Macrophage migration inhibitory factor (MIF) has been confirmed as an oncogene in solid tumor development, and its overexpression causes cell proliferation in T acute lymphoblastic leukemia (T‑ALL); however, the underlying mechanisms remain unclear. The overexpression of MIF promotes cellular transformation and proliferation, in part, through interaction with UHRF1. Nevertheless, overexpression of UHRF1 cannot upregulate MIF expression in T‑ALL. New insights into MIF regulation in T‑ALL are imperative to offer the opportunity for therapeutic intervention. In the present study, using RT‑qPCR, western blot analysis, confocal microscopy and RNA sequence, we report the identification and validation of UHRF1 as a negative regulator of MIF, which functions to downregulate MIF expression by binding to the CATT repeat sequence of the MIF promoter. By contrast, HMG‑box protein 1 (HBP1) functions as a positive regulator of MIF. AGK2 supplier Moreover, we demonstrated that HBP1 suppressive signaling is reduced by UHRF1 through promotion of the interaction between MIF and HBP1. MIF deficiency caused by UHRF1 knockdown resulted in enhanced apoptosis in T‑ALL as compared with that caused by decreased MIF or increased HBP1 expression alone. These results identify UHRF1 as a key regulator of MIF transcription in T‑ALL, although these transcription factors possess opposite regulatory functions. Thus, this mechanism may provide insight into how to effectively prevent MIF‑dependent oncogenic activity. Finally, T‑ALL mice possessing high HBP1 or low UHRF1 expression levels are associated with longer survival as compared with control mice, with UHRF1‑knockdown mice living the longest. Taken together, these findings indicate that MIF and its regulators are potential treatment targets and biomarkers for the prediction of prognosis in T‑ALL.Following the publication of this article, the authors have realized that the two affiliation addresses in the paper were written incorrectly “The First People’s Hospital” and “The Second People’s Hospital” should have appeared as “The First People’s Hospital of Linhai” and “The Second People’s Hospital of Linhai”, respectively. Therefore, the author affiliations and addresses in this paper should have appeared as follows Jixin Li1, Caili Yang1 and Yan Wang2. 1Department of Neurology, The First People’s Hospital of Linhai, Taizhou, Zhejiang 317000; 2Department of Neurology, The Second People’s Hospital of Linhai, Taizhou, Zhejiang 317016, P.R. China. The authors regret these errors in the presentation of the affiliation addresses, and apologize for any inconvenience caused.[the original article was published in Molecular Medicine Reports 23 Article no. 165, 2021; DOI 10.3892/mmr.2020.11804].Inability of early detection as well as lack of proper therapeutic intervention, both add to the complexity of pancreatic cancer. Understanding of the basic cellular processes is of the utmost importance and autophagy is one of these processes. Considering the importance of this process in normal cellular functions as well as in pathological states, elaboration of the updated information on the mechanism of autophagy was initially carried out. Autophagy is a process for degradation of damaged cellular organelles, abnormal proteins and even nutrients which happen via formation of autophagosomes. Incidentally, autophagy has been shown to play both oncogenic and tumour‑suppressive functions in cancer and has also been shown to modulate stemness of cancer cells, recurrence and resistance to chemotherapeutic agents. The contribution of autophagy genes and pathways in pancreatic tumorigenesis was also evaluated. Regulation is the key step in any such cellular phenomenon and noncoding RNA‑mediated regulation is an emerging field. While miRNAs participate mainly in post‑transcriptional regulation, long noncoding RNAs and circular RNAs have more diverse regulatory functions. Noncoding RNAs are also shown to modulate both the tumour‑promoting and tumour‑suppressing functions of autophagy in pancreatic cancer. The implication of noncoding RNA‑mediated regulation with respect to radio‑resistance and chemo‑resistance of pancreatic cancer cells was also assessed. To the best of our knowledge, this is the first ever attempt trying to decipher the cross‑talk between autophagy‑noncoding RNAs and genes involved in the development and progression of pancreatic cancer.Renal ischemia/reperfusion (I/R) injury can lead to acute renal failure, delayed graft function and graft rejection. Nucleotide‑binding oligomerization domain NOD‑like receptor containing pyrin domain 3 (NLRP3)‑mediated inflammation participates in the development of renal injury. Nrf2 accelerates NLRP3 signaling pathway activation and further regulates the inflammatory response. In addition, hydrogen sulfide serves a protective role in renal injury; however, the detailed underlying mechanism remains poorly understood. The present study investigated whether Nrf2 and NLRP3 pathway participate in hydrogen sulfide‑regulated renal I/R‑induced activation of the inflammatory response and apoptosis. Wild‑type and Nrf2‑knockout (KO) mice underwent surgery to induce renal I/R via clamping of the bilateral renal pedicles. A total of 20 mg/kg MCC950 (an NLRP3 inhibitor) was injected intraperitoneally daily for 14 days prior to surgery. Renal tissue and blood were collected from the I/R model mice to analyze NLRP3 and Nrf2 mRNA expression levels, NLRP3, PYD and CARD domain containing, caspase‑1, IL‑1β, Nrf2 and heme oxygenase 1 protein expression levels, cell apoptosis, the secretion of tumor necrosis factor‑α, IL‑1β and IL‑6 cytokines and renal histopathology and function. Renal I/R activated the NLRP3 and Nrf2 signaling pathways. Conversely, MCC950 treatment inhibited activation of the NLRP3 signaling pathway, and prevented I/R‑induced renal injury, release of cytokines and apoptosis in renal I/R model mice. Sodium hydrosulfide (NaHS) not only alleviated upregulation of NLRP3 protein expression levels, but also relieved renal injury, release of cytokines and cell apoptosis induced by renal I/R in wild‑type mice, but not in Nrf2‑KO mice. NaHS alleviated NLRP3 inflammasome activation, renal injury, the inflammatory response and cell apoptosis via the Nrf2 signaling pathway in renal I/R model mice.