Saturated fatty acid-induced miR-195 impairs insulin signaling and glycogen metabolism in HepG2 cells

MicroRNAs (miRNAs) play an important role in insulin signaling and insulin secretion, but the role of miRNAs in the association between obesity and hepatic insulin resistance is largely unknown. This study reports that saturated fatty acid (SFA) and high fat diet (HFD) significantly induce miR-195 expression in hepatocytes, and that the insulin receptor (INSR), not insulin receptor substrate-1 (IRS-1), is a direct target of miR-195. Furthermore, the ectopic expression of miR-195 suppresses the expression of INSR, thereby impairing the insulin signaling cascade and glycogen synthesis in HepG2 cells. These findings suggest that the dysregulation of miR-195 by SFA is a detrimental factor for hepatic insulin sensitivity.     

MiR-517a-3p accelerates lung cancer cell proliferation and invasion through inhibiting FOXJ3 expression

Aims

Aberrant expression of microRNAs (miRNAs) results in alterations of various biological processes (e.g., cell cycle, cell differentiation, and apoptosis) and cell transformation. Altered miRNAs expression was associated with lung carcinogenesis and tumor progression. This study aimed to investigate the function and underlying molecular events of miR-517a-3p on regulation of lung cancer cell proliferation and invasion.

Main methods

Transfected miR-517a-3p mimics or inhibitors into 95D and 95C cells respectively, the effects of miR-517a-3p on lung cancer cell proliferation, migration, and invasion were detected. Bioinformatics software forecasted potential target genes of miR-517a-3p and dual luciferase reporter gene system and western blot verified whether miR-517a-3p regulates FOXJ3 expression directly.

Key findings

MiR-517a-3p was differentially expressed in lung cancer 95D and 95C cell lines that have different metastatic potential. Manipulation of miR-517a-3p expression changed lung cancer cell proliferation, migration and invasion capacity. MiR-517a-3p directly regulated FOXJ3 expression by binding to FOXJ3 promoter.

Significance

This study demonstrated that miR-517a-3p promoted lung cancer cell proliferation and invasion by targeting of FOXJ3 expression.     

miR-200a 及AFP 在肝癌、肝硬化患者血清中表达比较分析*

目的:分析miR-200a及AFP在肝癌、肝硬化患者血清中的表达水平并进行比较,探索其成为肝癌早期诊断血清标志物的可能性。方法:临床收集肝正常、肝硬化、肝癌患者血液标本。运用实时定量PCR技术检测血清miR-200a的相对表达情况,血清AFP水平从临床资料中提取。结果:临床标本分析结果显示,miR-200a在肝硬化及肝癌患者中均显著下调(P<0.05),AFP仅在肝癌患者中出现异常表达。结论:血清miR-200a极大程度地参与了肝癌发生,对肝硬化及肝癌具有一定的诊断价值。     

MicroRNAs-126（miR-126）的生物学功能

MicroRNAs(MiRNAs)负向调控基因的表达,在细胞分化和细胞功能调节中起着重要作用,且涉及血管新生。应用克隆和测序方法,检测出miR-126在人内皮细胞高度表达。MiR-126与许多肿瘤关系密切,miR-126通过信号传导通路负向调控肿瘤细胞增殖、迁移和侵袭,并且抑制肿瘤生长延长患者存活率;相反的,在某些肿瘤中miR-126也可通过促进肿瘤细胞血管生长加速肿瘤进展,可能是未来作为相关肿瘤治疗的手段之一。本文就miR-126在生理进程和病理进程的表达及其作用进行综述。     

miR-30b 的组织特异性研究

目的:研究miR-30b的组织特异性,检测其在心,肝,脑,肾,脾和骨骼肌中的表达情况。方法:选取C57BL/6J雄性小鼠6只,用real-time PCR方法检测小鼠心,肝,脑,肾,脾和骨骼肌中miR-30b的表达量。结果:miR-30b在小鼠肝脏中表达量最低,与肝相比,在心,脑,肾,脾和骨骼肌中的相对表达量分别为13.13±0.899,9.497±0.717,4.478±1.031,6.751±0.596,2.538±0.79。且与肝相比均具有统计学意义(P<0.05)。结论:miR-30b在各组织中的表达存在差异,在心脏中的表达量最高,提示miR-30b可能与心脏的发生发展密切相关,为深入探索miR-30b的功能奠定了基础。     

