Diabetic foot wound ulcers management by vacuum sealing drainage: A meta-analysis.

The meta-analysis aimed to assess and compare diabetic foot wound ulcer management by vacuum sealing drainage. Using dichotomous or contentious random- or fixed-effects models, the outcomes of this meta-analysis were examined, and the odds ratio (OR) and the mean difference (MD) with 95% confidence intervals (CIs) were computed. Twenty-three examinations from 2000 to 2023 were enrolled for the present meta-analysis, including 1928 individuals with diabetic foot ulcers. Vacuum sealing drainage had significantly lower wound healing (OR, 2.35; 95% CI, 1.79-3.08, p < 0.001), lower duration of therapy (MD, -6.19; 95% CI, -10.06 to -2.32, p = 0.002), higher wound size reduction (MD, 4.22; 95% CI, 0.87-7.56, p = 0.01) and lower complication (OR, 0.32; 95% CI, 0.13-0.80, p = 0.01) compared with standard therapy in patients with diabetic foot ulcers. The examined data revealed that vacuum sealing drainage had significantly lower wound healing, duration of therapy and complication rates, as well as higher wound size reduction, compared with standard therapy in patients with diabetic foot ulcers. Yet, attention should be paid to its values since most of the selected examinations had a low sample size.

Sternal wound infections following internal mammary artery grafts for a coronary bypass: A meta-analysis.

The meta-analysis aims to evaluate and compare the sternal wound infections following internal mammary artery grafts for a coronary bypass. Examinations comparing bilateral internal mammary artery to single internal mammary artery for coronary artery bypass grafting were among the meta-analyses from various languages that met the inclusion criteria. Using dichotomous random- or fixed-effect models, the results of these investigations were examined, and the Odd Ratio (OR) with 95% confidence intervals (CIs) was computed. A total of 31 examinations from 2001 to 2023 were recruited for the current analysis including 181 503 personals with coronary artery bypass grafting. Bilateral internal mammary artery had significantly higher sternal wound infection (OR, 1.51; 95% CI, 1.37-1.68, p < 0.001), superficial sternal wound infection (OR, 1.72; 95% CI, 1.16-2.56, p = 0.007), deep sternal wound infection (OR, 1.62; 95% CI, 1.41-1.86, p < 0.001), sternal wound infection in diabetics (OR, 1.48; 95% CI, 1.16-1.90, p = 0.002), sternal wound infection in elderly (OR, 1.38; 95% CI, 1.22-1.57, p < 0.001), sternal wound infection in pedicled preparation (OR, 1.70; 95% CI, 1.30-2.23, p < 0.001) and sternal wound infection in skeletonized preparation (OR, 1.40; 95% CI, 1.09-1.81, p = 0.009) compared to single internal mammary artery in personals with coronary artery bypass grafting. Bilateral internal mammary artery grafting is linked to a higher risk of impaired wound healing, particularly in diabetic individuals, elderly, pedicled preparation, and skeletonized preparation. Nevertheless, caution should be exercised while interacting with its values since examinations were performed by different surgeons with different skills on different types of personals.

The hepatic and pancreatic tumour resection risk factors for surgical site wound infections: A meta-analysis.

A meta-analysis was conducted to measure hepatic and pancreatic tumour resection (HPTR) risk factors (RFs) for surgical site wound infections (SSWIs). A comprehensive literature inspection was conducted until February 2023, and 2349 interrelated investigations were reviewed. The nine chosen investigations included 22 774 individuals who were in the chosen investigations' starting point, 20 831 of them were with pancreatic tumours (PTs), and 1934 with hepatic tumours (HTs). Odds ratio (OR) and 95% confidence intervals (CIs) were used to compute the value of the HPTR RFs for SSWIs using dichotomous and continuous approaches, and a fixed or random model. HT patients with biliary reconstruction had significantly higher SSWI (OR, 5.81; 95% CI, 3.42-9.88, P < .001) than those without biliary reconstruction. Nevertheless, there was no significant difference between individuals with PT who underwent pancreaticoduodenectomy and those who underwent distal pancreatectomy in SSWI (OR, 1.63; 95% CI, 0.95-2.77, P = .07). HT individuals with biliary reconstruction had significantly higher SSWI compared with those without biliary reconstruction. Nevertheless, there was no significant difference between PT individuals who underwent pancreaticoduodenectomy and those who underwent distal pancreatectomy in SSWI. However, owing to the small number of selected investigations for this meta-analysis, care must be exercised when dealing with its values.

