LncRNA AB073614 promotes tumor migration and invasion by repressing CDKN1A in non-small cell lung cancer.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "LncRNA AB073614 promotes tumor migration and invasion by repressing CDKN1A in non-small cell lung cancer, by W.-D. Zhao, B.-X. Zhang, X.-H. Cui, J. Zhang, N. Du, Y.-F. Zhang, published in Eur Rev Med Pharmacol Sci 2019; 23 (13): 5815-5822-DOI: 10.26355/eurrev_201907_18320-PMID: 31298333" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18320.

MicroRNA-148a regulates the MAPK/ERK signaling pathway and suppresses the development of esophagus squamous cell carcinoma via targeting MAP3K9.

OBJECTIVE: Esophagus squamous cell carcinoma (ESCC) was a dominant histological type of esophagus cancer, which has a very high incidence due to distant metastasis and local invasion. MicroRNA-148a (miR-148a) functioned as a tumor suppressor in a variety of cancers. The purpose of our study was to explore the vital role of miR-148a in esophagus squamous cell carcinoma. PATIENTS AND METHODS: The Kaplan-Meier method was applied to calculate the 5-year overall survival of esophagus squamous cell carcinoma patients. Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) and Western blot were conducted to calculate the mRNA levels of miR-148a and genes. The cell counting kit-8 (CCK-8) and transwell assays were performed to measure the proliferative and invasive ability. RESULTS: MiR-148a was observed to be significantly downregulated and the downregulation of miR-148 predicted poor prognosis of esophagus squamous cell carcinoma patients. MAP3K9 was a target gene of miR-148a and its expression was mediated by miR-148a through directly binding to the 3'-untranslated region (3'-UTR) of its mRNA in the esophagus squamous cell carcinoma. Moreover, miR-148a remarkably inhibited the proliferation and invasion through directly targeting to MAP3K9 via extracellular-signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway and epithelial-mesenchymal transition (EMT) in the ESCC cells. In addition, overexpression of miR-148a inhibited the growth of ESCC in vivo. CONCLUSIONS: MiR-148a inhibited the proliferation and invasion through directly targeting to MAP3K9 by ERK/MAPK pathway and EMT in ESCC cells. The newly identified miR-148a/MAP3K9 axis provides a novel insight into the pathogenesis of the esophagus squamous cell carcinoma.

LncRNA AB073614 promotes tumor migration and invasion by repressing CDKN1A in non-small cell lung cancer.

OBJECTIVE: Some researches have showed that long noncoding RNAs (lncRNAs) take part in varieties of biological behaviors during the tumor progression. This study aims to determine whether lncRNA AB073614 functioned in the metastasis of non-small cell lung cancer (NSCLC). PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was used to detect AB073614 expression in NSCLC tissues. Besides, wound healing assay and transwell assay were conducted in NSCLC cells. Furthermore, the mechanism assays were performed to identify how AB073614 functioned in metastasis of NSCLC cells. RESULTS: By comparing with the expression level in adjacent tissues, the AB073614 expression level in NSCLC samples was significantly higher. Moreover, after AB073614 was knocked down, invasion and migration of NSCLC cells were inhibited. And after AB073614 was overexpressed, invasion and migration of NSCLC cells were promoted. Also, mRNA and protein expression level of CDKN1A was upregulated via knockdown of AB073614, while mRNA and protein expression level of CDKN1A was downregulated via overexpression of AB073614. Besides, the expression of CDKN1A in NSCLC tissues was negatively correlated to the expression of AB073614. CONCLUSIONS: Our results indicated that AB073614 could enhance cell migration and cell invasion in NSCLC through repressing CDKN1A, which might offer a potential therapeutic choice for patients with NSCLC.

A novel frameshift mutation of Chediak-Higashi syndrome and treatment in the accelerated phase

Chediak-Higashi syndrome (CHS) is a rare autosomal recessive immunodeficiency disease characterized by frequent infections, hypopigmentation, progressive neurologic deterioration and hemophagocytic lymphohistiocytosis (HLH), known as the accelerated phase. There is little experience in the accelerated phase of CHS treatment worldwide. Here, we present a case of a 9-month-old boy with continuous high fever, hypopigmentation of the skin, enlarged lymph nodes, hepatosplenomegaly and lung infection. He was diagnosed with CHS by gene sequencing, and had entered the accelerated phase. After 8 weeks of therapy, the boy had remission and was prepared for allogenic stem cell transplantation.

An insufficient glucose supply causes reduced lactose synthesis in lactating dairy cows fed rice straw instead of alfalfa hay.

