Long non-coding RNA OR3A4 facilitates cell proliferation and migration in colorectal cancer through the Wnt/ß-catenin signaling pathway.

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, "Long non-coding RNA OR3A4 facilitates cell proliferation and migration in colorectal cancer through the Wnt/ß-catenin signaling pathway, by W. Sun, G.-R. Chen, J. Wang, X.-Y. Yu, X.-F. Hao, M.-Y. Hu, published in Eur Rev Med Pharmacol Sci 2020; 24 (10): 5360-5366-DOI: 10.26355/eurrev_202005_21319-PMID: 32495870" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/21319.

LINC00473 functions as an oncogene and predicts poor prognosis in pancreatic cancer via the cAMP/ß-catenin axis.

OBJECTIVE: To investigate the expression and function of LINC00463 in pancreatic cancer (PC), and to demonstrate the relationship between LINC00473 expression and clinical pathological characteristics and prognosis of PC. PATIENTS AND METHODS: Expressions of LINC00473 in PC tissues and cell lines were detected using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). LINC00473 siRNA was synthesized to knock down the LINC00473 expression in PANC-1 cells. Proliferation, invasion, and migration abilities of experimental cells were analyzed using cell counting kit-8 (CCK-8) assay and transwell assay, respectively. cAMP activity was detected and protein expression of ß-catenin was measured to explain the underlying mechanism of LINC00473 in PC. The prognosis and clinical pathological features of PC patients were illustrated. RESULTS: LINC00473 was highly expressed in PC tissues and cells. Higher level of LINC00473 was relative with larger tumor size, worse tumor node metastasis (TNM) stage, worse tumor differentiation, higher rates of perineural invasion, and lymphatic invasion. Knockdown of LINC00473 significantly inhibited cell growth, invasion, and migration of PANC-1 cells. LINC00473 activated cAMP and then promoted the phosphorylation of ß-catenin to promote the progression of PC. Furthermore, high expression of LINC00473 and ß-catenin remarkedly indicated poor prognosis of PC patients. CONCLUSIONS: LINC00473 was upregulated in PC tissues and cells, indicating a poor prognosis and clinical pathological features of PC. It promoted PC progression via activating the cAMP/ß-catenin axis, which provided a novel target for the prediction for PC diagnosis, biological therapy, and prognosis.

Long non-coding RNA OR3A4 facilitates cell proliferation and migration in colorectal cancer through the Wnt/ß-catenin signaling pathway.

OBJECTIVE: Colorectal cancer (CRC) remains one of the most ordinary cancers worldwide. Recently, researches have suggested the important role of long noncoding RNAs (lncRNAs) in the progression of tumorigenesis. This study aims to identify how lncRNA OR3A4 functions in the development of CRC. PATIENTS AND METHODS: OR3A4 expressions in 54 paired CRC tissues and CRC cell lines were detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Moreover, the in vitro functions of OR3A4 in CRC cells were identified by performing proliferation assay, wound healing assay, and transwell assay. Besides, the underlying mechanism of OR3A4 in CRC development was explored through Western blot and RT-qPCR. RESULTS: OR3A4 expression was significantly higher in CRC tissues than adjacent normal ones. Cell proliferation, migration, and CRC were inhibited after OR3A4 was knocked down in vitro, which were promoted after upregulation of OR3A4. Moreover, OR3A4 could activate the Wnt/ß-catenin pathway, thus influencing phenotypes of CRC cells. CONCLUSIONS: OR3A4 enhances CRC cell proliferation and migration by activating the Wnt/ß-catenin signaling pathway.

MiR-142-5p reverses the resistance to gefitinib through targeting HOXD8 in lung cancer cells.

