Recent studies have shown that oxidative phosphorylation (OXPHOS) is a target for the effective attenuation of cancer drug resistance. OXPHOS inhibitors can improve treatment responses to anticancer therapy in certain cancers, such as melanomas, lymphomas, colon cancers, leukemias and pancreatic ductal adenocarcinoma (PDAC). However, the effect of OXPHOS on cancer drug resistance is complex and associated with cell types in the tumor microenvironment (TME). Cancer cells universally promote OXPHOS activity through the activation of various signaling pathways, and this activity is required for resistance to cancer therapy. Resistant cancer cells are prevalent among cancer stem cells (CSCs), for which the main metabolic phenotype is increased OXPHOS. CSCs depend on OXPHOS to survive targeting by anticancer drugs and can be selectively eradicated by OXPHOS inhibitors. In contrast to that in cancer cells, mitochondrial OXPHOS is significantly downregulated in tumor-infiltrating T cells, impairing antitumor immunity. In this review, we summarize novel research showing the effect of OXPHOS on cancer drug resistance, thereby explaining how this metabolic process plays a dual role in cancer progression. We highlight the underlying mechanisms of metabolic reprogramming in cancer cells, as it is vital for discovering new drug targets.

Characterized by multiple complex mutations, including activation by oncogenes and inhibition by tumor suppressors, cancer is one of the leading causes of death. Application of CRISPR-Cas9 gene-editing technology in cancer research has aroused great interest, promoting the exploration of the molecular mechanism of cancer progression and development of precise therapy. CRISPR-Cas9 gene-editing technology provides a solid basis for identifying driver and passenger mutations in cancer genomes, which is of great value in genetic screening and for developing cancer models and treatments. This article reviews the current applications of CRISPR-Cas9 gene-editing technology in various cancer studies, the challenges faced, and the existing solutions, highlighting the potential of this technology for cancer treatment.

Background: Although tripartite motif-containing protein 11 (TRIM11) is known to be associated with a variety of cancers, its role in nasopharyngeal carcinoma (NPC) is unclear. Methods and results: To investigate the role of TRIM11 in NPC, TRIM11 was stably overexpressed in 6–10B and CNE2 cells with lentiviral vectors and knocked down in S18 and 5–8F cells using the CRISPR/Cas9 system. Transwell assays and wound-healing assays revealed that TRIM11 facilitated the migration and invasion of NPC cells. Mechanistically, we found that p53 inhibits TRIM11 expression by binding to its promoter. Conclusions: TRIM11 may serve as a potential diagnostic marker for NPC and has a certain therapeutic value.