1,725,184 research outputs found
miR-3607-3p overexpression inhibited cell proliferation, colony formation, and migration in NSCLC cell lines.
No full text(A) RNA level of miR-3607-3p in six NSCLC cell lines. (B) Quantitation of miR-3607-3p level after the transfection of miR-3607-3p mimic (50 ng/L) in H157 cell lines. (C) Cell growth curve measured by MTS after the transfection of miR-3607-3p mimic (50 ng/L) in H157 cell lines; all OD 570 values were normalized to the starting point (0 hour). (D) Representative images and quantitative results of colony formation were obtained after transfection with miR-3607-3p mimic (50 ng/L) in H157 cell lines. (E) Representative images and quantitative results of the Transwell assay were obtained after transfection with miR-3607-3p mimic (50 ng/L) in H157 cell lines. (F) miR-3607-3p induced cell cycle arrest at G1/S phase. Data are presented as means ± standard deviation from triplicate experiments. *, P < 0.05.</p
3607-3p expression and clinicopathological parameters of NSCLC patients.
No full text3607-3p expression and clinicopathological parameters of NSCLC patients.</p
miR-3607-3p suppressed tumor growth and metastasis <i>in vivo</i>.
No full text(A) Levels of miR-3607-3p in stable miR-3607-3p knockdown A549 cells (Lenti-inhibitor) and control A549 cells (Lenti-vector). (B-D) Stable miR-3607-3p knockdown A549 cells were subcutaneously injected into nude mice to form solid tumors and representative images of tumor volumes and weights were analyzed by in vivo luciferase imaging on the endpoint day (n = 5 for each group). (E-G) The numbers of metastatic nodules were observed and quantified in the lungs and brain of mice treated with stable miR-3607-3p knockdown A549 cells or control vector cells by tail vein injection. (H-J) The A549 cells were subcutaneously injected into nude mice to form solid tumors and were treated with miR-3607-3p agomir or miR agomir NC (n = 5 for each group). A 10-nmol miR-3607-3p agomir and the miRNA negative control in 0.1 ml saline buffer were locally injected into the tumor masses once every 5 days for 6 weeks. (K) Immunohistochemistry of Ki67, TGFBR1, and CCNE2 in tumor tissues dissected from nude mice treated with miR-3607-3p agomir or miR angomir NC. (L) TGFBR1 and CCNE2 protein expression measured by immunohistochemistry in 162 NSCLC samples and association with lung cancer survival. (M-N) Spearman correlation analysis of the negative correlation between the expression of miR-3607-3p and TGFBR1/ CCNE2. *, P < 0.05.</p
The relationship between miR-3607-3p expression levels in NSCLC tissues or serum and clinical significances.
No full text(A) Kaplan-Meier overall survival curves according to high and low miR-3607-3p expression in 162 patients with NSCLC. (B) Quantitation of miR-3607-3p was performed using qRT-PCR in 107 NSCLC (T) and adjacent normal (N) tissues. The fold changes were calculated by relative quantification (2-ΔCt, U6 as the internal control). (C-D) miR-3607-3p expression was detected in primary tumor tissues and the patients were grouped according to lymph node metastasis status (C) or clinical stages (D). (E) Kaplan-Meier curves depicting overall survival according to the expression of miR-3607-3p from the validation set. (F) The expression levels of serum miR-3607-3p in 80 NSCLC patients and 40 healthy controls were measured by qRT-PCR and normalized to U6. (G-H) Serum miR-3607-3p expression was low in patients with NSCLC, indicated by lymph node metastasis (G) and different clinical stages (H). (I) Receiver operating characteristic (ROC) curve analysis of the miR-3607-3p assay ratio for detecting NSCLC patients. *, P < 0.05.</p
Repression of miR-3607-3p expression significantly promoted cell growth, colony formation, and migration in A549 cells.
