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Fig. 5 | BMC Cancer

Fig. 5

From: Depletion of PCAT-1 in head and neck cancer cells inhibits tumor growth and induces apoptosis by modulating c-Myc-AKT1-p38 MAPK signalling pathways

Fig. 5

Therapeutic potential of PCAT-1 in HNSCC xenograft model. a: JHU029 cells (1.4 × 106) cells were implanted subcutaneously into the flank of nude mice. After three weeks of palpable tumors (~ 75–90 mm3), 10 μg of siRNA to PCAT-1 or control oligoes were injected intratumorally at an interval of 4 days for a total of ten times. Representative images of tumors in different groups. b: Tumors were measured using a slide calliper, and tumor volumes were calculated (first delivery is indicated by arrow). Small bar indicates standard error (*, p < 0.05). c: Expression of PCAT-1 was examined from RNA of experimental and control tumors by qRT-PCR. 18 s gene was used as internal control. Small bar indicates standard error (***p < 0.001). d: Control or siPCAT-1 treated tumor lysates were subjected to Western blot analysis for c-Myc and AKT1 using specific antibodies. The membrane was reprobed with antibody to actin as an internal control. Right panel shows quantitative representation of Western blot band intensities using Image-J software. Small bar indicates standard error (*, p < 0.05; ** p < 0.01). e: Control or siPCAT-1 treated tumor lysates were subjected to Western blot analysis for PARP using a specific antibody. The membrane was reprobed with antibody to actin as an internal control. f: Schematic diagram showing effect PCAT-1 knockdown on c-Myc -AKT1- p38 MAPK signalling pathway in regulation of cell proliferation and apoptosis. Solid arrows indicate activation and blunt arrows indicate inhibition. Dotted arrows indicate upregulation and downregulation following inhibition of PCAT-1 by siRNA

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