LncRNA ACTA2-AS1 suppress colon adenocarcinoma progression by sponging miR-4428 upregulation BCL2L11.

BACKGROUND: Long non-coding RNA is considered to be essential to modulate the development and progression of human malignant cancers. And long non-coding RNA can act as crucial modulators by sponging the corresponding microRNA in tumorigenesis. We aimed to elucidate the function of ACTA2-AS1 and its molecular mechanism in colon adenocarcinoma. MATERIALS AND METHODS: The expression of ACTA2-AS1, miR-4428 and BCL2L11 in colon adenocarcinoma tissues were detected via qRT-PCR. SW480 and HT29 cells were transfected with shRNA ACTA2-AS1, OE ACTA2-AS1, miRNA mimics of miR-4428, miR-4428 inhibitor, si-BCL2L11 and over-expression of si-BCL2L11. Cell proliferation, colony formation and apoptosis were respectively assessed using CCK-8 assay, colony assay and flow cytometry. Luciferase reporter assay was performed to verify the targets of ACTA2-AS1 and miR-4428. Tumor subcutaneous xenograft mode was constructed to explore tumor growth in vivo. RESULTS: ACTA2-AS1 was obviously downregulated in human colon adenocarcinoma tissues and colon adenocarcinoma cell lines. Silence or over-expression of ACTA2-AS1 promoted or inhibited cell proliferation and colony formation abilities, and regulated apoptosis. The silence of ACTA2-AS1 resulted in the decrease of Bax and increase of Bal2, while restored in OE ACTA2-AS1 group when compared with the control transfected cells. In addition, luciferase reporter assay revealed that ACTA2-AS1 interacted with miR-4428 and suppressed its expression. miR-4428 could bind to 3' untranslated region of BCL2L11 and modulated the expression of BCL2L11 negatively. Knockdown of ACTA2-AS1 and over-expression of BCL2L11 reversed the biological function that ACTA2-AS1 mediated by knockdown ACTA2-AS1 alone. CONCLUSION: Our data demonstrated that ACTA2-AS1 could suppress colon adenocarcinoma progression via sponging miR-4428 to regulate BCL2L11 expression.

Telmisartan Mitigates High-Glucose-Induced Injury in Renal Glomerular Endothelial Cells (rGECs) and Albuminuria in Diabetes Mice.

Diabetic nephropathy (DN) is a common and severe complication of diabetes, impacting millions of people worldwide. High concentrations of serum glucose-associated injury of renal glomerular endothelial cells (rGECs) are involved in the DN pathogenesis. We found that exposure to high glucose increased the expression of angiotensin II type 1 receptor (AT1R) in human rGECs (hrGECs). To block the increased AT1R level, we used the newly developed antagonist Telmisartan. This study investigated whether Telmisartan possessed a beneficial effect against high-glucose-induced insults in hrGECs and explored the underlying mechanism. Our findings indicate that Telmisartan ameliorated high-glucose-induced mitochondrial dysfunction by increasing mitochondrial membrane potential. Also, Telmisartan attenuated oxidative stress by reducing the levels of two oxidative stress biomarkers 8-hydroxy-2 deoxyguanosine (8-OHDG) and malondialdehyde (MDA). Further, we found that Telmisartan prevented high-glucose-induced expression of NADPH oxidase 2 (NOX-2). Interestingly, exposure to high glucose resulted in the increased endothelial permeability of renal glomerular endothelial cells, which was mitigated by treatment with Telmisartan. Mechanistically, these effects are mediated by the MLCK/MLC-2/occludin signaling pathway. In the leptin-deficient db/db diabetic mouse model, we proved that Telmisartan treatment ameliorated the reduction of occludin and albuminuria. In conclusion, our findings demonstrate that Telmisartan possesses protective effects on high-glucose-induced injury to renal glomerular endothelial cells; its antagonizing of AT1R could be a potential therapeutic target in diabetic nephropathy.

lncRNA LIFR-AS1 suppresses invasion and metastasis of non-small cell lung cancer via the miR-942-5p/ZNF471 axis.

