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Long noncoding RNA LINC01111 suppresses pancreatic cancer aggressiveness by regulating DUSP1 expression via

Shutao Pan1, Ming Shen1, Min Zhou1

  • 1Department of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, 430030, Wuhan, Hubei, China.

Cell Death & Disease
|November 27, 2019
PubMed

Insights

This study identifies LINC01111 as a tumor suppressor long noncoding RNA (lncRNA) in pancreatic cancer (PC). Its downregulation correlates with poor prognosis, and it inhibits PC progression by regulating the miR-3924/DUSP1/SAPK/JNK pathway.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Long noncoding RNAs (lncRNAs) are implicated in human cancer, but their specific roles in pancreatic cancer (PC) remain largely uncharacterized.
  • Understanding the molecular mechanisms of lncRNAs in PC is crucial for developing novel diagnostic and therapeutic strategies.

Purpose of the Study:

  • To investigate the function and mechanism of the novel lncRNA, LINC01111, in pancreatic cancer.
  • To determine if LINC01111 can serve as a diagnostic biomarker and therapeutic target for PC.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) was used to assess LINC01111 and miR-3924 expression levels in PC tissues and plasma.
  • In vitro assays (proliferation, cell cycle, invasion, migration) and in vivo studies (tumorigenesis, metastasis) were performed using LINC01111 overexpression and knockdown models.
  • Western blotting and luciferase reporter assays were employed to elucidate the molecular mechanism involving miR-3924, DUSP1, and the SAPK/JNK pathway.

Main Results:

  • LINC01111 was significantly downregulated in PC tissues and plasma, with lower levels correlating with advanced TNM stage and poorer patient survival.
  • Overexpression of LINC01111 suppressed PC cell proliferation, invasion, migration, and tumorigenesis, while knockdown enhanced these processes.
  • LINC01111 upregulated DUSP1 by sequestering miR-3924, leading to SAPK/JNK pathway inactivation and reduced PC aggressiveness.

Conclusions:

  • LINC01111 functions as a tumor suppressor in pancreatic cancer.
  • The LINC01111/miR-3924/DUSP1 axis is a novel regulatory pathway that impacts PC initiation and development.
  • LINC01111 holds potential as a diagnostic biomarker and therapeutic target for pancreatic cancer.

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