in the SCC15 cell line. (b) Following FAP knockout in SCC15 cells, WB data clearly reveal a notable downregulation of FAP expression. (c) qPCR assays provide further evidence of the efficiency of FAP silencing in SCC15 cells. (d) A significant decline in SCC15 cell proliferation was observed post-FAP knockout, as confirmed by CCK8 assays. (e and f) Apoptotic status of SCC15 cells post-FAP knockout: (e) depicts a representative micrograph of apoptotic cells, and (f) offers a quantitative assessment of apoptosis. (g) WB data confirm a marked increase in FAP expression following its overexpression in HN6 cells. (h) qPCR assays validate the efficiency of FAP overexpression in HN6 cells. (i) FAP overexpression led to a noticeable enhancement in the proliferation of HN6 cells, as evidenced by CCK8 assays. (j and k) Apoptotic status of HN6 cells post-FAP overexpression: (j) shows a typical image of apoptotic cells, and (k) presents a quantitative analysis of apoptosis. ∗∗ p < 0.01 and ∗∗∗ p < 0.001.

Article Snippet: HNSCC cell lines, procured from the China Center for Type Culture Collection, were cultured in DMEM medium (Gibco) and maintained at 37°C in a 5% CO 2 atmosphere.

Techniques: Western Blot, Expressing, Knock-Out, Over Expression