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MicroRNA-137 down-regulates KIT and inhibits small cell lung cancer cell proliferation

Peipei Li1, Lijie Ma2, Yongjuan Zhang3

  • 1Department of Respiration, Tangdu Hospital, Fourth Military Medical University, 710038 Xi'an, China; Department of Respiration, Harrison International Peace Hospital, 053000 Hengshui, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|January 14, 2014
PubMed

Insights

MicroRNA-137 (miR-137) is linked to multidrug resistance (MDR) in small lung cancer (SCLC). Modulating miR-137 levels can alter cisplatin resistance, potentially by regulating KIT expression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Small lung cancer (SCLC) exhibits multidrug resistance (MDR), a significant clinical challenge.
  • Dysregulation of microRNAs (miRNAs) is implicated in cancer progression and drug resistance.

Purpose of the Study:

  • To investigate the role of miR-137 in the development of cisplatin resistance in SCLC.
  • To explore the relationship between miR-137, KIT expression, and drug sensitivity in SCLC.

Main Methods:

  • Compared miR-137 and KIT expression in parental (H446) and cisplatin-resistant (H446/CDDP) SCLC cell lines.
  • Utilized miR-137 inhibitors and mimics for transfection to modulate miR-137 levels.
  • Assessed changes in miR-137 and KIT expression, and evaluated drug sensitivity post-transfection.

Main Results:

  • H446/CDDP cells showed lower miR-137 expression and higher KIT expression compared to H446 cells.
  • Inhibition of miR-137 in H446 cells decreased cisplatin sensitivity.
  • Overexpression of miR-137 in H446/CDDP cells increased cisplatin sensitivity and affected KIT expression.

Conclusions:

  • miR-137 plays a crucial role in SCLC multidrug resistance.
  • Interfering with miR-137 expression can potentially reverse cisplatin resistance in SCLC.
  • KIT may be a downstream target of miR-137 involved in SCLC MDR.
Keywords:
KITMDRMiR-137SCLC

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