Amygdalin-mediated inhibition of non-small cell lung cancer cell invasion in vitro.

Abstract

Lung cancer is a common malignant tumor claiming the highest fatality worldwide for a long period of time. Unfortunately, most of the current treatment methods are still based on the characteristics of cancer cells in the primary lesion and the prognosis is often much poorer in patients with metastatic cancers. Amygdalin, a natural product of glycosides and lots of evidence shows that amygdalin can inhibit the proliferation of some kinds of cancer cells. In this study, we first obtained the highly metastatic NSCLC cell lines H1299/M and PA/M and further treated these cells with amygdalin. We found that the in vitro proliferability of H1299/M and PA/M was inhibited, but such inhibition required higher concentration of amygdalin. When lower concentration of amygdalin was used for the experiments, we observed that the in vitro invasive and migration capacities of H1299/M and PA/M were significantly inhibited. These results strongly suggested that amygdalin was likely to have anti-metastatic NSCLC effect. This study offers information of the role of amygdalin that may be useful as a therapeutic target in lung tumors.

• Authors: Liyu Qian, Bo Xie, Yaguo Wang, Jun Qian
• Journal: International journal of clinical and experimental pathology (Int J Clin Exp Pathol) Vol. 8 Issue 5 Pg. 5363-70 ( 2015) ISSN: 1936-2625 [Electronic] United States
• PMID: 26191238 (Publication Type: Journal Article)

Chemical References

• Antineoplastic Agents, Phytogenic
• Intracellular Signaling Peptides and Proteins
• Amygdalin

Topics

• Amygdalin (pharmacology)
• Antineoplastic Agents, Phytogenic (pharmacology)
• Carcinoma, Non-Small-Cell Lung (drug therapy, metabolism, secondary)
• Cell Line, Tumor
• Cell Movement (drug effects)
• Cell Proliferation (drug effects)
• Dose-Response Relationship, Drug
• Humans
• Intracellular Signaling Peptides and Proteins (metabolism)
• Lung Neoplasms (drug therapy, metabolism, pathology)
• Neoplasm Invasiveness
• Phosphorylation
• Signal Transduction (drug effects)