Additional file 1 of The miR-1185-2-3p—GOLPH3L pathway promotes glucose metabolism in breast cancer by stabilizing p53-induced SERPINE1
Creators: name: Xu, Youqin
name: Chen, Wancheng
name: Liang, Jing
name: Zeng, Xiaoqi
name: Ji, Kaiyuan
name: Zhou, Jianlong
name: Liao, Shijun
name: Wu, Jiexian
name: Xing, Kongyang
name: He, Zilong
name: Yang, Yang
name: Liu, Qianzhen
name: Zhu, Pingyi
name: Liu, Yuchang
name: Li, Li
name: Liu, Minfeng
name: Chen, Wenxiao
name: Huang, Wenhua
Publisher: name: figshare
Year: 2021
Subjects: subject: Biochemistry
subject: Cell Biology
subject: Genetics
subject: FOS: Biological sciences
subject: Molecular Biology
subject: Pharmacology
subject: Biological Sciences not elsewhere classified
subject: Cancer
subject: Hematology
subject: Plant Biology

description: Additional file 1:Supplementary Figure 1. GOLPH3L regulated the tumorigenic activities of BT474 cells. (A) Knockdown of GOLPH3L in MCF-10A, BT474 and T47D cells with five distinct siRNAs. (B) The overexpression (oe) of GOLPH3L in MCF-10A, BT474 and T47D cells. (C) The expression of GOLPH3L in BT474 cells promotes their proliferation, n = 3, * p &lt; 0.05, ** p &lt; 0.01. (D) GOLPH3L expression suppresses the apoptosis of BT474 cells, n = 3, ** p &lt; 0.01. (E) Knockdown of GOLPH3L inhibits the migration of BT474 cells using a transwell assay, n = 3, * p &lt; 0.05, ** p &lt; 0.01. (F) The suppression of GOLPH3L significantly blocks the BT474 cell cycle at G0/ G1 phase, n = 3, * p &lt; 0.05, ** p &lt; 0.01. Supplementary Figure 2. miR-1185-2-3p negatively regulates the tumorigenesis of BT474 cells. (A) The predicted miRNAs which were most likely to regulate with GOLPH3L. (B) The overexpression of miR-1185-2-3p was achieved with miRNA mimics and inhibition miR-1185-2-3p was achieved with miRNA inhibitor in T47D and BT474, n = 3, ** p &lt; 0.01. (C) The overexpression of miR-1185-2-3p inversely correlated with the proliferation of BT474 cells, n = 3, ** p &lt; 0.01. (D) The overexpression of miR-1185-2-3p promoted the apoptosis of BT474 cells, n = 3, * p &lt; 0.05. (E) miR-1185-2-3p overexpression could significantly inhibited the migration of BT474 cells, n = 3, * p &lt; 0.05. (F) The overexpression of miR-1185-2-3p could block the cell cycle at G0/ G1 phase, n = 3, * p &lt; 0.05. Supplementary Figure 3. miR-1185-2-3p overexpression partially reversed the tumorigenesis induced by GOLPH3L overexpression. (A) The overexpression of miR-1185-2-3p inversely correlated with the up-regulation of proliferation induced by GOLPH3L overexpression in T47D cells, n = 3, * p &lt; 0.05, ** p &lt; 0.01. (B) miR-1185-2-3p partially reversed the apoptosis induced by GOLPH3L overexpression in T47D cells, n = 3. * p &lt; 0.05. (C) Overexpressed miR-1185-2-3p inhibited the up-regulation of migration caused by GOLPH3L up-regulation using transwell assay, n = 3. * p &lt; 0.05. (D) The overexpression of miR-1185-2-3p affected the cell cycle regulation by GOLPH3L, n = 3, * p &lt; 0.05, ** p &lt; 0.01.Supplementary Figure 4. p53 pathway promotes the transcription of SERPINE1. (A) Volcano plots of fold changes and p-values of altered metabolites after GOLPH3L suppression in the Positive Ion Mode (top panel) and Negative Ion Mode (bottom panel). (B) Volcano plots of fold changes and p-values of RNA-seq data after silencing GOLPH3L expression in T47D cells. (C) STRING analysis predicted protein-protein network indicating that SERPINE1 interacted with p53 (top panel) and the role of SERPINE1 in p53 signaling pathway after GOLPH3L knockdown in T47D cells (bottom panel).