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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
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Updated: Apr 16, 2026

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
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Arteannuin B Inhibits NSCLC Cells via Regulating miR-194-3p/CLDN2 Axis.

Ting-Sha He1, Rong-Hui Chen1,2, Jing Feng1,2

  • 1Department of Pharmacology, College of Pharmacy, Jinan University, Guangzhou, China.

Cancer Medicine
|April 14, 2026
PubMed
Summary

Arteannuin B combats non-small cell lung cancer (NSCLC) chemoresistance by upregulating miR-194-3p, which inhibits CLDN2. This pathway overcomes cisplatin resistance and offers a new therapeutic strategy for NSCLC patients.

Keywords:
CLDN2Arteannuin BNSCLCchemoresistancemiR‐194‐3p

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genomics

Background:

  • Non-small cell lung cancer (NSCLC) often develops chemoresistance, limiting treatment efficacy.
  • Claudin-2 (CLDN2) is upregulated in NSCLC and contributes to tumor progression and drug resistance.
  • Identifying novel therapeutic targets is crucial for overcoming NSCLC chemoresistance.

Purpose of the Study:

  • To investigate the mechanism by which Arteannuin B (Art B) overcomes chemoresistance in NSCLC.
  • To identify key molecular players involved in Art B's anticancer effects.
  • To explore CLDN2 as a potential therapeutic target and prognostic biomarker in NSCLC.

Main Methods:

  • Integrated transcriptomic profiling and functional validation in NSCLC models.
  • Analysis of CLDN2 expression in NSCLC tissues and paired normal tissues.
  • Luciferase reporter assays to confirm miR-194-3p binding to CLDN2 3' UTR.
  • Assessment of Art B's effect on miR-194-3p, CLDN2, and chemoresistance.

Main Results:

  • Art B treatment upregulated miR-194-3p expression in NSCLC cells.
  • miR-194-3p directly targets and suppresses CLDN2 expression.
  • CLDN2 upregulation promotes NSCLC proliferation and cisplatin resistance via MRP2.
  • Art B's antitumor effects are mediated by the miR-194-3p/CLDN2 axis, resensitizing cells to cisplatin.

Conclusions:

  • Art B overcomes NSCLC chemoresistance by activating the miR-194-3p/CLDN2 pathway.
  • CLDN2 is a critical mediator of Art B's anticancer activity and a potential prognostic biomarker.
  • Targeting the miR-194-3p/CLDN2 axis represents a promising therapeutic strategy for NSCLC patients with treatment failure.