BACKGROUND: MicroRNA 942-5p (miR-942-5p) has been reported to promote migration and invasion in non-small cell lung cancer (NSCLC), but the underlying mechanism is not completely understood. The interplay between long non-coding RNAs (lncRNAs) and miRNAs plays a crucial role in tumor progression. METHODS: In the present study, we performed bioinformatic and biochemical analyses to identify miR-942-5p-interacting lncRNAs. The function and clinical significance of the candidate lncRNA(s) in NSCLC were determined. RESULTS: We identified LIFR-AS1 as a pivotal miR-942-5p-interacting lncRNA. Overexpression of miR-942-5p caused a reduction of LIFR-AS1 in NSCLC cells. LIFR-AS1 showed the ability to sponge miR-942-5p, leading to derepression of ZNF471. Functionally, LIFR-AS1 overexpression inhibited NSCLC cell migration and invasion, whereas LIFR-AS1 silencing yielded an opposite effect. In vivo studies confirmed that LIFR-AS1 overexpression suppressed lung metastasis of NSCLC cells. Rescue experiments demonstrated that enforced expression of miR-942-5p or depletion of ZNF471 restored the migration and invasion capacity of LIFR-AS1-overexpressing cells. Moreover, overexpression of ZNF471 restrained NSCLC cell invasion. Clinically, LIFR-AS1 downregulation was significantly correlated with TNM stage, lymph node metastasis, and reduced overall survival in NSCLC patients. CONCLUSIONS: we provide first evidence for the involvement of the LIFR-AS1/miR-942-5p/ZNF471 axis in NSCLC invasion and metastasis. LIFR-AS1 may represent a novel target for the treatment of NSCLC.

Hsa-miR-132 inhibits proliferation of hepatic carcinoma cells by targeting YAP.

MicroRNAs and Yes-associated protein (YAP) play an important role in the occurrence and development of hepatic carcinomas. However, the interaction between microRNAs and YAP was seldom elucidated. In this study, we showed that miR-132 could target YAP gene by using dual-luciferase reporter system. Further quantitative polymerase chain reaction analysis and western blotting showed that miR-132 could significantly reduce the expression of YAP at mRNA and protein levels. Results of annexin V-fluorescein isothiocyanate, 5-ethynyl-2'-deoxyuridine staining and transwell assays showed that miR-132 significantly promoted the cell apoptosis and effectively inhibited the proliferation and invasion of hepatoma cells. These results indicated that miR-132 could inhibit the growth of hepatoma cells by targeting YAP gene and reducing its expression level. Taken together, results from this study would help us to understand the mechanisms for occurrence and development of hepatic carcinoma and provide new targets for diagnosis and treatment of liver cancer.

MicroRNA-520c-3p inhibits hepatocellular carcinoma cell proliferation and invasion through induction of cell apoptosis by targeting glypican-3.

AIM: Glypican-3 (GPC3) is a membrane-associated heparan sulfate proteoglycan involved in regulation of cell proliferation, cell survival, cell migration and differentiation process. MicroRNAs (miRNAs) are single-stranded, non-coding functional RNAs that are important in many biological processes. GPC3 and miRNAs have been found to play essential roles in the development and progression of hepatocellular carcinoma (HCC). However, little information about the relationship between GPC3 and miRNAs is available nowadays. Therefore, this study aims to examine the relationship between GPC3 and miRNAs. METHODS: Dual-luciferase reporter assay was used to validate the direct target of GPC3. Fluorescence quantitative PCR and Western blotting were used to examined the gene expression at mRNA and protein levels. Cell apoptosis was evaluated by flow cytometric analysis and Annexin V-FITC staining. Invasion of cells was evaluated by Transwell matrigel assay. RESULTS: The results showed that miR-520c-3p could specifically target GPC3 in HCC cells. GPC3 protein levels decreased with unchanged transcription efficiency after miRNA transfection, and there was negative correlation of miR-520c-3p expression in HCC in relate to GPC3 protein levels. Moreover, miR-520c-3p not only induced HCC cell apoptosis, but also inhibited the growth and invasion of the cells. Interestingly, overexpression of GPC3 could effectively reverse apoptosis induced by miR-520c-3p transfection in HCC. CONCLUSIONS: Taken together, these results supported that miR-520c-3p may decrease GPC3 protein levels to inhibit proliferation of HCC cells. Therefore, GPC3 could be a new target for genetic diagnosis and treatment of HCC.

