Scholarlink

Background <p>Triglyceride (TG) metabolism and circular RNAs (circRNAs) are implicated in pancreatic adenocarcinoma (PAAD), but their interconnections remain unclear. This study aims to elucidate the role of hsa_circ_0041150 (circ_0041150) in metabolic mechanism and PAAD progression.</p> Methods <p>RNA/protein levels were detected by qRT-PCR/Western blot. Cell proliferation was evaluated using CCK-8 and EdU assays. TG accumulation was assessed via BODIPY 493/503 staining and a commercial TG assay kit. Interactions among circ_0041150, miR-1178-3p, and AADAC mRNA were analyzed via bioinformatics tools, RNA pull-down, dual-luciferase reporter, and RNA immunoprecipitation (RIP) assays.</p> Results <p>circ_0041150 was downregulated in PAAD tissues and cell lines, and its expression correlated with key clinicopathological features of PAAD. Mechanistically, circ_0041150 acts as a competing endogenous RNA (ceRNA) to sponge miR-1178-3p, thereby upregulating AADAC expression, and inhibiting TG accumulation and PAAD cell proliferation. Knockdown of circ_0041150 promoted proliferation and TG accumulation, and these effects were partially reversed by miR-1178-3p inhibition or AADAC overexpression.</p> Conclusion <p>circ_0041150 regulates AADAC by sponging miR-1178-3p, inhibiting PAAD progression and TG accumulation, and providing diagnostic and therapeutic targets via the circ_0041150/miR-1178-3p/AADAC axis.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Circ_0041150 inhibits proliferation of pancreatic adenocarcinoma cells by regulating triglyceride accumulation via the miR-1178-3p/AADAC axis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月5日

查看全文
  • Jing-jing Zhao,
  • Na-ya Hu,
  • Hui-ru Wang,
  • Cui-juan Qian,
  • Jun Yao

摘要

Background

Triglyceride (TG) metabolism and circular RNAs (circRNAs) are implicated in pancreatic adenocarcinoma (PAAD), but their interconnections remain unclear. This study aims to elucidate the role of hsa_circ_0041150 (circ_0041150) in metabolic mechanism and PAAD progression.

Methods

RNA/protein levels were detected by qRT-PCR/Western blot. Cell proliferation was evaluated using CCK-8 and EdU assays. TG accumulation was assessed via BODIPY 493/503 staining and a commercial TG assay kit. Interactions among circ_0041150, miR-1178-3p, and AADAC mRNA were analyzed via bioinformatics tools, RNA pull-down, dual-luciferase reporter, and RNA immunoprecipitation (RIP) assays.

Results

circ_0041150 was downregulated in PAAD tissues and cell lines, and its expression correlated with key clinicopathological features of PAAD. Mechanistically, circ_0041150 acts as a competing endogenous RNA (ceRNA) to sponge miR-1178-3p, thereby upregulating AADAC expression, and inhibiting TG accumulation and PAAD cell proliferation. Knockdown of circ_0041150 promoted proliferation and TG accumulation, and these effects were partially reversed by miR-1178-3p inhibition or AADAC overexpression.

Conclusion

circ_0041150 regulates AADAC by sponging miR-1178-3p, inhibiting PAAD progression and TG accumulation, and providing diagnostic and therapeutic targets via the circ_0041150/miR-1178-3p/AADAC axis.