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Role of c-Myc in lung cancer: Progress, challenges, and prospects
Nicholas J Wallbillich1,2, Hua Lu1,2
1Department of Biochemistry and Molecular Biology, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA.
Abstract:
Lung cancer remains the leading cause of cancer-related deaths worldwide. Despite the recent advances in cancer therapies, the 5-year survival of non-small cell lung cancer (NSCLC) patients hovers around 20%. Inherent and acquired resistance to therapies (including radiation, chemotherapies, targeted drugs, and combination therapies) has become a significant obstacle in the successful treatment of NSCLC. c-Myc, one of the critical oncoproteins, has been shown to be heavily associated with the malignant cancer phenotype, including rapid proliferation, metastasis, and chemoresistance across multiple cancer types. The c-Myc proto-oncogene is amplified in small cell lung cancers (SCLCs) and overexpressed in over 50% of NSCLCs. c-Myc is known to actively regulate the transcription of cancer stemness genes that are recognized as major contributors to tumor progression and therapeutic resistance; thus, targeting c-Myc either directly or indirectly in mitigation of the cancer stemness phenotype becomes a promising approach for development of a new strategy against drug resistant lung cancers. This review will summarize what is currently known about the mechanisms underlying c-Myc regulation of cancer stemness and its involvement in drug resistance and offer an overview on the current progress and future prospects in therapeutically targeting c-Myc in both SCLC and NSCLC.
Insights
Targeting c-Myc, a key oncoprotein, offers a promising strategy to overcome therapeutic resistance in lung cancer. This approach aims to mitigate cancer stemness, improving survival for non-small cell lung cancer patients.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Lung cancer is a leading cause of cancer mortality globally, with poor survival rates for non-small cell lung cancer (NSCLC).
- Therapeutic resistance, both inherent and acquired, significantly hinders effective NSCLC treatment.
- The oncoprotein c-Myc is implicated in cancer progression, metastasis, and chemoresistance across various cancer types.
Purpose of the Study:
- To review the mechanisms by which c-Myc regulates cancer stemness.
- To summarize c-Myc's role in drug resistance in lung cancer.
- To provide an overview of therapeutic strategies targeting c-Myc for lung cancer treatment.
Main Methods:
- Literature review of studies on c-Myc, cancer stemness, and drug resistance in lung cancer.
- Analysis of the role of c-Myc in regulating stemness genes.
- Examination of current and future therapeutic approaches targeting c-Myc.
Main Results:
- c-Myc overexpression is common in NSCLC and amplification occurs in small cell lung cancer (SCLC).
- c-Myc directly regulates genes associated with cancer stemness, promoting tumor progression and therapeutic resistance.
- Targeting c-Myc presents a potential strategy to overcome drug resistance in both SCLC and NSCLC.
Conclusions:
- c-Myc plays a critical role in driving lung cancer stemness and therapeutic resistance.
- Targeting c-Myc, directly or indirectly, is a promising avenue for developing novel lung cancer therapies.
- Further research into c-Myc-targeted strategies could significantly improve outcomes for lung cancer patients.
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