The objective of the present study was to investigate the nutrient availability for milk production in the mammary gland of lactating cows fed different forage-based diets. The 3 diets contained 30% corn stover (CS), 30% rice straw (RS), or 23% alfalfa hay plus 7% Chinese wild rye hay (AH) as a forage source. All diets contained 15% of DM as corn silage and 55% of DM as concentrate. The percentage of milk lactose was always lower in the RS-fed cows than in the cows fed AH or CS during the 12-wk feeding trial ( < 0.01). Ruminal propionate concentrations were lower in the RS group than in the AH group ( = 0.03). The ratio of insulin to glucagon in the mammary venous plasma was greater in the AH group than in the CS or RS group ( = 0.04). The abundance of the pyruvate carboxylase mRNA in the liver was lower in the RS group than in the AH or CS group ( = 0.04), and the abundance of mitochondrial phosphoenolpyruvate carboxykinase, IGF-1 receptor, and phosphofructokinase-liver, phosphofructokinase-muscle, and phosphofructokinase-platelet mRNA in the liver were lower in the RS group than in the AH group ( < 0.05). The mammary glucose uptake was greater in the AH-fed cows than in the CS- or RS-fed cows ( = 0.02). The mRNA abundance of the glucose transporters in the mammary gland was similar among the 3 treatments. The mRNA abundance of α-lactalbumin in the mammary gland of the cows fed RS tended to be greater compared with that of the cows fed AH or CS. The milk potassium concentration was greater in the cows fed RS than those fed AH or CS ( < 0.01). In summary, the insufficient ruminal propionate concentrations in the cows fed RS were associated with lower gluconeogenesis in the liver, resulting in the shortage of glucose supply for mammary utilization.

Rechargeable anticandidal denture material with sustained release in saliva.

OBJECTIVE: Candida-induced denture stomatitis is a common debilitating problem among denture wearers. Previously, we described the fabrication of a new denture material that released antifungal drugs when immersed in phosphate buffered saline. Here, we use more clinically relevant immersion conditions (human saliva; 37°C) and measure miconazole release and bioactivity. MATERIALS AND METHODS: Disks were prepared by grafting PNVP [poly(N-vinyl-2-pyrrolidinone)] onto PMMA [poly(methylmethacrylate)] using plasma initiation (PMMA-g-PNVP) and then loaded with miconazole. Drug-loaded disks were immersed in 10-100% human saliva (1-30 days). Miconazole release was measured and then tested for bioactivity vs miconazole-sensitive and miconazole-resistant Candida isolates. RESULTS: HPLC was used to quantify miconazole levels in saliva. Miconazole-loaded disks released antifungal drug for up to 30 days. Higher drug release was found with higher concentrations of saliva, and, interestingly, miconazole solubility was increased with higher saliva concentrations. The released miconazole retained its anticandidal activity. After immersion, the residual miconazole could be quenched and the disks recharged. Freshly recharged disks displayed the same release kinetics and bioactivity as the original disks. Quenched disks could also be charged with chlorhexidine that displayed anticandidal activity. CONCLUSIONS: These results suggest that PMMA-g-PNVP is a promising new denture material for long-term management of denture stomatitis.

Randomized clinical trial comparing infrahepatic inferior vena cava clamping with low central venous pressure in complex liver resections involving the Pringle manoeuvre.

BACKGROUND: Control of bleeding remains key to successful hepatic resection. The present randomized clinical trial compared infrahepatic inferior vena cava (IVC) clamping with low central venous pressure (CVP) during complex hepatectomy using portal triad clamping (PTC). METHODS: Consecutive patients undergoing complex hepatectomy were allocated randomly to PTC combined with infrahepatic IVC clamping or to PTC with low CVP. Primary outcome was blood loss during parenchymal transection. Secondary outcomes were intraoperative surgical and haemodynamic parameters, postoperative recovery of liver and renal function, postoperative morbidity and mortality, and duration of hospital stay. RESULTS: Between January 2008 and September 2010, 192 patients were randomized. Compared with low CVP, infrahepatic IVC clamping significantly decreased blood loss during parenchymal transection (mean(s.e.m.) 243(158) versus 372(197) ml; P < 0·001), was associated with faster recovery of liver function, and caused less impairment in renal function and fewer haemodynamic changes. The degree of cirrhosis correlated positively with CVP (R(2) = 0·963, P = 0·019) and with infrahepatic IVC pressure (R(2) = 0·950, P = 0·025). For patients with moderate or severe cirrhosis, infrahepatic IVC clamping was more efficacious in controlling blood loss during parenchymal transection (mean(s.e.m.) 2·9(1·8) versus 6·1(2·4) ml/cm(2); P < 0·001). CONCLUSION: PTC combined with infrahepatic IVC clamping is more efficacious in controlling bleeding during complex hepatectomy than PTC with low CVP, especially in patients with moderate to severe cirrhosis. REGISTRATION NUMBER: NCT01355887 (http://www.clinicaltrials.gov).

Combined hepatocellular cholangiocarcinoma originating from hepatic progenitor cells: immunohistochemical and double-fluorescence immunostaining evidence.