The efficacy and safety of hydrotherapy in patients with knee osteoarthritis: a meta-analysis of randomized controlled trials.

BACKGROUND: Currently, there is poor evidence of the effect of hydrotherapy on patients with knee osteoarthritis (OA). The authors performed a meta-analysis from randomized controlled trials to determine the efficacy and safety of a hydrotherapy program on measures of pain and knee function in individuals living with knee OA. METHODS: A literature review included PubMed, EMBASE, Cochrane Library, Science Citation Index, ScienceDirect, and Ovid. Studies evaluating the efficacy of hydrotherapy for knee OA up to August 2023 were included. The research was reported based on the preferred reporting items for systematic reviews and meta-analysis guidelines to ensure the reliability and verity of results. Statistical analysis was performed using Stata/SE version 15.0. RESULTS: A total of six randomized controlled trials were included for data extraction and meta-analysis. The present study revealed that there were significant differences between the two groups regarding the pain intensity at 1 week (WMD=-0.429; 95% CI: -0.679 to -0.179; P =0.001), 4 week (WMD=-0.308; 95% CI: -0.587 to -0.030; P =0.030) and 8 week (WMD=-0.724; 95% CI: -1.099 to -0.348, P <0.001). Furthermore, hydrotherapy was associated with improved outcome of the Western Ontario and McMaster Universities Arthritis index at 1 week (WMD=-3.314; 95% CI: -6.484 to -0.145, P =0.040), 4 week (WMD= -3.630; 95% CI: -6.893 to -0.366, P =0.029) and 8 week (WMD=-3.775; 95% CI: -7.315 to -0.235; P =0.037). No serious adverse events were observed in all patients who received hydrotherapy. CONCLUSION: Hydrotherapy is efficacious and safe for reducing pain and improving functional status in individuals with knee OA, without increasing the risk of adverse effects.

The effect of subcutaneous Lixisenatide on weight loss in patients with type 2 Diabetes Mellitus: Systematic review and Meta-Analysis of randomized controlled trials.

BACKGROUND: The impacts of subcutaneous Lixisenatide on body weight in patients with type 2 DM, remain inadequately understood; consequently, this systematic review and meta-regression analysis of randomized controlled trials (RCTs) was conducted to evaluate the influence of subcutaneous Lixisenatide administration on BW and BMI values in individuals with Type 2 diabetes. METHODS: A comprehensive literature search was conducted across four databases, spanning from their inception to February 2023. We computed effect sizes employing the random-effects model and reported results in terms of weighted mean differences (WMD) along with their corresponding 95% confidence intervals (CI). RESULTS: 23 articles with 26 RCT arms were included in the meta-analysis. The combined findings from a random-effects model demonstrated a significant reduction in body weight (WMD: -0.97 kg, 95 % CI: -1.10, -0.83, p < 0.001) and BMI (WMD: -0.48 kg/m2, 95 % CI: -0.67, -0.29, P < 0.001) after subcutaneous administration of Lixisenatide. Furthermore, a more pronounced reduction in body weight was discovered in RCTs lasting less than 24 weeks (WMD: -1.56 kg, 95 % CI: -2.91, -0.20, p < 0.001), employing a daily dosage of subcutaneous Lixisenatide lower than 19 Âµg per day (WMD: -1.94 kg, 95 % CI: -2.54, -1.34, p < 0.001) and with a mean participant age of 60 years or more (WMD: -1.86 kg, 95 % CI: -3.16, -0.57, p = 0.005). CONCLUSIONS: Lixisenatide was found to significantly decrease BW and BMI in patients with type 2 DM and could be considered as a therapeutic option for those suffering from weight gain caused by other anti-diabetic agents. However, while prescribing Lixisenatide, careful consideration of patient-specific factors is recommended.

Knockdown of GPC3 inhibits the proliferation of Huh7 hepatocellular carcinoma cells through down-regulation of YAP.

