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Efforts in cancer immunotherapy aim to counteract evasion mechanisms and stimulate the immune system to recognise and attack cancer cells effectively. Combination therapies that target multiple aspects of immune evasion are being investigated to enhance the overall efficacy of cancer immunotherapy. PD-1 (Programmed Cell Death Protein 1), CTLA-4 (Cytotoxic T-Lymphocyte Antigen 4), LAG-3 (Lymphocyte-Activation Gene 3), and TIM-3 (T Cell Immunoglobulin and Mucin Domain-Containing Protein3) are all immune checkpoint receptors that play crucial roles in regulating the immune response and maintaining self-tolerance often exploited by cancer cells to evade immune surveillance. Antibodies targeted against immune checkpoint inhibitors such as anti-PD-1 antibodies (e.g., pembrolizumab, nivolumab), anti-CTLA-4 antibodies (e.g., Ipilimumab), and experimental drugs targeting LAG-3 and TIM-3, aim to block these interactions and unleash the immune system’s ability to recognise and destroy cancer cells. The US FDA has approved different categories of immune checkpoint inhibitors that have been utilised successfully in some patients with metastatic melanoma, renal cell carcinoma, head and neck cancers, and non-small lung cancer. Although several immune checkpoint inhibitor antibodies have been developed, they exhibited immune-related adverse effects, resulting in hypophysitis, diabetes, and neurological issues. These adverse effects of antibodies can be reduced by developing aptamer against the target. Aptamers offer several advantages over traditional antibodies, such as improved specificity, reduced immunogenicity, and flexible design for reduced adverse effects that specifically target and block protein–protein or receptor-ligand interactions involved in immune checkpoint pathways. The current study aims to review the function of particular immune checkpoint inhibitors along with developed aptamer-mediated antitumor cytotoxicity in cancer treatment.

Lung cancer is the most devastating cause of death among all cancers worldwide, and non-small cell lung cancer (NSCLC) accounts for 80% of all the lung cancer cases. Beyond common genetic research and epigenomic studies, the extraordinary investigations of non-coding RNAs have provided insights into the molecular basis of cancer. Existing evidence from various cancer models highlights that the regulation of non-coding RNAs is crucial and that their deregulation may be a common reason for the development and progression of cancer, and competition of cancer therapeutics. Non-coding RNAs, such as long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), are increasingly recognized as potential cancer biomarkers for early detection and application of therapeutic strategies. The miRNAs have gained importance as master regulators of target mRNAs by negatively regulating their expression. The lncRNAs function as both tumor suppressors and oncogenes, and also compete with miRNAs that influence the translational inhibition processes. This review addresses the role of lncRNAs in lung cancer development, highlights their mechanisms of action, and provides an overview of the impact of lncRNAs on lung cancer survival and progression via miRNA sponging. The improved understanding of lung cancer mechanisms has opened opportunities to analyze molecular markers and their potential therapeutics.