OncomiR-181a promotes carcinogenesis by repressing the extracellular matrix proteoglycan decorin in hepatocellular carcinoma.

BACKGROUND: Proteoglycans are important tumor microenvironment extracellular matrix components. The regulation of key proteoglycans, such as decorin (DCN), by miRNAs has drawn attention since they have surfaced as novel therapeutic targets in cancer. Accordingly, this study aimed at identifying the impact of miR-181a in liver cancer and its regulatory role on the extracellular matrix proteoglycan, DCN, and hence on downstream oncogenes and tumor suppressor genes. RESULTS: DCN was under-expressed in 22 cirrhotic and HCC liver tissues compared to that in 11 healthy tissues of liver transplantation donors. Conversely, miR-181a was over-expressed in HCC liver tissues compared to that in healthy liver tissues. In silico analysis predicted that DCN 3'UTR harbors two high-score oncomiR-181a binding regions. This was validated by pmiRGLO luciferase reporter assay. Ectopic miR-181a expression into HuH-7 cells repressed the transcript and protein levels of DCN as assessed fluorometrically and by western blotting. DCN siRNAs showed similar results to miR-181a, where they both enhanced the cellular viability, proliferation, and clonogenicity. They also increased Myc and E2F and decreased p53 and Rb signaling as assessed using reporter vectors harboring p53, Rb, Myc, and E2F response elements. Our findings demonstrated that miR-181a directly downregulated the expression of its direct downstream target DCN, which in turn affected downstream targets related to cellular proliferation and apoptosis. CONCLUSION: To our knowledge, this is the first study to unveil the direct targeting of DCN by oncomiR-181a. We also highlighted that miR-181a affects targets related to cellular proliferation in HCC which may be partly mediated through inhibition of DCN transcription. Thus, miR-181a could be a promising biomarker for the early detection and monitoring of liver cancer progression. This would pave the way for the future targeting of the oncomiR-181a as a therapeutic approach in liver cancer, where miR-181a-based therapy approach could be potentially combined with chemotherapy and immunotherapy for the management of liver cancer.

Peripartum veno-venous extracorporeal membrane oxygenation in patients with severe CoViD-19-related-ARDS.

We describe a case series of five pregnant or postpartum women with severe CoViD-19-related ARDS requiring VV ECMO at our centre between Jan 1 and Sep 30, 2021. All patients were cannulated at the referring hospitals by our team before transferring to our centre. None of the women were vaccinated against CoViD-19. All had severe ARDS with Murray's Lung Injury Score of 3-4 and met the severity threshold for ECMO initiation that was used in the EOLIA study. All patients were discharged alive to home, acute rehabilitation, or lung transplant centre. One patient suffered intrauterine death before ECMO initiation and another while on ECMO. VV ECMO for refractory CoViD-19 related ARDS in the peripartum period is safe, and in this small series, it was associated with good maternal survival rates.

Oncological outcomes of laparoscopic versus open gastrectomy after neoadjuvant chemotherapy for locally advanced gastric cancer: a retrospective multicenter study.

BACKGROUND: The oncological outcomes of laparoscopic gastrectomy (LG) and open gastrectomy (OG) following neoadjuvant chemotherapy have been investigated in a few studies. Our purpose was to evaluate the oncological outcomes of LG and OG after neoadjuvant chemotherapy in patients with locally advanced gastric cancer (GC) and to determine the advantages, preferences, and ease of use of the two techniques after chemotherapy. METHODS: We conducted a retrospective chart review of all patients who underwent either OG (n = 43) or LG (n = 41). The neoadjuvant treatment regimen consisted of capecitabine plus oxaliplatin for three cycles, which was then repeated 6 to 12 weeks after the operation for four cycles. RESULTS: The hospital stay time and intraoperative blood loss in the LG group were significantly lower than those in the OG group. The mortality rate and the 3-year survival rate for patients in the LG group were comparable to those of patients in the OG group (4.6% vs. 9.7% and 68.3% vs. 58.1%, respectively). Similar trends were observed regarding the 3-year recurrence rate and metastasis. The mean survival time was 52.9 months (95% confidence interval [CI], 44.2-61.6) in the OG group compared with 43.3 (95% CI, 36.6-49.8) in the LG group. Likewise, the mean disease-free survival was 56.1 months (95% CI, 46.36-65.8) in the LG group compared with 50.9 months (95% CI, 44.6-57.2) in the OG group. CONCLUSION: LG is a feasible and safe alternative to OG for patients with locally advanced GC receiving neoadjuvant chemotherapy.

