Figure 2.

Mitochondrial dysfunction and fission promote HCC progression. Mutations in mtDNA and defects in mitochondrial enzymes, such as SDH, FH and IDH are closely related to familial and sporadic cancers. The accumulation of ROS, Ca²⁺ or carcinogenic metabolites can participate in tumor transformation. Moreover, mitochondrial morphology is interchangeable between fused and fission states. Mitochondrial fission begins with interaction with endoplasmic reticulum. DRP1 is recruited to mitochondria upon stress, where it interacts with its mitochondrial receptors. DRP1 is responsible for mitochondrial fission as it physically confines mitochondria by forming a ring structure in the region of future mitochondrial fission. The level of mitochondrial fission significantly affects the malignant biological behaviors of HCC.