Fig. 8: UPF1 regulates ECSC initiation via the LINC00963/miR-508-5p axis in vivo. | Cell Death & Disease

Fig. 8: UPF1 regulates ECSC initiation via the LINC00963/miR-508-5p axis in vivo.

From: UPF1 contributes to the maintenance of endometrial cancer stem cell phenotype by stabilizing LINC00963

Fig. 8: UPF1 regulates ECSC initiation via the LINC00963/miR-508-5p axis in vivo.The alternative text for this image may have been generated using AI.

Tumorigenicity assessed by the A morphology, B volumes, and C weights of xenografts formed from ECSCs transfected with sh-NC and sh-UPF1 (n = 3, each group). D Tumorigenicity initiating capacity of the minimum number of ECSCs transfected with sh-NC and sh-UPF1 (n = 6, each group). E The nude mice carrying tumors from the respective groups are shown. The sample tumors from the respective groups are shown (n = 3, each group). F Tumor growth curves are shown (n = 3, each group). G Expression of SOX2, OCT4, and NANOG from the respective groups assessed using western blotting (n = 3, each group). The results are presented as the ratio of the integrated density values of SOX2, OCT4, and NANOG versus Tubulin. The graphs represent the alteration in relation to the control group (protein of interest/Tubulin equal to 1). H Apoptosis of tumors from the respective groups detected using TUNEL assays (n = 3, each group). I The primary and secondary spheres numbers of xenograft-derived cells detected by serial sphere formation assay (n = 3, each group). J The proposed mechanism underlying the UPF1/LINC00963/miR-508-5p/SOX2 axis in ECSCs. Data are presented as the means ± SEM (n = 3, each group), *P < 0.05, **P < 0.01, ***P < 0.001 vs. Control group, #P < 0.05, ##P < 0.01 vs. sh-UPF1 group, △△P < 0.01 vs. sh-LINC00963 group, ▲P < 0.05, ▲▲P < 0.01 vs. Agomir-508-5p group. Scale bars, 50 μm.

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