Objective: With the highest cancer related mortality and morbidity, lung cancer has become a predominant problem world-wide. The antitumor property of vitamin C (VC) has already been demonstrated. However, the precise mechanism and the targets of VC against lung cancer are yet to be discovered. This study is conducted to identify potential targets and underlying mechanisms of VC against lung cancer by bioinformatics analysis of network pharmacology and molecular docking. Methodology: Targets of VC and lung cancer were obtained from various data bases. From the 142 pharmacological targets of VC, 136 overlapping targets with lung cancer were mapped. The 10 potential core targets of VC were identified from mapped proteins. These 10 core targets are subjected to Gene Ontology and Kyoto Encyclopaedia of Genes and Genomes pathway enrichment analysis. The top 20 biological processes, molecular functions, cellular components and pathways were presented. Results: EGFR, ADRA2C, CHRM2, CCR5, MAPK1, BDKRB2, DRD2, AGTR2, ADRA2A and ADRA2B were found to be the key targets involved. Molecular docking studies revealed that VC has highest binding affinity to B2 bradykinin receptor (BDKRB2). The mechanism of VC in lung cancer may be associated with regulation of catecholamine release by inhibiting BDKRB2 receptor. Conclusion: VC can suppress tumour development and progression in lung cancer. Further pre-clinical studies are required for VC before it is used as a therapeutic agent in lung cancer.Objective: With the highest cancer related mortality and morbidity, lung cancer has become a predominant problem world-wide. The antitumor property of vitamin C (VC) has already been demonstrated. However, the precise mechanism and the targets of VC against lung cancer are yet to be discovered. This study is conducted to identify potential targets and underlying mechanisms of VC against lung cancer by bioinformatics analysis of network pharmacology and molecular docking. Methodology: Targets of VC and lung cancer were obtained from various data bases. From the 142 pharmacological targets of VC, 136 overlapping targets with lung cancer were mapped. The 10 potential core targets of VC were identified from mapped proteins. These 10 core targets are subjected to Gene Ontology and Kyoto Encyclopaedia of Genes and Genomes pathway enrichment analysis. The top 20 biological processes, molecular functions, cellular components and pathways were presented. Results: EGFR, ADRA2C, CHRM2, CCR5, MAPK1, BDKRB2, DRD2, AGTR2, ADRA2A and ADRA2B were found to be the key targets involved. Molecular docking studies revealed that VC has highest binding affinity to B2 bradykinin receptor (BDKRB2). The mechanism of VC in lung cancer may be associated with regulation of catecholamine release by inhibiting BDKRB2 receptor. Conclusion: VC can suppress tumour development and progression in lung cancer. Further pre-clinical studies are required for VC before it is used as a therapeutic agent in lung cancer.