OBJECTIVE: To investigate the role and potential mechanism of micro ribonucleic acid (miR)-142-5p in the acquired resistance to gefitinib in lung cancer cells. MATERIALS AND METHODS: The drug resistance of PC9/G cells was detected via methyl thiazolyl tetrazolium (MTT) assay. Expression levels of miR-142-5p and HOXD8 in PC9 and PC9/G cells were detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) and Western blotting. PC9/G cells were transfected with miR-142-5p mimic, while PC9 cells were transfected with miR-142-5p inhibitor. Subsequently, expression changes of HOXD8 were determined using qRT-PCR and Western blotting, cell sensitivity to gefitinib was detected through MTT assay, and the apoptosis was detected via flow cytometry. Moreover, Dual-Luciferase reporter assay was conducted to determine the relationship between HOXD8 and miR-142-5p. Finally, potential involvement of HOXD8 in miR-142-5p-regulated gefitinib sensitivity was confirmed via rescue tests. RESULTS: PC9/G cells were more significantly resistant to gefitinib compared with its parental PC9 cells. MiR-142-5p was down-regulated in PC9/G cells, while that of HOXD8 was up-regulated in PC9/G cells. Transfection of miR-142-5p mimic could inhibit the expression level of HOXD8 in PC9/G cells and reverse its resistance to gefitinib. Conversely, transfection of miR-142-5p inhibitor could upregulate HOXD8 in PC9 cells and promote its resistance to gefitinib. According to the Dual-Luciferase reporter assay, miR-142-5p could suppress the expression of HOXD8 through the targeted binding to the HOXD8 3'UTR. Moreover, miR-142-5p could regulate mitochondrial apoptosis pathway by targeting HOXD8. Finally, rescue tests confirmed that miR-142-5p regulated the sensitivity of PC9 cells to gefitinib by acting on the target gene HOXD8. CONCLUSIONS: Down-regulation of miR-142-5p induces the resistance of lung cancer PC9 cells to gefitinib by upregulating HOXD8.

[Effects of platelet-rich plasma combined with polylactic acid/polycaprolactone on healing of pig deep soft tissue defect caused by fragment injury].

Objective: To investigate the effects of platelet-rich plasma (PRP) combined with polylactic acid/polycaprolactone (PLA/PCL) on healing of mininature pig deep soft tissue defect caused by fragment injury. Methods: Two male Bama miniature pigs with 11 to 12 months (the same below) were selected by lottery to prepare PRP. The other twenty-seven male Bama miniature pigs were used to reproduce deep soft tissue defect caused by high-explosive ammunition fragment injury on bilateral posterior femoral region. According to the random number table, 27 pigs were divided into control group, material group, and PRP+material group, with 9 pigs in each group. After debridement, wounds of pigs in material group and PRP+material group were filled with PLA/PCL and PLA/PCL+2 mL activated PRP, respectively. Pigs in each group received suture of full-thickness skin to close the wounds. The operative duration was recorded. The length and volume of wounds of pigs in the above groups were measured immediately after surgery. In 1, 2, and 4 weeks after surgery, 3 pigs in each group were sacrificed to collect femoral wounds tissue on two sides, and PLA/PCL were collected from wounds of pigs in material group and PRP+material group for general observation of wounds tissue and degradation of the material. In 2 and 4 weeks after surgery, wounds tissue was obtained to observe the histological changes by hematoxylin-eosin staining, and expressions of transforming growth factor ß (TGF-ß) and vascular endothelial growth factor (VEGF), and angiogenesis were determined by immunohistochemical method. In 1, 2, and 4 weeks after surgery, wounds tissue was collected to determine mRNA expressions of TGF-ß and VEGF by real-time quantitative reverse transcription polymerase chain reaction. Data were processed with analysis of variance of factorial design, one-way analysis of variance, and least significant difference-t test. Results: (1) There were no significantly statistical differences in length and volume of the wounds of pigs among the three groups (F=0.336, 0.282, P>0.05). The operative duration in control group [(30.9±2.1)min] was significantly shorter than that of material group [(39.7±2.2)min] and PRP+material group[(40.0±2.6)min], t=-11.45, -11.88, P<0.01. (2) There were respectively 10, 7, and 5 wounds tissue with infection in pigs of control group, material group, and PRP+material group. In 1, 2, 4 weeks after surgery, all of the wounds tissue of pigs was infected in control group, while none of wounds tissue of pigs was infected in material group and PRP+material group. In pigs of material group and PRP+material group, materials and tissue were easily separated in 1 week after surgery; some materials were integrated with tissue and showed a tendency of degradation in 2 weeks after surgery; materials were completely embedded with tissue in 4 weeks after surgery. (3) In pigs of control group, erythrocytes and inflammatory cells infiltration in wounds tissue were observed in 2 weeks after surgery, and necrotic tissue and inflammatory cells infiltration in wounds tissue were still observed in 4 weeks after surgery. In pigs of material group and PRP+material group, a large number of erythrocytes and inflammatory cells infiltration were observed in 2 weeks after surgery. Compared with that of material group, wounds tissue of pigs in PRP+material group had no inflammatory cells infiltration in 4 weeks after surgery. (4) Protein expressions of TGF-ß in fibroblasts and multinuclear macrophagocytes, VEGF in fibroblasts and vascular endothelial cells, and blood vessel formation in wounds tissue of pigs in PRP+material group were significantly more than those of pigs in control group and material group in 2 and 4 weeks after surgery. (5) The mRNA expression of TGF-ß in wounds tissue of pigs in material group was significantly higher than that in control group in 4 weeks after surgery (t=-3.93, P<0.01). Compared with those of pigs in control group and material group, the mRNA expression of TGF-ß in wounds tissue of pigs in PRP+material group was significantly increased at each time point (t=9.23, 13.81, 11.73, -7.51, -12.04, -7.80, P<0.01). The mRNA expression of VEGF in wounds tissue of pigs increased significantly in material group compared with that of pigs in control group in 4 weeks after surgery (t=-3.94, P<0.01). Compared with those of pigs in control group and material group, the mRNA expression of VEGF in wounds tissue increased significantly in wound tissue of pigs in PRP+material group at each time point (t=12.33, 3.95, 7.97, -11.36, -2.97, -4.04, P<0.01). Conclusions: PRP combined with PLA/PCL can accelerate wound healing of deep soft tissue defect of mininature pigs caused by fragment injury by providing physical scaffold for newborn tissue growth, promoting mRNA and protein expressions of TGF-ß and VEGF.

