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Lin-28 reactivation is required for let-7 repression and proliferation in human small cell lung cancer cells

Lin Pan1, Zhaohui Gong, Zhiwei Zhong

  • 1Institute of Biochemistry and Molecular Biology, School of Medicine, Ningbo University, 818 Fenghua Road, Ningbo 315211, China.

Molecular and Cellular Biochemistry
|May 10, 2011
PubMed

Insights

Lin-28 protein inhibits let-7 microRNA (miRNA) production, promoting lung cancer cell proliferation and cell cycle progression. Inhibiting Lin-28 impairs cancer cell growth and affects cell cycle phases.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • The let-7 miRNA family functions as tumor suppressors and is frequently downregulated in lung cancer.
  • The RNA-binding protein Lin-28 inhibits let-7 miRNA biogenesis by interfering with Drosha and Dicer processing and promoting precursor decay.

Purpose of the Study:

  • To investigate if Lin-28 promotes cell proliferation and affects the cell cycle by negatively regulating let-7 miRNA biogenesis in NCI-H446 small cell lung cancer cells.
  • To determine the role of Lin-28 in lung cancer progression.

Main Methods:

  • Real-time RT-PCR to quantify let-7 and lin-28 mRNA levels.
  • MTT assay to assess cell proliferation.
  • Cell cycle analysis via flow cytometry following lin-28 knockdown.

Main Results:

  • Lin-28 mRNA was upregulated in NCI-H446 cells, correlating with a high c-Myc state.
  • pri-let-7a-1/7g and mature let-7g were significantly downregulated, while lin-28 expression was inversely correlated with mature let-7g.
  • Lin-28 inhibition impaired lung cancer cell proliferation, increased the G1/G0 phase cell proportion, and decreased the S phase proportion.

Conclusions:

  • Lin-28 induction mediates the repression of let-7 family members.
  • Lin-28 promotes cell cycle progression and suppresses cell proliferation in lung cancer.
  • Targeting Lin-28 may represent a therapeutic strategy for lung cancer.

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