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  • 标题:Author Correction: Integrated network analysis identifies hsa-miR-4756-3p as a regulator of FOXM1 in Triple Negative Breast Cancer
  • 本地全文:下载
  • 作者:Yuanliang Gu ; Wenjuan Wang ; Xuyao Wang
  • 期刊名称:Scientific Reports
  • 电子版ISSN:2045-2322
  • 出版年度:2021
  • 卷号:11
  • DOI:10.1038/s41598-021-99328-3
  • 语种:English
  • 出版社:Springer Nature
  • 摘要:Correction to: Scientific Reports 10.1038/s41598-019-50248-3, published online 25 September 2019 The original version of this Article contained an error in Figure 2F where the cell line for trained MDA-MB-231 was used instead of MDA-MB-231. The original Figure  2 and accompanying legend appear below. Similarly, in Figure 4D, the MDA-MB-231 cell line was used instead of the trained MDA-MB-231. The original Figure  4 and accompanying legend appear below. The original Article has been corrected. Figure 2 Increased of hsa-miR-4756-3p induced apoptosis, cell cycle arrest and inhibit cell proliferation, migration in vitro. Control miRNA and hsa-miR-4756-3p mimic was transfected in TNBC cell line MDA-MB-231 cells for 48 h, then using ( A) Annexin V APC/7-AAD double staining to detect the change of cell apoptosis. ( B) CCK8 to detect cell proliferation change. ( C) Wound healing assay to assess cell migration change. ( D) High concentration PI staining to assess cell cycle change. ( E) MDA-MB-231 cell was transfected with hsa-miR-4756-3p mimic, then TGFβ-1 pathway molecules TGFβ-1, TGFβ-1 type 1 receptor, TGFβ-1 type 2 receptor, SMAD3, p-SMAD3 were detected by western blot. ( F) MDA-MB-231 cell were injected in mammary gland fat pad of nude mice, then control miRNA and hsa-miR-4756-3p inhibitor were inject in nude mice using DOPC liposomes, after 1 months, mice were sacrificed, and primary tumor diameter were assessed. Figure 4 hsa-miR-4756-3p regulated TNBC metastasis in vitro and in vivo through FOXM1-TGFβ1-Smad3-EMT pathway. ( A) Control sgRNA and FOMX1 KO were transfected in MDA-MB-231 cells, after single clone selection, using western blot to detect change of FOXM1 expression. ( B) MDA-MB-231 cells was divided into control, hsa-miR-4756-3p inhibitor, hsa-miR-4756-3p inhibitor + FOXM1 KO group, control group transfected with control miRNA, hsa-miR-4756-3p inhibitor transfected with hsa-miR-4756-3p inhibitor, hsa-miR-4756-3p inhibitor + FOXM1 KO group was 231-FOXM1 KO transfected with hsa-miR-4756-3p inhibitor, then using wound healing assay to assess the migration change. ( C) Employing QPCR and western blot to find the hsa-miR-4756-3p (left) and FOXM1(right) expression in 231 and trained 231 cells. ( D) 15 nude mice were divided into control, hsa-miR-4756-3p inhibitor, hsa-miR-4756-3p inhibitor + FOXM1 KO group, control, hsa-miR-4756-3p inhibitor group were injected trained 231 in mammary gland fat pad, hsa-miR-4756-3p inhibitor + FOXM1 KO group were injected with FOXM1 KO trained 231 cells, then control miRNA was injected control nude mice using DOPC liposomes, hsa-miR-4756-3p inhibitor was injected in other 2 groups, after 2 months, mice lung metastasis were detected. ( E) In control, hsa-miR-4756-3p inhibitor, hsa-miR-4756-3p inhibitor + FOXM1 KO group nude mice primary tumor, protein was extracted and TGFβ1 signal pathway, EMT pathway were assess.
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