No full text(A) Quantitative measurement of miR-3607-3p level after the transfection of miR-3607-3p inhibitor (100 ng/L) in A549 cell lines. (B) Cell growth curve measured by MTS after transfection with miR-3607-3p inhibitor (100 ng/L) in A549 cell lines; all OD 570 values were normalized to the starting point (0 hour). (C) Representative images and quantitative results of colony formation were obtained after transfection with miR-3607-3p inhibitor (100 ng/L) in A549 cell lines. (D) Representative images and quantitative results of the Transwell assay were obtained after the transfection of miR-3607-3p inhibitor (100 ng/L) in A549 cell lines. (E) miR-4317 induced cell cycle arrest at G1/S phase. Data are presented as means ± standard deviation from triplicate experiments. *, P < 0.05.</p
Serum expression levels of miR-3607-3p and clinicopathological characteristics in patients with NSCLC.
No full textSerum expression levels of miR-3607-3p and clinicopathological characteristics in patients with NSCLC.</p
In situ hybridization to detect miR-3607-3p expression in 162 paired NSCLC and adjacent non-cancerous tissue samples.
No full textA negative or positive cytoplasmic signal for miR-3607-3p was observed in lung tissues. (A) Scrambled miRNA negative control (no expression). (B) U6 snRNA positive control (strong expression). (C) miR-3607-3p expression in adjacent normal lung tissues (strong expression). (D) miR-3607-3p expression in NSCLC tissues (left figure: low expression, middle figure: moderate expression, right figure: low expression).</p
<i>TGFBR1</i> and <i>CCNE2</i> are two direct target genes of miR-3607-3p.
No full text(A-B) TGFBR1 and CCNE2 were identified as potential regulatory targets of miR-3607-3p by considering the downregulation genes using prediction tools and the qRT-PCR method. (C-D) The expression levels of TGFBR1 and CCNE2 mRNA and protein were measured by qRT-PCR and western blot analysis using GAPDH as the loading control after transfection of miR-3607-3p mimic in H157 and H292 cell lines, respectively. (E-F) The expression levels of TGFBR1 and CCNE2 mRNA and protein were measured by qRT-PCR and western blot analysis using GAPDH as the loading control after transfection of miR-3607-3p inhibitors in A549 and H1299 cell lines, respectively. (G-H) Dual-luciferase reporter assay. The relative luciferase activity was normalized to the Renilla luciferase activity after co-transfection of cells with miR-3607-3p mimic and pmiR-RB-REPORT construct containing WT or MUT TGFBR1 and CCNE2 3’-UTR region in H157 and H292 cell lines. Data are presented as means ± standard deviation from triplicate experiments. *, P < 0.05.</p
Data_Sheet_1_Natural Killer Cell-Derived Exosomal miR-3607-3p Inhibits Pancreatic Cancer Progression by Targeting IL-26.DOCX
No full textIncreasing evidences have suggested that natural killer (NK) cells in the tumor microenvironment are involved in the regulation of cancer development. However, the potential biological roles and regulatory mechanisms of NK cells in pancreatic cancer (PC) remain unclear. Co-culture system of NK cells with PC cells is used to test the ability of cancer cell proliferation, migration and invasion both in vitro and in vivo. And tail vein intravenous transfer was used to test metastasis in vivo. Meanwhile, extracellular vesicles (EVs) were separated and examined. Furthermore, reporter assay and Biotin-RNA pull down assay were performed to verify the interaction between molecules. NK cells can inhibit the malignant transformation of co-cultured PC cells both in vivo and in vitro, which requires miR-3607-3p. miR-3607-3p is found enriched in the EVs of NK cells and transmitted to PC cells, and low level of miR-3607-3p predicts poor prognosis in PC patients. It can also inhibit proliferation, migration and invasion of PC cells in vitro. Importantly, IL-26 is found to be a direct target of miR-3607-3p in PC cells. miR-3607-3p enriched in EVs derived from NK cells can inhibit the malignant transformation of PC probably through directly targeting of IL-26.</p
Rescue assays were performed to confirm that TGFBR1 and CCNE2 are the functional targets of miR-3607-3p.
No full text(A-C) The mRNA and protein levels of TGFBR1 and CCNE2 in H157 and H292 cell lines with co-transfection of miR-3607-3p mimic and pEGFP-C1 plasmid containing TGFBR1 and CCNE2 CDS sequence. (D-E) Transwell assay of co-transfection cell with miR-3607-3p mimic and TGFBR1 and CCNE2 plasmid. Data are presented as means ± standard deviation from triplicate experiments. *, P < 0.05.</p
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