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In addition, the current status of ACE2 as a targeted therapy for COVID‑19 is discussed in order to provide new insight into the clinical prevention and treatment of COVID‑19.Following the publication of this article and after having solicited the opinions of all the participating authors, the Editorial Office was contacted by the authors to explain that the following changes are required to the list of contributing authors on the paper. The corresponding author of the article should be changed to the first author (Gang Chen), and a request was made that the name of the final author in the author list (Xiaotang Yang), who was also the original corresponding author, be removed. Therefore, the author affiliations and addresses, and the corresponding author information, in this paper have been revised as follows GANG CHEN1, ZHIFENG ZHENG2, JUNSHENG LI3, PEIGANG ZHANG4, ZHENJUN WANG5, SHIPING GUO1, JUN MA6, JIAN SHEN7 and HUIXIN LI8. 1The Secondary Department of Thoracic Surgery, The Tumor Hospital Affiliated to Shanxi Medical University, Taiyuan, Shanxi 030013; 2Department of General Thoracic Surgery, Linfen People's Hospital, Linfen, Shanxi 041000; 3Department of Cardiothoracic Surge authors regret this error in the presentation of these affiliations, and apologize for any inconvenience caused. [the original article was published in Molecular Medicine Reports 23 212, 2021; DOI 10.3892/mmr.2021.11851].The present study evaluated the expression levels of nuclear factor I B (NFIB) in gastric cancer (GC) specimens and cells, and its regulatory roles were further elucidated. The expression levels of NFIB were examined in GC and paired normal specimens, and in human GC and normal gastric epithelial cells by reverse transcription‑quantitative PCR. A circular RNA (circRNA) microarray was performed to identify the novel downstream circRNA of NFIB. Cell proliferation was determined by Cell Counting Kit‑8 assay. Furthermore, cell cycle distribution and apoptosis were assessed using flow cytometry. Interactions between RNA were examined by RNA pulldown assay and the stability of target mRNA was evaluated using a mRNA stability assay. The results of the present study revealed that NFIB was upregulated in GC. Ipatasertib Furthermore, silencing NFIB suppressed the proliferation of GC cells, whereas cell cycle arrest and apoptosis were enhanced. In addition, significant downregulation of circMAP7D1 (hsa_circ_0004093) was observed in GC cells infected with short hairpin RNA‑NFIB. These findings indicated that circMAP7D1 may be a promising downstream molecule of NFIB in GC, and further functional analyses indicated that circMAP7D1 was involved in NFIB‑modulated GC cell proliferation and apoptosis. Moreover, human epidermal growth factor receptor 2 (HER2) was identified as a novel target of circMAP7D1 in GC, and NFIB was able to increase the stability of HER2 mRNA through regulating circMAP7D1. In conclusion, the present findings indicated that NFIB expression was increased in GC. In addition, NFIB may promote the proliferation of GC cells and function through stabilizing HER2 mRNA by upregulating circMAP7D1. Notably, NFIB and its novel downstream signaling pathway may serve essential roles during the development of GC, and NFIB may be considered a promising candidate for the treatment of patients with GC.Malignant tumors of the central nervous system (CNS) are among the types of cancer with the poorest prognosis and glioma is the commonest primary CNS tumor. A mitochondrial DNA (mtDNA)‑depleted cell line C6ρ0 was generated from C6 glioma cells after long‑term exposure to ethidium bromide and 2',3'‑dideoxycytidine in order to determine the effect of mtDNA damage on cell proliferation and pathological changes in glioma cells. Single cell clones were isolated and identified after 42 days of incubation. Repopulated cybrids were formed when the clonal C6ρ0 cells were fused with rat platelets and no difference was observed in their growth in a selective medium without uridine and pyruvate compared with the growth of the parent C6 cells. Disruption of mtDNA resulted in changes in mitochondrial morphology, decreased cell proliferation, reduced intracellular reactive oxygen species and intracellular ATP, along with decreased mtDNA and mitochondrial membrane potential in C6ρ0 cells compared with the C6 cells. Taken together, C6ρ0 cells without mtDNA were established for the first time and their characteristics were compared with parent cells. This C6ρ0 cell line could be used to explore the contribution of mitochondrial dysfunction and mtDNA mutations in the pathogenesis of glioma.Ovarian cancer (OC) is a major contributor to cancer‑related mortality in women. Despite numerous drugs being available for the treatment and improving the prognosis of OC, resistance to clinical chemotherapy remains a major obstacle for the treatment of advanced OC. Therefore, determining how to reverse the chemoresistance of OC has become a research hotspot in recent years. The present study aimed to reveal the potential mechanism of OC chemoresistance. Reverse transcription‑quantitative PCR and western blot analysis were performed to detect the expression levels of Ubiquitin‑specific peptidase 46 (USP46) and Pumilio 2 (PUM2) in OC. Cell viability and apoptosis were evaluated by Cell Counting Kit‑8 assay and flow cytometry, respectively. The association between USP46 and PUM2 was assessed by RNA immunoprecipitation. The results of the present study revealed that the expression levels of USP46 which is associated with tumor progression, was downregulated, while PUM2 expression levels were upregulated in cispreas those of caspase‑3, caspase‑9 and Bax were upregulated compared with the small interfering‑USP46 group. Similarly, in SKOV3/DDP cells, the overexpression of PUM2 could reverse DDP sensitivity induced by the overexpression of USP46. In conclusion, the findings of the present study suggested that the downregulation of USP46 expression levels may promote DDP resistance in OC, which may be regulated by PUM2. Therefore, targeting PUM2/USP46 may be an effective way to reverse DDP resistance in OC.