Effects of 1,25(Oh)2d3 on microrna-130b and transforming growth factor beta 1 in renal tissue of rat models of diabetic nephropathy / 中国组织工程研究

BACKGROUND: 1,25(OH)2D3 plays an important regulatory role in the development of diabetic nephropathy. OBJECTIVE: To explore the effect of 1,25(OH)2D3 on the expression of microRNA-130b and transforming growth factor pi in kidney of diabetic nephropathy rats. METHODS: The study was approved by the Laboratory Animal Ethical Committee of Laboratory Animal Center of Xinjiang Medical University. Twenty-five clean Sprague-Dawley rats were randomly divided into normal control group, diabetic nephropathy+1,25(OH)2D3 group and diabetic nephropathy+peanut oil group. The latter two groups were given calcitriol (1,25(OH)2D3, active vitamin D3, 0.03 jg/kg

Effect of lncRNA HULC knockdown on rat secreting pituitary adenoma GH3 cells

Pituitary adenoma is one of the most common tumors in the neuroendocrine system. This study investigated the effects of long non-coding RNAs (lncRNAs) highly up-regulated in liver cancer (HULC) on rat secreting pituitary adenoma GH3 cell viability, migration, invasion, apoptosis, and hormone secretion, as well as the underlying potential mechanisms. Cell transfection and qRT-PCR were used to change and measure the expression levels of HULC, miR-130b, and FOXM1. Cell viability, migration, invasion, and apoptosis were assessed using trypan blue staining assay, MTT assay, two-chamber transwell assay, Guava Nexin assay, and western blotting. The concentrations of prolactin (PRL) and growth hormone (GH) in culture supernatant of GH3 cells were assessed using ELISA. The targeting relationship between miR-130b and FOXM1 was verified using dual luciferase activity. Finally, the expression levels of key factors involved in PI3K/AKT/mTOR and JAK1/STAT3 pathways were evaluated using western blotting. We found that HULC was highly expressed in GH3 cells. Overexpression of HULC promoted GH3 cell viability, migration, invasion, PRL and GH secretion, as well as activated PI3K/AKT/mTOR and JAK1/STAT3 pathways. Knockdown of HULC had opposite effects and induced cell apoptosis. HULC negatively regulated the expression of miR-130b, and miR-130b participated in the effects of HULC on GH3 cells. FOXM1 was a target gene of miR-130b, which was involved in the regulation of GH3 cell viability, migration, invasion, and apoptosis, as well as PI3K/AKT/mTOR and JAK1/STAT3 pathways. In conclusion, HULC tumor-promoting roles in secreting pituitary adenoma might be via down-regulating miR-130b, up-regulating FOXM1, and activating PI3K/AKT/mTOR and JAK1/STAT3 pathways.

Onco-microRNA miR-130b promoting cell growth in children APL by targeting PTEN

Objective: To study the expression of microRNA-130b (miR-130b) in children acute promyelocytic leukemia (APL) and its role for regulating PTEN expression. Methods: A total of 50 children APL marrow tissues and 15 normal marrow tissues between January and December in 2012 were collected into our study. The expression of miR-130b in APL and normal marrow tissues were detected by quantitative real-time polymerase chain reaction. MiR-130b inhibitor was transfected into HL-60 cells. Cell Counting Kit-8 assay and flow cytometry were used to measure cell proliferation and apoptosis, respectively. The expression of PTEN, a potential target of miR-130b, and its downstream genes, Bcl-2 and Bax, in transformed cells were detected by quantitative real-time polymerase chain reaction and western-blot. Results: The expression of miR-130b was significantly higher in children APL marrow tissues than in normal marrow tissues (P < 0.05). Down-regulation of miR-130b could significantly suppress cell proliferation and induce apoptosis in HL-60 cells (P < 0.05). PTEN expression was upregulated when miR-130b was knocking-down (P < 0.05). As downstream genes of PTEN, the expression of Bcl-2 and Bax were regulated as well. Conclusions: MiR-130b is overexpressed in children APL marrow tissues and associated with cell growth. MiR-130b may promote children APL progression by inducing cell proliferation and inhibiting apoptosis.

