Mitochondria are double-walled organelles that generate energy in the form of ATP. ATP is an energy-rich compound and a driver of fundamental cell functions. Mitochondria-oriented studies help design advanced therapies to target lung cancer. Lung cancer is the leading cause of cancer incidences and death globally. Various studies have supported that mitochondrial function is disrupting cancerous cells. Mitochondrial dysfunctions lead to dysregulated ATP synthesis, disturbed respiratory chain, unbalanced mitochondrial fission or fusion, disturbed cellular redox homeostasis, dysregulated apoptosis, and interfered non-smooth intracellular calcium signaling. Dysfunction mitochondria are associated with cancer cell proliferation, metastasis, and death. In this review, we have tried to elaborate on how normal cell mitochondria function differently from the mitochondria of lung cancer cells. It includes various targets such as mitochondrial proteins and related pathways, along with new drug molecules like Militarin analog-1, Dihydromyricetin, and papuamine. As mitochondrial metabolism is associated with the proliferation and metastasis of lung cancer cells, finding interlinks between malfunctioning mitochondria and the process of lung cancer can promote the development of new treatments.