{"doi":"10.3389/fonc.2022.1111724","title":"Editorial: Developing combined modality therapy with mitochondria-targeting strategy","abstract":"A broad array of molecular and cellular events is associated with developing resistance to treatment resistance, such as deregulation of the cell cycle, inhibition of DNA damage repair mechanisms, and metabolic alterations.Most cancer therapy-induced responses, including resistance, involve the dysfunction of mitochondria.Mitochondria have acquired numerous functions throughout evolution, controlling energy production, cellular metabolism, cell survival, apoptosis and autophagy within host cells. Tumor cells can develop defects in mitochondrial function, presenting a potential strategy for designing selective anticancer therapies. However, nonspecific targeting of mitochondrial functions may have significant unwarranted effects on normal cell growth and survival. Therefore, treatments conjugated with other anticancer therapy are needed to precisely target specific mitochondrial proteins involved in tumor progression and the acquisition of cancer resistance.In the present Research Topic, we have garnered several contributors to provide evidence-informed insights into the mechanistic and pathogenic role of mitochondrial proteins to support the discovery of novel therapeutic targets for directed mitochondrial treatment and eventually facilitating enablers of knowledge translation. After a rigorous peer-review process, seven articles have been collected, consisting of two comprehensive review and five original research articles. Notably, these articles were contributed by renowned academic institutes from North America, Europe and Asia engaged in mitochondria-based biology and translational research, demonstrating the great interest in this hot area.Cancer cells exhibit metabolic plasticity that endows them with a selective advantage to face harsh microenvironmental alterations and orchestrate nutrient sensing and upload, signaling, and redox circuits. The finely tuned reactive oxygen species (ROS) generation and scavenging within a certain sub-toxic tumorigenic range are two aspects fundamental to cancer cells as ROS mediate cell signaling to significantly impact a wide range of pathways involved in cancer development and progression. That is the reason why ROS have recently become an attractive target for anticancer therapies. Ippolito et al outlined several crucial functions of mitochondrial redox activity in different cancer stages by elaborating effects of mitochondrial ROS (mROS) on tumor initiation, progression, energy metabolism, stemness achievement, metastases and tumor immune environment (Ippolito et al., 2020). They also explored the impact of mROS on treatment response in cancers, such as tumor chemosensitivity. Because mitochondrial redox homeostasis crucially regulates cancer cell behavior and several cancer hallmarks, the authors also attempted to point out the potential redox-based targeted therapeutic strategies, either single or combined modality. It is worth mentioning that two new mROS-targeted treatments, photothermal and photodynamic therapy, have rendered their effectiveness in curing and preventing cancer. Criscuolo and his colleagues reviewed the available literature on the coordinated regulation of mitochondrial and cytosolic mRNA translation, as well as their effects on the integrity of the mitochondrial proteome and functions. The purpose of this review paper is to highlight the importance of mitochondrial protein quality control systems in coordinating mitochondrial and cytosolic protein translation (Criscuolo et al., 2021).More than that, this critical review also hints that mitochondrial protein homeostasis dysfunctions are tightly associated with cancer development, and thus the most relevant therapeutics hold great promises as anticancer strategies.Mitochondrial dependency of leukemia cells and their altered oxidative metabolism have already been explored as a common abnormality existing in acute myeloid leukemia (AML). Accumulating evidence suggests that AML may be particularly sensitive to chemo","journal":"Frontiers in Oncology","year":2023,"id":402259,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":0,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9518,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2023-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":105721,"name":"Yong Teng","orcid":"0000-0002-1856-7289","position":0,"is_corresponding":true}],"reference_count":0,"raw_metadata":null,"created_at":"2026-07-19T01:20:23.920156Z","pmid":"36686773","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}