AIMS: Combined hepatocellular cholangiocarcinoma (CHC) is a rare form of primary liver cancer, showing a mixture of hepatocellular and biliary features. Data suggest that most CHC arise from hepatic progenitor cells (HPCs). The aim was to investigate the origin of CHC. METHODS AND RESULTS: Twelve cases of CHC were studied by immunohistochemistry for hepatocytic (hepPar1, alpha-fetoprotein), cholangiocytic cytokeratin [(CK) 7, CK19], hepatic progenitor cell (OV-6), haematopoietic stem cell (c-kit, CD34), as well as CD45 and chromogranin-A markers. The combination of double-fluorescence immunostaining consisted of HepPar1 with CK19, and c-kit with OV-6. All 12 cases demonstrated more or less transitional areas, with strands/trabeculae of small, uniform, oval-shaped cells including scant cytoplasm and hyperchromatic nuclei embedded within a thick, desmoplastic stroma; however, two cases were found to consist entirely of such transitional areas. Simultaneous co-expression of hepPar1 and CK7, or CK19, was demonstrated in 10/12 (83.3%) cases of CHC. c-kit expression was noted in 10/12 (83.3%) cases, of which 7/10 (70%) showed co-expression of OV-6. CONCLUSIONS: The results suggest that CHC are of HPC origin, supporting the concept that human hepatocarcinogenesis may originate from the transformation of HPCs.

Metallothionein I and II gene knock-out mice exhibit reduced tolerance to 24-h sodium lauryl sulphate patch testing.

BACKGROUND: Metallothioneins (MTs) are a group of proteins widely distributed in tissues regulating metal metabolism, scavenging free radicals, and taking part in immunological reactions. Knockout mice for MT genes I and II (MT(-/-)) exhibit reduced tolerance to ultraviolet B injury in vivo. Upregulation of MT proteins can be found at positive allergy patch-test sites; however, the role of MTs in skin irritation has not been investigated. AIM: To evaluate the role of MT genes in sodium lauryl sulphate (SLS)-induced skin irritation. SLS is a well-known model irritant in the study of experimental irritant contact dermatitis. METHODS: Skin irritation was induced in mice by applying closed-patch testing of 2.5%, 5%, 7.5% and 10% SLS in distilled water on the right dorsal skin of MT(-/-) mice for 24 h. Skin irritation was evaluated visually and by the number of infiltrated inflammatory cells in SLS-irritated skin. Homozygous wild-type mice with intact MT genes (MT(+/+)) tested at the same time served as controls. RESULTS: MT(-/-) mice showed a much higher degree of skin inflammation than did MT(+/+) mice. Numbers of infiltrated inflammatory cells were 312.8 +/- 50.9 vs. 136.2 +/- 13.1 for 2.5%, 430.2 +/- 49.3 vs. 242.6 +/- 28.6 for 5%, 540.2 +/- 28.4 vs. 437.6 +/- 22.2 for 7.5%, and 690.6 +/- 31.0 vs. 559.0 +/- 37.8 for 10% SLS in MT(-/-) and MT(+/+) mice, respectively (P < 0.05, Mann-Whitney U test). CONCLUSIONS: These results clearly suggest that the MTI and MTII genes may play an important protective role in SLS irritation. It would be valuable to study whether topical MTs can prevent or treat skin irritation.

Metallothionein-null mice exhibit reduced tolerance to ultraviolet B injury in vivo.

Events that induce expression of the metallothionein (MT) gene, such as injection of cadmium chloride, cold stress or topical application of 1,25-dihydroxyvitamin D3, can deplete the number of ultraviolet (UV) B-induced sunburn cells (SBC) in mouse skin in vivo. MT-null mouse skin explants exhibit reduced tolerance to UVB injury in vitro. However, the in vivo response of MT-null mice to UVB injury has not been investigated. In the present study, we investigated the role of the MT gene on UVB injury in vivo. MT-null mice that are deficient in MT-I and MT-II genes were studied and compared with homozygous wild-type mice. Mouse dorsal skin was irradiated with 0.05, 0.70 and 1.40 J/cm2 UVB. The thickness of the dorsal skin was measured with a spring micrometer before and 24 h after UVB irradiation. In addition, SBC were counted 24 h after UVB irradiation. No significant difference was found in the change of skin thickness between MT-null mice and control mice irradiated with low-dose UVB (0.05 J/cm2) (Student's t-test, t = 1.519, P = 0.167). At higher doses (0.70 and 1.40 J/cm2), the skin of MT-null mice became much thicker than that of control mice (Student's t-test, t = 6.576, P < 0.01 and t = 3.142, P = 0.007, respectively). More SBC were detected in MT-null mice skin irradiated with the highest dose of UVB (1.40 J/cm2) (Student's t-test, t = 4.258, P < 0.01). These results suggest that the MT gene in mice has a photoprotective role in vivo.