Corrigendum: Evaluation and management of systemic corticosteroids-induced ocular hypertension in children with non-Hodgkin lymphoma.

[This corrects the article DOI: 10.3389/fped.2022.982224.].

Evaluation and management of systemic corticosteroids-induced ocular hypertension in children with non-Hodgkin lymphoma.

Purpose: To investigate the effect of systemic corticosteroids (CSs) on ocular hypertension (OHT) and to evaluate the management of OHT in children with non-Hodgkin lymphoma (NHL). Methods: Medical records of children with NHL treated in our institution between October 2016 and October 2019 were reviewed. The enrolled patients were divided into the mature B-cell lymphoma (MBL) group and lymphoblastic lymphoma (LBL) group based on pathology. Data on routine ophthalmic examinations and management of OHT were recorded. Results: Of the 54 recruited patients, 38 patients (70.4%) had LBL, and 16 (29.6%) had MBL. Thirty-one patients (57.4%) developed OHT, 24 patients (77.4%) in the LBL group, and 7 (22.6%) in the MBL group. Twelve patients (38.7%) were identified as high responders (10 with LBL and 2 with MBL). Symptomatic patients had a higher mean peak IOP than asymptomatic patients (p=0.006). A total of 74.2% of OHT was controlled with antiglaucoma medications (100% in the MBL group vs. 66.7% in the LBL group, significant variation, p < 0.001). In total, 8 patients (25.8%) underwent tapering of the CSs dose. The duration of OHT was shorter in the MBL group than in the LBL group (p = 0.003). No patients were found to have glaucomatous damage or cataracts. Conclusions: Patients receiving systemic CSs had a higher risk of developing OHT, but the pattern of CSs administration might be a critical factor in the risk and severity of OHT. Tapering of CSs dose should be considered the first line for the management of OHT during high-dose CSs therapy.

Long Noncoding RNA VPS9D1-AS1 Sequesters microRNA-525-5p to Promote the Oncogenicity of Colorectal Cancer Cells by Upregulating HMGA1.

BACKGROUND: The long noncoding RNA VPS9D1 antisense RNA 1 (VPS9D1-AS1) has emerged as a critical regulator in non-small-cell lung, gastric, and prostate cancers. In this study, we measured the expression levels of VPS9D1-AS1 in colorectal cancer (CRC) and determined the role of VPS9D1-AS1 in regulating the biological activities of CRC cells. In addition, we thoroughly elucidated the molecular mechanism mediating the oncogenic activities of VPS9D1-AS1 in CRC. METHODS: The expression levels of VPS9D1-AS1 in CRC tissues and cell lines were detected via quantitative reverse transcription-polymerase chain reaction. Loss-of-function experiments were performed to detect the effects of VPS9D1-AS1 silencing on CRC cell proliferation, apoptosis, migration, and invasion as well as on tumor growth in vivo. Bioinformatics analysis predicted the potential microRNAs (miRNAs) interacting with VPS9D1-AS1, and this prediction was further confirmed via RNA immunoprecipitation and luciferase reporter assays. RESULTS: Our results demonstrated the upregulated expression of VPS9D1-AS1 in CRC tissues and cell lines. Functionally, VPS9D1-AS1 interference suppressed CRC cell proliferation, migration, and invasion and promoted cell apoptosis in vitro. In addition, the loss of VPS9D1-AS1 hindered tumor growth in vivo. Mechanistic studies identified VPS9D1-AS1 as a competing endogenous RNA in CRC cells, in which VPS9D1-AS1 acted as a molecular sponge of miR-525-5p and consequently increased the expression of high-mobility group AT-hook 1 (HMGA1). Moreover, rescue experiments revealed that the regulatory effects of VPS9D1-AS1 deficiency on CRC cells were abolished after miR-525-5p inhibition or HMGA1 restoration. CONCLUSION: The newly identified competing endogenous RNA pathway involving VPS9D1-AS1, miR-525-5p, and HMGA1 is implicated in the control of CRC progression and may provide an effective target for CRC diagnosis and therapy.

MicroRNA-374b reduces the proliferation and invasion of colon cancer cells by regulation of LRH-1/Wnt signaling.

Deregulation of microRNA (miRNA) has been suggested as a critical event in colon cancer development and progression. Recent studies have suggested that miR-374b is a novel cancer-related miRNA involved in several cancer types. Thus far, very little is known about the role of miR-374b in colon cancer; therefore, the goal of this study was to investigate the potential role of miR-374b in colon cancer. Here, we showed that miR-374b expression was significantly downregulated in colon cancer tissues and cell lines. Overexpression of miR-374b inhibited the proliferation and invasion of colon cancer cells, while miR-374b suppression promoted colon cancer cell proliferation and invasion. Liver receptor homolog-1 (LRH-1) was identified as a target of miR-374b in colon cancer cells. Both the mRNA and protein expression of LRH-1 were regulated by miR-374b. In addition, an inverse correlation between LRH-1 mRNA and miR-374b expression was evidenced in colon cancer specimens. Notably, overexpression of miR-374b also downregulated the Wnt signaling in colon cancer cells. Furthermore, restoration of LRH-1 expression significantly abolished the antitumor effect of miR-374b in colon cancer cells. These findings suggest that miR-374b inhibits colon cancer cell proliferation and invasion through downregulation of LRH-1 expression. Inhibiting LRH-1 by miR-374b may represent a novel therapeutic strategy for the treatment of colon cancer.