Vestibular function assessment following cochlear implantation using rotatory chair testing.

PURPOSE: Study aimed to assess short- and long-term impact of unilateral cochlear implantation in children on the angular vestibulo-ocular reflex using rotatory chair test. METHODS: Two groups; A (early postoperative evaluation) and B (later on evaluation) were included, each consisted of 23 cochlear implant candidates' children with unilateral implant surgeries were performed in El-Galaa Hospital, Cairo, Egypt. They were assessed by rotatory chair test; sinusoidal harmonic acceleration paradigm. Three parameters: average gain, asymmetry, and phase results of each group were compared with the manufacturer's norms and with each other. Further analysis by comparing each group implanted side specific gain results with the same group non-implanted side specific gain and with the other group implanted side specific gain results. RESULTS: Group A versus norms showed only significant differences in average gain and phase at 0.02 Hz and 0.01 Hz test frequencies respectively. However, three parameters in group B showed no significant differences when compared with norms. When comparing the results of both groups relieved significant differences only in average gain at 0.02 Hz and in phase at both 0.01 Hz and 0.04 Hz. Comparing specific gain results for both sides of group A showed significance at 0.32 Hz test frequency, while those of group B showed no significant differences. The analysis of implanted sides gain results of both groups showed differences at 0.16 Hz and 0.32 Hz. CONCLUSION: Bilateral restoration and improvement of angular vestibulo-ocular reflexes after unilateral cochlear implantation was reported with long-term assessment by rotatory chair test.

Competing Endogenous RNAs in Hepatocellular Carcinoma-The Pinnacle of Rivalry.

The role of noncoding transcripts in gene expression is nowadays acknowledged to keep various diseases at bay-despite being referred to as "junk" DNA several years ago. Believed to be at the heart of multiple regulatory pathways, microRNAs (miRNAs) are small noncoding RNAs (ncRNAs) involved in posttranscriptional gene regulation. Recently, the discovery of ncRNAs that compete for shared miRNA pools has dimmed the light on the solo performance of miRNAs in genomic regulation. Indeed, several studies describe RNAs such as long noncoding RNAs, mRNAs, circular RNAs, pseudogenes, and viral RNAs as competing endogenous RNAs (ceRNAs) that sequester miRNAs, allowing for de-repression of downstream miRNA targets. Such integration between coding and noncoding transcripts forms complex ceRNA networks that when dysregulated lead to several diseases such as hepatocellular carcinoma. Here, the authors review perturbed ceRNA networks in hepatocellular carcinoma, describe the role of each in tumorigenesis, and discuss their various clinical implications.

Epigallocatechin gallate (EGCG) and miR-548m reduce HCV entry through repression of CD81 receptor in HCV cell models.

Epigallocatechin gallate (EGCG) is the most abundant component in green tea extract, that has powerful antioxidant and antiviral effects. It has been previously reported to inhibit HCV entry via several mechanisms. Hence, this study aimed at further investigating the potential impact of EGCG on HCV entry through regulation of the expression of tetraspanin receptor CD81 by the novel predicted miR-548m. Liver biopsies were obtained from 29 HCV patients and 10 healthy controls for expression profiling. Huh7 cells were stimulated with EGCG and subsequently miR-548m expression was assessed. Naïve, HCV- ED43/JFH-1 and HCV-JFH-1 infected Huh7 cells were transfected by miR-548m mimics and inhibitors. Consequently, CD81 protein and mRNA levels were assessed using flow cytometry and qRT-PCR, respectively. Additionally, these cells were used to investigate HCV permissiveness into Huh7 cells using qRT-PCR for viral quantification. Direct binding confirmation of miR-548m to CD81 was done using luciferase reporter assay. In-silico analysis revealed miR-548m to have two potential binding sites in the 3'UTR of CD81 mRNA. EGCG boosted miR-548m expression in Huh7 cells. Additionally, miR-548m caused a downregulation of CD81 protein and mRNA levels as well as reduction in HCV infectivity of Huh7 cells. Luciferase binding assay confirmed the binding of miR-548m to CD81 mRNA at the two predicted binding sites. Intriguingly, miR-548m expression was not detected in healthy liver biopsies but was found in liver biopsies of HCV patients. This study shows that EGCG might act as an anti-HCV agent that reduces cellular infectivity via enhancing miR-548m expression and repressing CD81 receptor.