Onco-microRNA miR-130b promoting cell growth in children APL by targeting PTEN

OBJECTIVE@#To study the expression of microRNA-130b (miR-130b) in children acute promyelocytic leukemia (APL) and its role for regulating PTEN expression.@*METHODS@#A total of 50 children APL marrow tissues and 15 normal marrow tissues between January and December in 2012 were collected into our study. The expression of miR-130b in APL and normal marrow tissues were detected by quantitative real-time polymerase chain reaction. MiR-130b inhibitor was transfected into HL-60 cells. Cell Counting Kit-8 assay and flow cytometry were used to measure cell proliferation and apoptosis, respectively. The expression of PTEN, a potential target of miR-130b, and its downstream genes, Bcl-2 and Bax, in transformed cells were detected by quantitative real-time polymerase chain reaction and western-blot.@*RESULTS@#The expression of miR-130b was significantly higher in children APL marrow tissues than in normal marrow tissues (P < 0.05). Down-regulation of miR-130b could significantly suppress cell proliferation and induce apoptosis in HL-60 cells (P < 0.05). PTEN expression was upregulated when miR-130b was knocking-down (P < 0.05). As downstream genes of PTEN, the expression of Bcl-2 and Bax were regulated as well.@*CONCLUSIONS@#MiR-130b is overexpressed in children APL marrow tissues and associated with cell growth. MiR-130b may promote children APL progression by inducing cell proliferation and inhibiting apoptosis.

Clinical significance of microRNA-130b in osteosarcoma and in cell growth and invasion

Objective: To investigate clinical significance of microRNA-130b (miR-130b) in osteosarcoma and its role in cell growth and invasion. Methods: miR-130b expression was detected in 68 samples of surgically resected osteosarcoma and matched normal tumor-adjacent tissues by qRT-PCR. The expression of miR-130b was altered by corresponding vectors in osteosarcoma cells, and then Western blot was used to detect the expression of PPARγ. BrdU cell proliferation and Transwell assays were performed to determine cell proliferation and invasion. Results: The expression of miR-130b in osteosarcoma tissues was significantly higher than that in normal tumor-adjacent tissues. Its expression in patients with metastasis was significantly higher than that in those without metastases. miR-130b expression in tumor tissues was significantly associated with tumor size, clinical stage and distant metastasis. And its expression was significantly correlated with overall survival and disease free survival. miR-130b overexpression obviously repressed the expression of PPARγ, and resulted in significant increase of Saos-2 cell proliferation and invasion. On the contrast, repressing miR-130b expression with its inhibitor significantly increased PPARγ expression, and inhibited MG-63 cell proliferation and invasion. Conclusions: The high-expression of miR-130b is correlated with the adverse clinicopathological features and poor prognosis in osteosarcoma. miR-130b may regulate proliferation and invasion of osteosarcoma cells by targeting PPARγ, suggesting miR-130b may play a key role in the progression of osteosarcoma.

Clinical significance of microRNA-130b in osteosarcoma and in cell growth and invasion

OBJECTIVE@#To investigate clinical significance of microRNA-130b (miR-130b) in osteosarcoma and its role in cell growth and invasion.@*METHODS@#miR-130b expression was detected in 68 samples of surgically resected osteosarcoma and matched normal tumor-adjacent tissues by qRT-PCR. The expression of miR-130b was altered by corresponding vectors in osteosarcoma cells, and then Western blot was used to detect the expression of PPARγ. BrdU cell proliferation and Transwell assays were performed to determine cell proliferation and invasion.@*RESULTS@#The expression of miR-130b in osteosarcoma tissues was significantly higher than that in normal tumor-adjacent tissues. Its expression in patients with metastasis was significantly higher than that in those without metastases. miR-130b expression in tumor tissues was significantly associated with tumor size, clinical stage and distant metastasis. And its expression was significantly correlated with overall survival and disease free survival. miR-130b overexpression obviously repressed the expression of PPARγ, and resulted in significant increase of Saos-2 cell proliferation and invasion. On the contrast, repressing miR-130b expression with its inhibitor significantly increased PPARγ expression, and inhibited MG-63 cell proliferation and invasion.@*CONCLUSIONS@#The high-expression of miR-130b is correlated with the adverse clinicopathological features and poor prognosis in osteosarcoma. miR-130b may regulate proliferation and invasion of osteosarcoma cells by targeting PPARγ, suggesting miR-130b may play a key role in the progression of osteosarcoma.