Highly virulent porcine reproductive and respiratory syndrome virus emerged in China.

A highly pathogenic pig disease emerged in China in 2006, which was characterized by prolonged high fever, red discoloration of the body, and blue ears associated with high mortality. Porcine reproductive and respiratory syndrome virus (PRRSV) was isolated as the single most prominent virus in the samples collected from affected pigs. The full-length genomic sequence of the virus revealed two distinct deletions in the non-structural protein 2 (NSP2) in comparison to all previously reported North American genotype PRRSV. Through extensive surveys in 14 different provinces, 56 additional PRRSV isolates were obtained from affected farms. All of the isolates were found to contain identical deletions in NSP2. To confirm the etiology, eight 60-day-old PRRSV-free pigs were divided into two groups and the test group was intranasally infected at a titer of 2 x 10(5.0) tissue culture infectious dose 50 per pig. The inoculated pigs all died at 7, 8, 12, 16, or 21 days post-inoculation with their clinical and pathological findings similar to those in the field. The viruses recovered from dead pigs were identical to the inoculated virus in NSP2 and GP5 genes. Our study shows that the recently emerged PRRSV in China is characterized by two discontiguous deletions in NSP2 and is the cause for the current epizootics in China.

Functional conservation of the cell cycle-regulating transcription factor DRTF1/E2F and its pathway of control in Drosophila melanogaster.

The cellular transcription factor DRTF1/E2F is implicated in the control of early cell cycle progression due to its interaction with important regulators of cellular proliferation, such as pocket proteins (for example, the retinoblastoma tumour suppressor gene product), cyclins and cyclin-dependent kinase subunits. In mammalian cells DRTF1/E2F is a heterodimeric DNA binding activity which arises when a DP protein interacts with an E2F protein. Here, we report an analysis of DRTF1/E2F in Drosophila cells, and show that many features of the pathway which regulate its transcriptional activity are conserved in mammalian cells, such as the interaction with pocket proteins, binding to cyclin A and cdk2, and its modulation by viral oncoproteins. We show that a Drosophila DP protein which can interact co-operatively with E2F proteins is a physiological DNA binding component of Drosophila DRTF1/E2F. An analysis of the expression patterns of a Drosophila DP and E2F protein indicated that DmDP is developmentally regulated and in later embryonic stages preferentially expressed in proliferating cells. In contrast, the expression of DmE2F-1 in late stage embryos occurs in a restricted group of neural cells, whereas in early embryos it is widely expressed, but in a segmentally restricted fashion. Some aspects of the mechanisms which integrate early cell cycle progression with the transcription apparatus are thus conserved between Drosophila and mammalian cells. The distinct expression patterns of DmDP and DmE2F-1 suggest that the formation of DP/E2F heterodimers, and hence DRTF1/E2F, is subject to complex regulatory cues.