Correction to: Ectopic delivery of miR-200c diminishes hepatitis C virus infectivity through transcriptional and translational repression of Occludin.

The author would like to correct the errors in the online published article.

MiR-615-5p depresses natural killer cells cytotoxicity through repressing IGF-1R in hepatocellular carcinoma patients.

miR-615-5p was characterized by our group as a tumour suppressor. IGF-1 R activates a downstream signalling pathway, well characterized in liver cells, however, its role in immunity especially Natural Killer cells (NKs) remains vague. This study aimed at investigating the regulatory role of miR-615-5p on IGF signalling and its impact on NKs cytotoxicity in HCC. Our results showed an upregulation in miR-615-5p and IGF-1 R in NKs of 130 HCC patients compared to 35 controls. Forcing the expression of miR-615-5p, repressed IGF-IR, attenuated NKs cytotoxicity, decreased CD56dim, increased CD56bright NK subsets and reduced the cytotoxic markers NKG2D, TNF-α and perforins. It repressed NKG2D ligand (ULBP2) in Huh-7 cells. In conclusion, miR-615-5p represses IGF-1 R in NKs and their target hepatocytes; however, it has a contradicting impact on HCC progression on both cell types. These findings might pave the way for better understanding the role of microRNAs in NKs function and HCC immune-pathogenesis.

Ectopic delivery of miR-200c diminishes hepatitis C virus infectivity through transcriptional and translational repression of Occludin.

Occludin (OCLN) is an essential factor for HCV entry through interacting with other surface receptors. The aim of this study was to investigate the epigenetic regulation of Occludin expression and to study its impact on viral infectivity. microRNAs expression was assessed using qRT-PCR, while OCLN protein expression was investigated by indirect immunofluorescence and Western blotting. Viral infectivity was assessed by measuring viral-load using qRT-PCR. In silico analysis predicted that miR-200c targeted the OCLN 3'UTR, which was further experimentally confirmed. miR-122 was previously validated to target the 3'UTR of OCLN and was used as a control. We report a significant down-regulation of miR-200c in liver tissues of HCV-infected patients. Ectopic expression of both miR-122 and miR-200c in Huh7 cells reduced OCLN mRNA and protein levels. Viral infectivity was significantly reduced by miR-200c but enhanced by miR-122. This work sheds light on miR-200c as a novel regulator of HCV infectivity through the regulation of OCLN.

Abrogating the interplay between IGF2BP1, 2 and 3 and IGF1R by let-7i arrests hepatocellular carcinoma growth.

IGF2BP 1, 2 and 3 control the fate of many transcripts. Immunoprecipitation studies demonstrated the IGF2BPs to bind to IGF1R mRNA, and our laboratory has recently shown them to post-transcriptionally regulate IGF1R. This study sought to identify a microRNA regulating the IGF2BPs and consequently IGF1R. All three IGF2BPs were among the top-ranked predicted targets of let-7i. Let-7i was downregulated in HCC tissues, and transfection of HuH-7 with let-7i inhibited malignant cell behaviors and decreased IGF2BPs transcripts. Direct binding of let-7i to IGF2BP2 and IGF2BP3 3'UTRs was confirmed, and the effect of let-7i caused a decrease in the IGF2BPs' target gene, the IGF1R. IGF1R mRNA was inversely correlated with let-7i in HCC tissues and was reduced upon let-7i transfection into HuH-7. Reporter assays validated IGF1R as a target of let-7i. Therefore, let-7i may control HCC tumorigenesis by regulating IGF1R directly and indirectly by interrupting the interplay between IGF1R and the IGF2BPs.

Contradicting interplay between insulin-like growth factor-1 and miR-486-5p in primary NK cells and hepatoma cell lines with a contemporary inhibitory impact on HCC tumor progression.

In this study, an impaired natural killer (NK) cell cytolytic activity in 135 hepatocellular carcinoma (HCC) patients parallel to a reduced expression level of insulin-like growth factor (IGF)-1 in NK cells of HCC patients has been revealed. Ectopic expression of miR-486-5p, a direct upstream regulator of IGF-1, restored the endogenous level of IGF-1 in NK cells of HCC patients, thus augmenting its cytolytic activity against Huh7 cells in an opposite manner to the IGF-1 siRNAs. Unorthodoxly, over-expression of miR-486-5p in target hepatocytes resulted in the repression of IGF-1, suppression of Huh7 cells proliferation and viability in a similar pattern to the IGF-1 siRNAs. Therefore, this study highlights a potential role of IGF-1 in modulating cytolytic potential of NK cells of HCC patients. miR-486-5p acts in a cell-specific manner, differentially modulating IGF-1 expression in NK cells and their target hepatocytes with a contemporary inhibitory impact on HCC progression.