Glypican-3 (GPC3), a membrane-associated heparan sulfate proteoglycan, is frequently upregulated in hepatocellular carcinoma (HCC). Yes-associated protein (YAP) is also found over-expressed in HCC and has been identified as a key effector molecule in Hippo pathway, which could control the organ size in animals through the regulation of cell proliferation and apoptosis and plays an important role in the development of malignant tumors. Studies have reported that GPC3 and YAP might collaborate to regulate the development of HCC. To elucidate the role of GPC3 in the development of HCC and its relationship with YAP, siRNA technique was employed to knock down GPC3 in Huh7 HCC cells. Moreover, recombinant human YAP-1 was used to examine the effects of GPC3 on Huh7 cells. The results of flow cytometric analysis and Annexin-V-FLUOS apoptosis assay showed that knockdown of GPC3-induced apoptosis in Huh7 cells, resulting in inhibition of cell proliferation as examined by EdU incorporation assay, migration, and invasion. GPC3 knockdown also suppressed the expression of YAP in mRNA and protein levels, as examined by fluorescence quantitative PCR and Western blot analysis. Moreover, addition of recombinant human YAP-1 effectively rescued the cells from apoptosis triggered by GPC3 knockdown. Taken together, our findings suggest that GPC3 regulates HCC cell proliferation with the involvement of Hippo pathway.

circ_0008285 Regulates Glioma Progression via the miR-384/HMGB1 Axis.

Background: Recent studies indicate that circular RNAs (circRNAs) have been implicated in the initiation or progression of a wide spectrum of diseases. In the current study, we explored the potential engagement of circ_0008285 in glioma and investigated the downstream regulators. Methods: The detection of circ_0008285 level in glioma specimens and cell lines was conducted by quantitative real-time polymerase chain reaction. The chi-squared test was employed to evaluate the relationship between the circ_0008285 level and the clinical features of glioma patients. The roles of circ_0008285 on the proliferation and apoptosis of glioma cells were studied by knockdown experiment. Meanwhile, the regulatory relationship of circ_0008285, miR-384, and high mobility group protein B1 (HMGB1) was explored in glioma cells, and we explored the effects of circ_0008285/miR-384/HMGB1 pathway on glioma cells. Results: In glioma specimens and cell lines, the expression of circ_0008285 was significantly increased, and a high circ_0008285 level was associated with a larger tumor size and more advanced grading in glioma patients. Furthermore, downregulating circ_0008285 suppressed proliferation and triggered apoptosis of glioma cells, which was associated with a cell cycle arrest at the G1/G0 phase. Mechanism studies indicated that circ_0008285 regulated HMGB1 by sponging miR-384. Functional experiments demonstrated that circ_0008285 promoted the malignant phenotype of glioma cells by miR-384/HMGB1 axis. Conclusion: Our study revealed circ_0008285 as a novel oncogenic factor in glioma through modulating the miR-384/HMGB1 pathway, suggesting that targeting circ_0008285 could serve as a strategy for glioma management.

Prognostic impact of prognostic nutritional index on renal cell carcinoma: A meta-analysis of 7,629 patients.

BACKGROUND: Prognostic nutritional index (PNI) is a parameter which reflects nutritional and inflammatory status. The prognostic value of PNI in renal cell carcinoma (RCC) remains in debate. The aim of this study is to evaluate the prognostic value and clinicopathological features of PNI in RCC. METHODS: A literature search was performed in the databases of PubMed, Embase, Web of Science, and Cochrane Library. Hazard ratios (HRs), odds ratios (ORs), and 95% confidence intervals (CIs) were extracted for meta-analysis. The association between PNI and overall survival (OS), cancer-specific survival (CSS), disease-free survival (DFS), progression-free survival (PFS), recurrence-free survival (RFS), and clinicopathological factors were evaluated. RESULTS: Eleven studies involving 7,629 patients were included for meta-analysis. A decreased PNI was shown to be a significant predictor of worse OS (HR = 2.00, 95%CI = 1.64-2.42, p<0.001), CSS (HR = 2.54, 95%CI = 1.61-4.00, p<0.001), and DFS/PFS/RFS (HR = 2.12, 95%CI = 1.82-2.46, p<0.001) in RCC. Furthermore, a low PNI was correlated with Fuhrman grade III-IV (OR = 1.96, 95%CI = 1.27-3.02, p = 0.002), T stage T3-T4 (OR = 2.21, 95%CI = 1.27-3.87, p = 0.005), presence of sarcomatoid differentiation (OR = 5.00, 95%CI = 2.52-9.92, p<0.001), and presence of tumor necrosis (OR = 3.63, 95%CI = 2.54-5.19, p<0.001). CONCLUSION: PNI is an independent prognostic indicator of survival and associated with Fuhrman grade, T stage, sarcomatoid differentiation, and tumor necrosis in patients with RCC.

