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<p>Long non-coding RNA MINCR performs a tumor-promoting role in various cancers. Accordingly, this research analyzed whether MINCR exerted tumor-promoting effects and facilitated gemcitabine (GEM) resistance in BC. MINCR, microRNA (miR)-876-5p, ZEB1, and PHGDH expression was detected in BC tissues and cells. Following the construction of GEM-resistant cells, MINCR expression was examined with RT-qPCR. Gain- and loss-of-function assays were conducted in GEM-resistant cells, followed by the measurement of cell proliferation, invasion, and apoptosis. The relationships among MINCR, miR-876-5p, and ZEB1 were assessed with dual-luciferase and RIP assays. Subcutaneous tumor formation in nude mice was conducted for in vivo corroboration. MINCR was up-regulated in BC tissues and cells and GEM-resistant BC cells. miR-876-5p expression was poor and ZEB1 and PHGDH expression was abundant in BC tissues. Mechanistically, MINCR enhanced ZEB1 expression in BC cells via competitive binding to miR-876-5p, and ectopic ZEB1 induced PHGDH up-regulation. MINCR silencing diminished proliferation and invasion while accelerating apoptosis in GEM-resistant BC cells, which was further advanced by miR-876-5p overexpression but nullified by ZEB1 overexpression. Meanwhile, MINCR silencing or miR-876-5p overexpression synergized with GEM to depress BC growth in vivo. MINCR silencing impedes GEM resistance in BC through the miR-876-5p/ZEB1/PHGDH axis.</p>

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Long non-coding RNA MINCR silencing contributes to suppressed gemcitabine resistance in bladder cancer by blocking the ZEB1/PHGDH axis through microRNA-876-5p up-regulation

  • 期刊论文

  • 发表日期：

    2025年7月9日

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  • Linfei Xu,
  • Yongfeng Lin,
  • Liming Zhang,
  • Xingzhang Lin,
  • Sheng Liu

摘要

Long non-coding RNA MINCR performs a tumor-promoting role in various cancers. Accordingly, this research analyzed whether MINCR exerted tumor-promoting effects and facilitated gemcitabine (GEM) resistance in BC. MINCR, microRNA (miR)-876-5p, ZEB1, and PHGDH expression was detected in BC tissues and cells. Following the construction of GEM-resistant cells, MINCR expression was examined with RT-qPCR. Gain- and loss-of-function assays were conducted in GEM-resistant cells, followed by the measurement of cell proliferation, invasion, and apoptosis. The relationships among MINCR, miR-876-5p, and ZEB1 were assessed with dual-luciferase and RIP assays. Subcutaneous tumor formation in nude mice was conducted for in vivo corroboration. MINCR was up-regulated in BC tissues and cells and GEM-resistant BC cells. miR-876-5p expression was poor and ZEB1 and PHGDH expression was abundant in BC tissues. Mechanistically, MINCR enhanced ZEB1 expression in BC cells via competitive binding to miR-876-5p, and ectopic ZEB1 induced PHGDH up-regulation. MINCR silencing diminished proliferation and invasion while accelerating apoptosis in GEM-resistant BC cells, which was further advanced by miR-876-5p overexpression but nullified by ZEB1 overexpression. Meanwhile, MINCR silencing or miR-876-5p overexpression synergized with GEM to depress BC growth in vivo. MINCR silencing impedes GEM resistance in BC through the miR-876-5p/ZEB1/PHGDH axis.