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LINC01001 Promotes Progression of Crizotinib-Resistant NSCLC by Modulating IGF2BP2/MYC Axis

Meiling Zhang1, Qian Wang1, Zihao Ke1

  • 1Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.

Frontiers in Pharmacology
|October 11, 2021
PubMed

Insights

Long non-coding RNA LINC01001 promotes crizotinib resistance in non-small cell lung cancer (NSCLC) by regulating the IGF2BP2/MYC axis. This study clarifies the molecular mechanism behind crizotinib resistance in NSCLC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Crizotinib is a tyrosine kinase inhibitor used for anaplastic lymphoma kinase (ALK)-rearranged non-small cell lung cancer (NSCLC).
  • The precise molecular mechanisms of crizotinib resistance in NSCLC remain incompletely understood.
  • This study investigates the role of LINC01001 in mediating crizotinib resistance via the IGF2BP2/MYC pathway.

Purpose of the Study:

  • To elucidate the molecular mechanism of crizotinib resistance in ALK-rearranged NSCLC.
  • To determine if LINC01001 regulates NSCLC progression through the IGF2BP2/MYC axis in the context of crizotinib treatment.

Main Methods:

  • Quantitative reverse transcription PCR (RT-qPCR) to measure mRNA levels of LINC01001, IGF2BP2, and MYC.
  • Cell viability, proliferation, and apoptosis assays (CCK-8, EdU, FACS, TUNEL) in crizotinib-resistant NSCLC cells.
  • Western blot for proliferation markers (PCNA, Ki-67) and immunohistochemistry for Ki-67 in patient tissues.
  • Crosslinking-immunoprecipitation (CLIP), RNA immunoprecipitation (RIP), and RNA pulldown assays to confirm molecular interactions.

Main Results:

  • LINC01001 was highly expressed in crizotinib-resistant NSCLC cells and correlated with poor patient survival.
  • Inhibition of LINC01001 or IGF2BP2 reduced crizotinib resistance in NSCLC cells.
  • LINC01001 directly interacts with IGF2BP2, which in turn binds to MYC mRNA, promoting crizotinib resistance.

Conclusions:

  • LINC01001 promotes the progression of crizotinib-resistant NSCLC by modulating the IGF2BP2/MYC axis.
  • This study clarifies a specific molecular mechanism contributing to crizotinib resistance in NSCLC treatment.
Keywords:
IGF2BP2LINC01001MYCcrizotinibcrizotinib-resistance NSCLC

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