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Published on: March 30, 2019
Mistletoe lectin inhibits growth of Myc-amplified small-cell lung cancer
Mohammad A Shatat1, Betsy Gauthier2, Suzy Yoon2
1Division of Pulmonary, Critical Care and Sleep Medicine, Case Western Reserve University, The Louis Stokes Cleveland VA Medical Center and Case Comprehensive Cancer Center, Ohio, Cleveland, USA.
Background:
Small-cell lung cancer (SCLC) is the deadliest form of lung cancer but lacks targeted therapies.
Methods:
We studied the effect of the natural product mistletoe lectin (ML) in pre-clinical models of SCLC, focusing on cell lines with amplification of the myc family oncogenes C-myc and N-myc.
Results:
We found that ML treatment inhibits growth of SCLC cell lines in culture and induces apoptosis. ML treatment also decreases the expression of the amplified myc proteins. Over-expression of either C-myc or N-myc results in enhanced SCLC cell sensitivity to ML. In a mouse xenograft model of SCLC, treatment with ML results in decreased tumor growth over 4 weeks with evidence of increased apoptosis in tumors from treated animals.
Conclusion:
Overall, our results demonstrate that ML exhibits therapeutic potential in SCLC, that is at least partially dependent on myc protein expression.
Insights
Mistletoe lectin (ML) shows promise in treating small-cell lung cancer (SCLC) by inhibiting tumor growth and inducing cell death. Its effectiveness is linked to myc protein expression in SCLC models.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Small-cell lung cancer (SCLC) is an aggressive malignancy with limited targeted treatment options.
- The myc family of oncogenes (C-myc, N-myc) is frequently amplified in SCLC, contributing to its poor prognosis.
Purpose of the Study:
- To investigate the therapeutic potential of mistletoe lectin (ML), a natural product, against SCLC.
- To explore the role of myc oncogene amplification in SCLC sensitivity to ML.
Main Methods:
- Pre-clinical evaluation of ML in SCLC cell lines and a mouse xenograft model.
- Assessment of ML's effects on cell growth, apoptosis, and myc protein expression.
Main Results:
- ML treatment significantly inhibited SCLC cell growth and induced apoptosis in vitro.
- ML decreased myc protein expression and enhanced SCLC cell sensitivity when C-myc or N-myc were over-expressed.
- In vivo, ML treatment reduced tumor growth and increased apoptosis in a mouse xenograft model.
Conclusions:
- Mistletoe lectin demonstrates significant therapeutic potential for small-cell lung cancer.
- The anti-cancer effects of ML in SCLC are, at least partially, dependent on myc protein expression.
