RESUMO
BACKGROUND: Glioma stem-like cells (GSCs) are greatly responsible for the progression of glioma. Long noncoding RNAs (lncRNAs) play an important role in glioma tumor progression. This study aims to explore the role and underlying mechanism of lncRNA SNHG9 in regulating GSC cell growth. METHODS: GSCs were obtained from glioma cells (U87 and U251) and referred to as GSC-87 and GSC-251, respectively. The interactions between miR-326 and SNHG9 or SOX9 were analyzed using luciferase reporter assay. Cell growth of GSCs was evaluated by EdU assay and sphere formation assay. RESULTS: SNHG9 expression was significantly higher in GSC-87 and GSC-251 cells than in U87 and U251 cells. SNHG9 overexpression promoted GSC cell growth, whereas SNHG9 knockdown inhibited GSC cell growth. Mechanistically, SNHG9 acted as a competitive endogenous RNA of miR-326 to elevate the expression of SOX9, a direct target of miR-326. Moreover, transfection with miR-326 inhibitor counteracted SNHG9 knockdown-mediated inhibition of GSC cell growth. CONCLUSIONS: SNHG9 facilitates growth of GSCs via the miR-326/SOX9 axis. This study provides a promising therapeutic target for glioma treatment.
Assuntos
Neoplasias Encefálicas , Glioma , MicroRNAs , Células-Tronco Neoplásicas , RNA Longo não Codificante , Fatores de Transcrição SOX9 , Neoplasias Encefálicas/genética , Neoplasias Encefálicas/patologia , Linhagem Celular Tumoral , Proliferação de Células/genética , Regulação Neoplásica da Expressão Gênica , Glioma/patologia , Humanos , MicroRNAs/genética , MicroRNAs/metabolismo , Células-Tronco Neoplásicas/metabolismo , Células-Tronco Neoplásicas/patologia , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Fatores de Transcrição SOX9/genética , Fatores de Transcrição SOX9/metabolismoRESUMO
AIM: To detect the expression of the long noncoding RNA HOTAIR in colon cancer and analyze its relationship with clinicopathological parameters of colon cancer. METHODS: Total RNA was extracted from 80 colon cancer tissues and matched tumor-adjacent normal colon tissues and reverse transcribed. Quantitative polymerase chain reaction was used to detect the expression of HOTAIR. The relationship between the expression of HOTAIR and clinicopathological parameters of colon cancer was analyzed. RESULTS: The expression of HOTAIR was significantly higher in colon cancer tissues than in matched tumor-adjacent normal colon tissues (P < 0.05). HOTAIR expression was significantly higher in cases with lymph node metastasis than in those without metastasis; in lowly differentiated and undifferentiated cases than in highly and moderately differentiated cases; and in stages III + IV cases than in stagesâ Iâ + II cases (P < 0.05). CONCLUSION: HOTAIR expression is upregulated in colon cancer, suggesting that HOTAIR plays an important role in the tumorigenesis, development and metastasis of colon cancer. HOTAIR may act as an oncogene and represents a new molecular target for the treatment of colon cancer.
Assuntos
Biomarcadores Tumorais/genética , Neoplasias do Colo/genética , RNA Longo não Codificante/genética , Idoso , Idoso de 80 Anos ou mais , Diferenciação Celular , Neoplasias do Colo/mortalidade , Neoplasias do Colo/patologia , Neoplasias do Colo/terapia , Feminino , Regulação Neoplásica da Expressão Gênica , Humanos , Estimativa de Kaplan-Meier , Metástase Linfática , Masculino , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Estudos Retrospectivos , Regulação para CimaRESUMO
OBJECTIVE: To investigate the protective effects of recombinant human growth hormone (rhGH) on intestinal mucosal barrier in rat sepsis and explore its possible mechanisms. METHODS: E. coli was injected intraperitoneally to produce rats sepsis models. Forty-two female SD rats were randomly divided into the control group (group C), sepsis group (group S) and treatment group (group T). Group S and group T were further divided into 1 d and 3 d subgroups (T1d,T3d, Sld, S3d), respectively. The expression of IGF-1 mRNA in liver, expression of Bcl-2 protein in intestine, bacteria translocation, the levels of growth hormone(GH) and insulin-like growth factor-1 (IGF-1) in plasma, and the histological appearance of intestine were determined dynamically by means of RT-PCR, radioimmunoassay, immunohistochemical staining and other corresponding methods, respectively. RESULTS: (1) rhGH could significantly attenuate intestinal mucosal injuries and ameliorate bacteria translocation on sepsis rats. (2) The levels of Bcl-2 protein expression in intestine in group T (T1d:2441 +/- 117; T3d: 3628 +/- 235) were obviously higher than those of group S (S1d: 321 +/- 36; S3d: 1873 +/- 57) (P < 0.01). (3) The plasma levels of GH in group T (T1d: 1.28 +/- 0.24 microg/L; T3d: 2.14 +/- 0.48 microg/L) increased markedly than those of group S (S1d: 0.74 -/+ 0.12 microg/L; S3d: 0.60 +/- 0.18 microg/L) (P < 0.01). (4) The plasma levels of IGF-1 in group T (Tld: 168.94 +/- 65.67 microg/L; T3d: 201.56 +/- 64.98 microg/L) elevated significantly than those of group S (Sld: 116.72 +/- 13.96 microg/L; S3d:107.50 +/- 23.53 microg/L) (P < 0.05). (5) The levels of liver IGF-1 mRNA in group T (Tld: 0.98 +/- 0.20; T3d: 1.76 +/- 0.17) were significantly higher than those in group S (S1d: 0.38 +/- 0.09; S3d: 0.46 +/- 0.10) (P < 0.01). CONCLUSION: rhGH conferred protective efficacy in maintaining the integrity of intestinal mucosal barrier against sepsis in rat. The possible mechanisms might involve the rhGH-diminished apoptosis of intestinal mucosa cells and the rhGH-maintained intestinal mucosa barrier via the roles of GH and IGF-1.