The arthritic patients' perspective of measuring treatment efficacy: Patient Reported Experience Measures (PREMs) as a quality tool.

OBJECTIVES: We aimed to assess the validity and reliability of a Patient Reported Experience Measures (PREMs) questionnaire which can be used in standard clinical practice to measure self-defined important experiences of inflammatory arthritis patients. METHODS: The Patient Reported Experience Measures (PREMs) questionnaire was conceptualised based on frameworks used by the WHO Quality of Life tool, as well as the PRO measurement information system (PROMIS). Cognitive interviews were conducted with 94 inflammatory arthritis patients (diagnosed according to EULAR/ACR criteria 2010), with a range of severity and disease activity to identify item pool of questions. Item selection and reduction was achieved based on patients as well as an interdisciplinary group of physicians, nurses, health educators and occupational therapy (OTs) feedback, in addition to clinometric and psychometric methods. The latter included Rasch and internal consistency reliability analyses. The PREMs questionnaire was developed centered around 5 categories: 1. Journey to diagnosis, 2. Impact of the disease on the patients' everyday life, 3. knowledge about the disease, 4. the care in the hospital, and 5. patient education and aftercare (including what to do in case of exacerbation). After analysis for ordered response options, content analysis and semi structured group discussion to cover these 5 categories, 32 questions were identified as the final item set. The routine clinic was used as a setting for the questionnaire evaluation. 183 patients were asked to complete the PROMs as well as PREMs questionnaires whilst sitting in the waiting area before being examined by the treating physician. Reliability and comprehensibility was assessed using the Test-retest reliability (reproducibility). RESULTS: The tool was derived from RA patients, therefore establishing its face validity. The PREMs questionnaire showed a high degree of comprehensibility (9.3). It demonstrated a relatively high-standardised alpha (0.892). The questionnaire items correlated significantly (p<0.01) with clinical parameters of disease activity, PROMs, self-helplessness and DAS-28 score supporting its construct validity. The domain of impact of arthritis correlated significantly (p<0.01) with health related quality of life (HRQOL) score as well as disease activity and damage measures, establishing its criterion validity. Patient education and aftercare correlated significantly (p<0.01) with adherence to therapy. CONCLUSIONS: The studied PREMs questionnaire had fair psychometric properties as it was valid, reliable and comprehensible. The patients were able to comprehend varying response options on a categorical scale, and could accurately respond to items using a 7-day recall period. It provides informative measure for the patients' experience with their disease, and in the meantime, facilitates incorporating the patients' feedback into the patients' management algorithm.

Progesterone suppresses interferon signaling by repressing TLR-7 and MxA expression in peripheral blood mononuclear cells of patients infected with hepatitis C virus.

This study aimed at investigating the effect of progesterone on interferon signaling pathways in peripheral blood mononuclear cells (PBMCs) of patients infected with hepatitis C virus (HCV). PBMCs were isolated from peripheral blood of 38 treatment-naïve HCV-infected patients, pooled, and stimulated with progesterone in the presence and absence of its receptor antagonist, mifepristone, along with interferon alpha (IFN-α) or imiquimod. Toll-like receptor (TLR) 7 and myxovirus resistance protein A (MxA) were quantified in PBMCs using RT-qPCR. Imiquimod alone or combined with progesterone did not change MxA expression in HCV-infected PBMCs. Progesterone decreased the inducing effect of IFN-α on TLR-7 expression in both males and females. Moreover, progesterone stimulation prior to IFN-α treatment attenuated the Jak/STAT pathway, which was reflected by decreased expression of MxA in females. Progesterone showed a negative impact on the IFN signaling pathway in HCV-infected PBMCs as it decreased the expression of TLR-7 in both genders, while MxA expression was decreased only in females.

Dual downregulation of microRNA 17-5p and E2F1 transcriptional factor in pediatric systemic lupus erythematosus patients.