Protective Effect of Iron Oxide Nanoparticles on Periodontal Injury in Rats by Inhibiting Collagenase-1 and Alkaline Phosphatase Expression.

This study intends to assess whether iron oxide nanoparticles affect periodontal injury and collagenase-1 (COL-1), and alkaline phosphatase (ALP) in rats. In this study, the ALP activity and Col-1 concentration in rats with periodontal injury were determined.We detected the periodontal histopathological changes and expression of periodontal pocket depth (PD) and attachment loss (AL) by Hematoxylin and eosin (HE) staining.We also detected Col-1 and ALP proteins in periodontal tissues by Western blot. Real-time reverse transcription-polymerase chain reaction (RT-PCR) detected Col-1 and ALP mRNA level in periodontal tissues of rats in each group, while ALP activity and Col-1 concentration in gingival crevicular fluid in model group increased compared to sham group (P < 0.05). After intervention by iron oxide nanoparticles, ALP activity and Col-1 concentration in the gingival crevicular fluid of model rats decreased greatly (P < 0.05). The gingival atrophy was more serious in model group, and many inflammatory cells infiltrated into the tissue and destroyed the alveolar tissue. Meanwhile, the periodontal tissue from rats in intervention group was greatly improved, and the degree of alveolar bone destruction was also significantly reduced, while the PD and AL periodontal indexes were significantly inhibited (P < 0.05). The protein and relative expression showed that the protein and mRNA expressions of ALP and Col-1 in periodontal tissue from model group were lower than those in sham group (P < 0.05). After intervention by iron oxide nanoparticles, the protein and mRNA expressions of ALP and Col-1 in the periodontal tissues in intervention group increased (P < 0.05). Iron oxide nanoparticles can thus inhibit the expression of ALP and COL-1 in periodontal injury rats, and improve the periodontal injury tissue.

Does bariatric surgery really benefit patients before total knee arthroplasty? A systematic review and meta-analysis.

PURPOSE: At present, whether bariatric surgery before total knee arthroplasty (TKA) affects the prognosis of subsequent TKA has been a topic of debate in the academic community. The primary purpose of this systematic review and meta-analysis was to investigate the effect of previous bariatric surgery on prosthetic revisions and postoperative complications after TKA. METHODS: We included prospective and observational studies published in English involving patients who had undergone bariatric surgery prior to TKA and compared them with morbidly obese patients with no history of bariatric surgery. The Newcastle-Ottawa Scale was used to assess the methodological quality of non-randomized case-control studies. The outcomes included revisions, infections, venous thromboembolism (VTE), blood transfusion, mortality, stiffness or manipulation under anesthesia (MUA), and medical complications. RESULTS: Of the 9 included studies with 166047 patients, 4 were matched cohort studies, 2 were unmatched cohort, and 3 were database studies. Methodological quality was high in ten studies and moderate in thirteen studies. Our analysis demonstrated that patients with TKA who had undergone prior bariatric surgery were associated with increased risks of long-term revision, long-term infection, long-term stiffness or MUA and blood transfusions, whereas prior bariatric surgery did not increase the risk of short-term complications and short-term revision. CONCLUSION: This meta-analysis highlights the risks of bariatric surgery prior to TKA and suggests that prior bariatric surgery may increase the risk of perioperative blood transfusion and also the risk of revision and infection in long-term follow-up. Surgeons can use this information to help counsel patients undergoing bariatric surgery before primary TKA.

LncRNA DUXAP8 induces breast cancer radioresistance by modulating the PI3K/AKT/mTOR pathway and the EZH2-E-cadherin/RHOB pathway.

