Hsa-miR-132 regulates apoptosis in non-small cell lung cancer independent of acetylcholinesterase.

Abstract

MiR-132 is enriched in the central nerve system and is thought to be involved in neuronal development, maturation and function, and to be associated with several neurological disorders including Alzheimer's disease. In addition to its documented neuronal functions, an emerging role for miR-132 in tumorigenesis has been suggested. Recently, hsa-miR-132 was shown to be modulated in different tumor types. However, its role in non-small cell lung cancer (NSCLC) remains unclear. Here, we show that hsa-miR-132 can initiate apoptosis in NSCLC cells to dramatically attenuate tumor formation in nude mice independent of its effect on the proliferation/apoptosis-associated gene, acetylcholinesterase (AChE). Interestingly, hsa-miR-132 has no pro-apoptotic effect in normal pulmonary trachea epithelium. Taken together, these results suggest that hsa-miR-132 represses NSCLC growth by inducing apoptosis independent of AChE.

• Authors: Bo Zhang, Lu Lu, Xuejin Zhang, Weiyuan Ye, Jun Wu, Qiliang Xi, Xuejun Zhang
• Journal: Journal of molecular neuroscience : MN (J Mol Neurosci) Vol. 53 Issue 3 Pg. 335-44 (Jul 2014) ISSN: 1559-1166 [Electronic] United States
• PMID: 24158730 (Publication Type: Journal Article)

Chemical References

• MIRN132 microRNA, human
• MicroRNAs
• Acetylcholinesterase

Topics

• Acetylcholinesterase (metabolism)
• Animals
• Apoptosis
• Carcinoma, Non-Small-Cell Lung (metabolism)
• HEK293 Cells
• HeLa Cells
• Humans
• Mice
• Mice, Inbred BALB C
• Mice, Nude
• MicroRNAs (genetics, metabolism)