The main objective of this study is to investigate the relative expression of miRNA 17-5p and one of its target genes E2F1 in the peripheral blood of systemic lupus erythematosus pediatric patients. The expression of miRNA 17-5p and its target E2F1 mRNA was analyzed by TaqMan real-time qPCR. Our results showed significant downregulation of miRNA 17-5p in SLE patients compared to healthy controls; moreover, miRNA 17-5p was more downregulated in patients on no treatment compared to those on treatment. Relative expression of E2F1, which is a target for miRNA 17-5p, was significantly downregulated as well on both mRNA and protein levels in SLE pediatric patients. In conclusion, our data show an unexpected dual downregulation of both miRNA 17-5p and its target gene E2F1 on the mRNA and protein levels. This may suggest an expression pattern of miRNA 17-5p and its target E2F1 that may be specific to SLE. [corrected].

Prevalence and Risk Factors of New-onset Diabetes after Transplant in East Africans.

Very little is known about the prevalence of new-onset diabetes after transplant (NODAT) in sub-Saharan and Eastern Africans. Most of the data are related to African Americans and to North and South Africans. The aims of this study were to examine the prevalence of NODAT in Sudanese renal transplant recipients, compare it with the published literature, and identify the risk factors for developing NODAT. In total, 150 patients who received a living-related kidney transplant between January 2015 and January 2016 were included in this study. Patients with diabetic nephropathy and pretransplant diabetes were excluded. Follow-up was for 2 years after the transplant. The variables studied were age, sex, body mass index, a family history of diabetes mellitus (DM), pretransplant steroid therapy, dyslipidemia, and hepatitis C virus infection. Twenty- three patients (15.3%) developed NODAT during the study period. The mean age of the patients who developed NODAT was 39 ± 14 years, and the mean time to develop NODAT was 5.78 ± 5.9 months. In the multivariate analysis, the risk factors for developing NODAT were a family history of DM (P = 0.01) and pretransplant steroid therapy (P = 0.01). The prevalence of NODAT in this study was 15.3%, which is in line with the reported literature from North Africa. However, it was significantly lower than the reported prevalence in African Americans.

Sustaining Life versus Altering Life-Saving Drugs: Insights to Explain the Paradoxical Effect of Extracorporeal Membrane Oxygenation on Drugs.

There has been a substantial increase in the use of extracorporeal membrane oxygenation (ECMO) support in critically ill adults. Understanding the complex changes that could affect drugs' pharmacokinetics (PK) and pharmacodynamics (PD) is of suitable need. Therefore, critically ill patients on ECMO represent a challenging clinical situation to manage pharmacotherapy. Thus, clinicians' ability to predict PK and PD alterations within this complex clinical context is fundamental to ensure further optimal and, sometimes, individualized therapeutic plans that balance clinical outcomes with the minimum drug adverse events. Although ECMO remains an irreplaceable extracorporeal technology, and despite the resurgence in its use for respiratory and cardiac failures, especially in the era of the COVID-19 pandemic, scarce data exist on both its effect on the most commonly used drugs and their relative management to achieve the best therapeutic outcomes. The goal of this review is to provide key information about some evidence-based PK alterations of the drugs used in an ECMO setting and their monitoring.

Arthritis education: the integration of patient-reported outcome measures and patient self-management.

OBJECTIVES: To assess the integration of PROMs and patient education, using the joint-fitness programme, and the effectiveness of this combined approach on disease activity and adherence to therapy. METHODS: This was a double-blind randomised controlled study which included 147 arthritic patients monitored over 18 months. Every patient completed a PROMs questionnaire. By the 6th month of treatment, the patients were randomly allocated to an active group (74 patients) that was able to view former self-reported PROMs scores and discuss the implementation of the joint fitness programme as a tool for psycho-educational interventions. The control group (73 patients) continued their treatment and management based on viewing their recorded PROMs and clinical assessment. The patients were assessed at 3 monthly intervals for another 12 months. The primary outcome was the change in the patients' adherence to their medications, disease activity score (DAS-28) and PROMs domains. RESULTS: The integration of patient education and PROMs led to a significant greater reduction of disease activity parameters, DAS-28 score, as well as improvement of the patients' adherence to therapy (p<0.01). The improvement of disease activity parameters was associated with the improvement in functional disability and quality of life scores. At 18-month-follow-up, both the self-management and cognitive behavioural therapy intervention demonstrated improvement for disease activity (effect size 1.4 and 1.2 respectively). CONCLUSIONS: The integration of patient education and PROMs succeeded in improving self-perceived health as well as disease activity. The patient education for patients with inflammatory arthritis is feasible in the standard clinical practice.

The optimum inhibitory effects of Alpha Interferon and Cisplatin in colon cancer, a comparative in vitro study.