Radiation resistance poses a major clinical challenge in breast cancer (BC) treatment, but little is known about how long noncoding RNA (lncRNA) may regulate this phenomenon. Here, we reported that DUXAP8 was highly expressed in radioresistant BC tissues, and high expression of DUXAP8 was associated with poor prognosis. We found that the overexpression of DUXAP8 promoted radioresistance, while the knockdown of DUXAP8 expression increased radiosensitivity. Further studies revealed that DUXAP8 enhanced the radioresistance of BC cells by activating the PI3K/AKT/mTOR pathway and by repressing the expression of E-cadherin and RHOB through interaction with EZH2. Together, our work demonstrates that the overexpression of DUXAP8 promotes the resistance of BC cells toward radiation through modulating PI3K/AKT/mTOR pathway and EZH2-E-cadherin/RHOB axis. Targeting DUXAP8 may serve as a potential strategy to overcome radioresistance in BC treatment.

LncRNA FGD5-AS1 Facilitates the Radioresistance of Breast Cancer Cells by Enhancing MACC1 Expression Through Competitively Sponging miR-497-5p.

Background: LncRNA-FGD5-AS1, as an oncogene, participates in the development and progress of various cancers. However, the exact role and the molecular mechanisms by which FGD5-AS1 regulates radiosensitivity in breast cancer (BC) remains largely unknown. Methods: We used X-Ray weekly-dose-increase method to establish radiation-resistance cell lines. Bioinformatics tools analyze the expression of FGD5-AS1 in breast cancer tissue and evaluated the relationship between FGD5-AS1 and clinic-pathological features. CCK-8 and colony formation were used to analyze cell proliferation. Western blotting and qPCR were applied to detect protein and gene expression, respectively. RNA interference was used to knock down the endogenous gene expression. Luciferase reporter system and immunoprecipitates were applied to verify the target of FGD5-AS1. Result: FGD5-AS1 was overexpressed in BC tissues and radiation-resistance cell lines. Higher levels of FGD5-AS1 predicted poorer clinical characteristics and prognosis. Loss-of-function FGD5-AS1 sensitized BC cells to X-ray, meanwhile, the cell gained radiation-resistance when exogenous FGD5-AS1 was expressed. FGD5-AS1 depletion arrested cells at G0/G1 and triggers cell apoptosis. The starBase database (ENCORI), predicted binding site of miR-497-5p in FGD5-AS1 sequence, and luciferase reporter system and immunoprecipitates verified miR-497-5p was the target of FGD5-AS1. Furthermore, MACC1 was predicted and verified as the target of miR-497-5p. Loss-of-function FGD5-AS1 sensitized ionizing radiation was rescued by the up-regulation of MACC1 and the inhibition of miR-497. Conclusion: FGD5-AS1 displays an oncogene profile in CRC; patients with high expression of FGD5-AS1 should benefit less from radiotherapy and need a more frequent follow-up. Besides, FGD5-AS1 may be a potential therapeutic target for CRC.

Corrigendum: LncRNA FGD5-AS1 Facilitates the Radioresistance of Breast Cancer Cells by Enhancing MACC1 Expression Through Competitively Sponging miR-497-5p.

[This corrects the article DOI: 10.3389/fonc.2021.671853.].

Upregulation of phosphatidylinositol glycan anchor biosynthesis class C is associated with unfavorable survival prognosis in patients with hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is one of the most common types of malignant tumor, and is the second highest cause of cancer-associated mortality, behind lung carcinoma. It is urgent to identify novel genes that can be used to confirm the diagnosis and prognosis of patients with HCC. The present study aimed to investigate the expression pattern of phosphatidylinositol glycan anchor biosynthesis class C (PIGC) in HCC and assess its clinical prognostic significance. Bioinformatics analyses were used to investigate PIGC mRNA expression levels in HCC and adjacent non-cancerous tissue samples. Furthermore, the present study detected the expression levels of PIGC protein in HCC and matched normal tissue samples via immunohistochemistry, and evaluated the prognostic significance of PIGC protein in HCC. The levels of PIGC mRNA and protein were found to be significantly higher in tissue from patients with HCC compared with non-cancerous liver tissue. The survival analysis showed that the expression levels of PIGC mRNA or protein were associated with the survival of patients with HCC. PIGC protein expression was significantly associated with Tumor-Node-Metastasis stage. A negative correlation between PIGC DNA methylation and mRNA expression was observed (Spearman r=-0.453). PIGC is an oncogene that is negatively regulated by DNA methylation, and high levels of PIGC mRNA or protein may predict an unfavorable prognosis in patients with HCC.