Department of Hepatobiliary Surgery, Affiliated Hospital of Guizhou Medical University, 28 Guiyi Street, Yunyan District, Guiyang, 550004, Guizhou, China.
Department of Otorhinolaryngology, Affiliated Hospital of Guizhou Medical University, 28 Guiyi Street, Yunyan District, Guiyang, 550004, Guizhou, China.
Mol Cell Probes. 2018 Aug;40:19-26. doi: 10.1016/j.mcp.2018.06.003. Epub 2018 Jun 13.
Dysregulation of miR-1297 has been detected in various human cancers, and miR-1297 can function as either an oncogene or tumor suppressor. However, the role of miR-1297 in pancreatic adenocarcinoma has not been previously reported. Here, we investigated miR-1297 expression in pancreatic cancer and the role it plays in the development and metastasis of pancreatic adenocarcinoma. In the present study, MiR-1297 and metadherin (MTDH) expression in pancreatic cancer tissue was detected using quantitative real-time PCR (qRT-PCR) and western blot methods. The CCK-8 assay and EdU incorporation assay were used to analyze the impact of miR-1297 and MTDH on cell proliferation. Flow cytometric and Hoechst 33342 staining methods were used to explore how miR-1297 and MTDH affect cell apoptosis. The Transwell assay and scratch wound healing assay were used to analyze cell migration and invasion capabilities. The dual-luciferase assay was used to confirm that miR-1297 targets MTDH. Here, we found that miR-1297 expression was decreased in pancreatic adenocarcinoma tissues, while MTDH expression was increased in those tissues. Furthermore, western blot and dual-luciferase assay results confirmed that MTDH was a direct target of miR-1297. Additionally, overexpression of miR-1297 or knockdown of MTDH suppressed BxPC-3 and PANC-1 cell proliferation, and upregulation of miR-1297 or suppression of MTDH promoted BxPC-3 and PANC-1 cell apoptosis. Finally, BxPC-3 and PANC-1 cell migration and invasion abilities were suppressed by either overexpression of miR-1297 or downregulation of MTHD. In conclusion, our results suggest that miR-1297 inhibits the growth and metastasis of pancreatic adenocarcinoma by downregulating MTDH expression, and the miR-1297/MTDH pathway is a potential target for treating pancreatic adenocarcinoma.
miR-1297 的失调已在各种人类癌症中被检测到，miR-1297 可以作为癌基因或肿瘤抑制因子发挥作用。然而，miR-1297 在胰腺腺癌中的作用尚未被报道。在这里，我们研究了胰腺癌细胞中 miR-1297 的表达及其在胰腺腺癌的发生和转移中的作用。在本研究中，使用实时定量 PCR（qRT-PCR）和 Western blot 方法检测胰腺癌细胞中 miR-1297 和 MTDH 的表达。CCK-8 检测和 EdU 掺入检测用于分析 miR-1297 和 MTDH 对细胞增殖的影响。流式细胞术和 Hoechst 33342 染色法用于探讨 miR-1297 和 MTDH 如何影响细胞凋亡。Transwell 检测和划痕愈合实验用于分析细胞迁移和侵袭能力。双荧光素酶报告基因实验用于证实 miR-1297 靶向 MTDH。在这里，我们发现 miR-1297 在胰腺腺癌组织中的表达降低，而 MTDH 的表达在这些组织中增加。此外，Western blot 和双荧光素酶报告基因实验结果证实 MTDH 是 miR-1297 的直接靶标。此外，过表达 miR-1297 或敲低 MTDH 抑制 BxPC-3 和 PANC-1 细胞的增殖，上调 miR-1297 或抑制 MTDH 促进 BxPC-3 和 PANC-1 细胞的凋亡。最后，过表达 miR-1297 或敲低 MTHD 抑制 BxPC-3 和 PANC-1 细胞的迁移和侵袭能力。总之，我们的结果表明，miR-1297 通过下调 MTDH 表达抑制胰腺腺癌的生长和转移，miR-1297/MTDH 通路可能是治疗胰腺腺癌的潜在靶点。
