Antibody–drug conjugates (ADCs) represent a transformative therapeutic class in non-small cell lung cancer (NSCLC), moving precision oncology beyond traditional targeted therapies. These agents, composed of a monoclonal antibody, linker, and potent cytotoxic payload, enable targeted drug delivery to tumor cells expressing specific antigens like TROP2, HER2, and c-MET. Recent clinical trials have demonstrated remarkable efficacy of ADCs, both as monotherapy in molecularly defined populations and in combination with immunotherapy, offering new hope for patients with advanced disease. This review summarizes the latest clinical progress of ADCs in NSCLC, highlighting key agents and their impact, while also addressing the associated challenges and future directions for optimizing this promising treatment modality.
Xi Chen, Sirui Wu, Feiyang Li et al.· Holistic Integrative Oncolog...· 0 citations
Eukaryotic translation initiation factors (eIFs) play a crucial role in tumor progression; however, which eIFs are most significant in cervical cancer (CC) remains unclear. In this study, eIF3A and eIF4E were found to be highly expressed in CC and associated with poor prognosis. Silencing either factor inhibited CC cell proliferation, induced apoptosis, and reduced glycolytic activity. Quantitative proteomic analysis and subsequent functional validation identified α-enolase (ENO1) as a common downstream effector of eIF3A and eIF4E, through which they promoted aerobic glycolysis and CC progression. Notably, eIF3A consistently exhibited a more pronounced functional effect than eIF4E. Further analyses demonstrated that eIF3A associated with N6-methyladenosine (m6A)-modified ENO1 mRNA and promoted its translation. eIF3A depletion reduced the abundance of ENO1 mRNA in actively translating polysomes and decreased the ENO1 protein-to-mRNA ratio without affecting total ENO1 mRNA abundance. Mutation of a key m6A site A359 in ENO1 mRNA similarly weakened its association with eIF3A and reduced ENO1 translation. Moreover, pharmacological inhibition of m6A-related regulation partially attenuated eIF3A-induced ENO1 expression, glycolytic activation, and tumor growth. Collectively, our results identify eIF3A as a key regulator of CC progression in an m6A-dependent ENO1 translation and suggest that targeting the eIF3A-m6A-ENO1 may have therapeutic potential for CC.
Linjuan Cai, Yu Jiang, Lingfeng Gu et al.· Cancer Genetics· 0 citations