Cisplatin is well known as a potent anti-cancer agent against colon cancer. However, alpha interferons are also widely used for cancer suppression. This in vitro study was designed to investigate and compare the cancer suppression function of alpha interferon in colon cancer with Cisplatin. The analysis used a human SW 480 cancer cell line with RPMI-1630 culture media. Six dilutions of interferon (2.5 µg/ml, 1.25 µg/ml, 0.562 µg/ml, 0.286 µg/ml, 0.143 µg/ml, and 0.057 µg/ml) and six dilutions of cisplatin (100 µg/ml, 50 µg/ml, 25 µg/ml, 6.25 µg/ml, and 3.125) were used at 24, 48 and 72 hours along with the presence of control groups. Following this, results were observed by ELISA plate reader, and percentage inhibition was calculated using ANOVA analysis. The interferon and cisplatin percentage of inhibition was comparable with higher inhibition rates observed with alpha interferon. The statistical analysis showed that the maximum inhibition was observed at a 0.143 µg/ml interferon concentration when exposed for 48 to 72 hours. This in vitro analysis demonstrated the anti-cancer activity of alpha interferon and its advanced inhibitory activity compared to Cisplatin.

Does Vitamin D Have a Role in Diabetes?

Vitamin D, a fat-soluble vitamin, acts in the calcium and phosphorus metabolism in its active form (1,25-dihydroxy vitamin D). It may help prevent and treat autoimmune diseases, including diabetes mellitus. Diabetes has become a significant global health issue with a rising incidence and prevalence. A recent focus has been on vitamin D supplementation as part of efforts to discover novel ways to prevent and treat diabetes. Most evidence points to the vitamin D receptors (VDRS) gene in both types of diabetes. The main objective of this study is to analyze how vitamin D affects both type 1 and type 2 diabetes. In this literature review, we searched the PubMed and Google Scholar databases to collect related articles from 13 papers of different study designs. We found a significant association between vitamin D deficiency and type 1 and type 2 diabetes development. It has been shown that vitamin D supplements have a promising effect in reducing glycated hemoglobin (HbA1c) in patients with type 1 diabetes, with no significant impact on the incidence or improvement of type 2 diabetes. Patients with diabetes and people at high risk of diabetes need the appropriate amount of vitamin D; therefore, regular testing and vitamin D supplementation are advised for the management and prevention of diabetes. Additional randomized studies with bigger sample sizes and longer-term trials are required to fully explore the benefits of vitamin D supplementation in patients with type 1 and type 2 diabetes.

Regulation of IGF2BP1 by miR-186 and its impact on downstream lncRNAs H19, FOXD2-AS1, and SNHG3 in HCC.

AIM: We have previously characterized oncogenic properties of IGF2BP1 in HCC, and its regulation by short noncoding RNAs (ncRNAs). Recent evidence suggests that IGF2BP1 itself may regulate long ncRNAs (lncRNAs). Therefore, this study aimed at exploring the interplay between IGF2BP1 and various upstream and downstream ncRNAs and its link to HCC pathogenesis. MATERIALS AND METHODS: Bioinformatic analysis was used to identify up- and downstream ncRNAs interacting with IGF2BP1. Huh-7 cells were transfected with siRNAs against IGF2BP1 and microRNA mimics. Relative gene expression was determined using RTqPCR and IGF2BP1 protein was quantified by western blot. Luciferase binding assay was used to explore the targeting of IGF2BP1 3'UTR. HCC tumorigenesis was measured by MTT assay, BrdU-incorporation assay, colony-forming assay, and scratch assay. KEY FINDINGS: Bioinformatic analysis identified three oncogenic lncRNAs - namely H19, FOXD2-AS1, and SNHG3 - potentially regulated by IGF2BP1. Knockdown of IGF2BP1 decreased the expression of all three oncogenic lncRNAs and inhibited malignant cell behaviors. miR-186 was revealed as a possible upstream regulator of IGF2BP1. miR-186 mimics decreased IGF2BP1 mRNA and protein levels. miR-186 was significantly lower while IGF2BP1 was elevated in cancerous tissues from ten HCC patients compared to five healthy controls. In addition, miR-186 mimics caused a downregulation of the oncogenic lncRNAs H19, SNHG3, and FOXD2-AS1 and a concomitant decrease in cell viability, proliferation, migration, and clonogenicity. SIGNIFICANCE: miR-186 may exert tumor suppressor effects in HCC by repressing oncogenic lncRNAs H19, SNHG3, and FOXD2-AS1 through its effect on IGF2BP1.