MicroRNA-129-5p inhibits 3T3-L1 preadipocyte proliferation by targeting G3BP1

MicroRNAs have been regarded to play a crucial role in the proliferation of different cell types including preadipocytes. In our study, we observed that miR-129-5p was down-regulated during 3T3-L1 preadipocyte proliferation, while the expression of G3BP1 showed a contrary tendency. 5-Ethynyl-2′-deoxyuridine (EdU) incorporation assay and flow cytometry showed that overexpression of miR-129-5p could bring about a reduction in S-phase cells and G2-phase arrest. Additional study indicated that miR-129-5p impaired cell cycle-related genes in 3T3-L1 preadipocytes. Importantly, it showed that miR-129-5p directly targeted the 3′UTR of G3BP1 and the expression of G3BP1 was inhibited by miR-129-5p mimic. Moreover, miR-129-5p mimic activated the p38 signaling pathway through up-regulating p38 and the phosphorylation level of p38. In a word, results in our study revealed that miR-129-5p suppressed preadipocyte proliferation via targeting G3BP1 and activating the p38 signaling pathway.     

MiR-185 inhibits 3T3-L1 cell differentiation by targeting SREBP-1

Adipogenesis involves a highly orchestrated series of complex events in which microRNAs (miRNAs) may play an essential role. In this study, we found that the miR-185 expression increased gradually during 3T3-L1 cells differentiation. To explore the role of miR-185 in adipogenesis, miRNA agomirs and antagomirs were used to perform miR-185 overexpression and knockdown, respectively. Overexpression of miR-185 dramatically reduced the mRNA expression of the adipogenic markers, PPARγ, FABP4, FAS, and LPL, and the protein level of PPARγ and FAS. MiR-185 overexpression also led to a notable reduction in lipid accumulation. In contrast, miR-185 inhibition promoted differentiation of 3T3-L1 cells. By target gene prediction and luciferase reporter assay, we demonstrated that sterol regulatory element binding protein 1 (SREBP-1) may be the target of miR-185. These results indicate that miR-185 negatively regulates the differentiation of 3T3-L1 cells by targeting SREBP-1, further highlighting the importance of miRNAs in adipogenesis.     

喉鳞状细胞癌组织miR-1207-5p、miR-186-5p表达水平与PI3K/Akt信号通路、临床病理特征和预后的关系

摘要 目的：探讨喉鳞状细胞癌（LSCC）组织miR-1207-5p、miR-186-5p表达水平与磷脂酰肌醇3-激酶/蛋白激酶B（PI3K/Akt）信号通路、临床病理特征和预后的关系。方法：选取2017年1月至2020年1月南充市中心医院收治的120例LSCC患者,取手术切除的LSCC组织和癌旁组织。检测miR-1207-5p、miR-186-5p、PI3K mRNA、Akt mRNA表达。患者出院后随访3年,统计总生存（OS）和无复发生存（RFS）情况。分析miR-1207-5p、miR-186-5p与PI3K、Akt的相关性以及影响LSCC患者预后的因素。结果：LSCC组织miR-1207-5p、miR-186-5p表达低于癌旁组织（P＜0.05）,PI3K mRNA、Akt mRNA表达高于癌旁组织（P＜0.05）。LSCC组织miR-1207-5p、miR-186-5p表达与PI3K mRNA、Akt mRNA表达呈负相关（P＜0.05）。肿瘤直径≥1 cm、低分化、TNM分期Ⅲ期、颈部淋巴结转移LSCC组织中miR-1207-5p、miR-186-5p表达低于肿瘤直径＜1 cm、中高分化、TNM分期Ⅰ～Ⅱ期、无颈部淋巴结转移（P＜0.05）。miR-1207-5p低表达、miR-186-5p低表达LSCC患者3年总生存（OS）率和无复发生存（RFS）率低于miR-1207-5p高表达、miR-186-5p高表达LSCC患者（P＜0.05）。多因素COX回归分析显示TNM III期、颈部淋巴结转移是LSCC患者复发和死亡的危险因素（P＜0.05）,高miR-1207-5p、高miR-186-5p是保护因素（P＜0.05）。结论：LSCC组织中miR-1207-5p和miR-186-5p表达均下调,与LSCC恶性病理特征、PI3K/Akt信号通路激活以及低生存率有关。