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The effects involving dietary fiber (oat bran) health supplement on blood pressure levels throughout sufferers together with crucial high blood pressure: A new randomized managed tryout.
MDM2 proto‑oncogene, E3 ubiquitin protein ligase (MDM2) is a well‑known oncogene and has been reported to be closely associated with epithelial‑to‑mesenchymal transition (EMT). The present study first demonstrated that the expression levels of MDM2 were markedly increased in TGF‑β‑induced EMT using quantitative PCR and western blotting. In addition, MDM2 was demonstrated to be associated with pathological grade in clinical glioma samples by immunohistochemical staining. Furthermore, overexpression of MDM2 promoted EMT in glioma, lung cancer and breast cancer cell lines using a scratch wound migration assay. Subsequently, the present study explored the mechanism by which MDM2 promoted EMT and revealed that MDM2 induced EMT by upregulating EMT‑related transcription factors via activation of the B‑Raf signaling pathway through tyrosine 3‑monooxygenase activation protein ε using RNA sequencing and western blotting. This mechanism depended on the p53 gene. Furthermore, in vivo experiments and the colony formation experiment demonstrated that MDM2 could promote tumor progression and induce EMT via the B‑Raf signaling pathway. Since EMT contributes to increased drug resistance in tumor cells, the present study also explored the relationship between MDM2 and drug sensitivity using an MTT assay, and identified that MDM2 promoted cell insensitivity to silibinin treatment in an EMT‑dependent manner. This finding is crucial for the development of cancer therapies and can also provide novel research avenues for future biological and clinical studies.Subsequently to the publication of the above article, the author realized that Fig. 5 on p. 486 contained some errors on account of the figure having been compiled incorrectly; essentially, the published version of the figure contained incorrect images for the panels presented in Fig. 5C and E. The authors were able to re‑examine their original data, and identify the data that was intended to have been shown for these figure parts. The corrected version of Fig. 5 is shown on the next page, featuring the correct data for Fig. 5C and E, including new bar charts showing the quantification of these data. The authors confirm that these data continue to support the main conclusions presented in their paper, and are grateful to the Editor of International Journal of Oncology for allowing them this opportunity to publish a Corrigendum. They also apologize to the readership for any inconvenience caused. [the original article was published in International Journal of Oncology 54 479‑490, 2019; DOI 10.3892/ijo.2018.4659].Gastric cancer (GC) is one of the most frequently diagnosed types of cancer worldwide, and exploring its potential therapeutic targets is particularly important for improving the prognosis of patients with GC. The aim of the present study was to investigate the association between serine/threonine kinase 17a (STK17A) expression and GC prognosis. STK17A expression was measured by quantitative real‑time PCR, western blotting and immunohistochemical staining. Standard stable transfection technology was also used to construct overexpression and knockdown cell lines. Wound healing, Transwell, Cell Counting Kit‑8 and colony formation assays, as well as other methods, were used to explore the function and underlying molecular mechanism of STK17A in GC. The results indicated that STK17A overexpression significantly promoted the proliferation and migration of GC cells. The clinical significance of STK17A in a cohort of 102 cases of GC was assessed by clinical correlation and Kaplan‑Meier analyses. Overexpression of STK17A was demonstrated to be associated with tumor invasion depth (P less then 0.001), lymph node metastasis (P less then 0.001) and poor prognosis in terms of 5‑year survival (P less then 0.001). In addition, Cox multivariate analysis revealed that STK17A expression was an independent risk factor for overall and progress‑free survival (P less then 0.001). Therefore, STK17A may be a valuable biomarker for the prognosis of patients with GC.Lung cancer is one of the most frequently diagnosed neoplasms and the leading cause of cancer‑related mortality worldwide. Its predominant subtype is non‑small cell lung cancer (NSCLC), which accounts for over 80% of the cases. Surprisingly, the majority of lung cancer‑related deaths are caused not by a primary tumour itself, but by its metastasis to distant organs. Therefore, it becomes especially important to identify the factors involved in lung cancer metastatic spread. Special AT‑rich binding protein 1 (SATB1) is a nuclear matrix protein that mediates chromatin looping and plays the role of global transcriptional regulator. During the past decade, it has received much attention as a factor promoting tumour invasion. In breast, colorectal and prostate cancers, SATB1 has been shown to influence the epithelial‑mesenchymal transition (EMT) process, which is thought to be crucial for cancer metastasis. The aim of this study was to analyse the possible correlations between the expression of SATB1 and major EMT‑associated proteins in NSCLC clinical samples. signaling pathway Additionally, the impact of EMT induction in NSCLC cell lines on SATB1 mRNA expression was also investigated. Immunohistochemistry was used to assess the expression of SATB1, SNAIL, SLUG, Twist1, E‑cadherin, and N‑cadherin in 242 lung cancer clinical samples. EMT was induced by TGF‑β1 treatment in the A549 and NCI‑H1703 lung cancer cell lines. Changes in gene expression profiles were analyzed using real‑time PCR and Droplet Digital PCR. SATB1 expression was positively correlated with the expression of SNAIL (R=0.129; P=0.045), SLUG (R=0.449; P less then 0.0001), and Twist1 (R=0.264; P less then 0.0001). Moreover, SATB1 expression significantly increased after in vitro EMT induction in A549 and NCI‑H1703 cell lines. The results obtained may point to the role of SATB1 as one of the regulators of EMT in NSCLC.Colorectal cancer (CRC), a commonly occurring carcinoma, now ranks the second in terms of cancer‑associated deaths around the world. Among the numerous factors that contribute to CRC tumor progression, a class of motor proteins known as the kinesins has been found to play a vital role. Kinesins are responsible for the intracellular trafficking of functional proteins, organelles and biomacromolecules along microtubules. Dysregulation of kinesins has been revealed to influence the cell cycle to cause abnormal cell growth and affect cell adhesion to promote epithelial‑mesenchymal transition in breast, bladder, ovarian and prostate cancer. Studies on the function of kinesins in CRC have also been performed, although, to the best of our knowledge, little is known about the underlying mechanisms of kinesins in CRC progression. The present review outlines the roles played by different kinesins in CRC carcinogenesis, mainly discussing the most studied subfamilies (kinesin 3‑6, 8, 10, 11 and 13), This review aims to illustrate the functions of kinesins in CRC cell growth, cancer metastasis and chemoresistance to provide insights regarding kinesins as potential targets for determining CRC prognosis and selecting therapy.MicroRNAs (miRNAs/miRs) are key regulators of renal interstitial fibrosis (RIF). The present study was designed to identify miRNAs associated with the development of RIF, and to explore the ability of these identified miRNAs to modulate the renal tubular epithelial‑to‑mesenchymal transition (EMT) process. To this end, miRNAs that were differentially expressed between normal and fibrotic kidneys in a rat model of mercury chloride (HgCl2)‑induced RIF were detected via an array‑based approach. Bioinformatics analyses revealed that miR‑101 was the miRNA that was most significantly downregulated in the fibrotic renal tissue samples, and this was confirmed by RT‑qPCR, which also demonstrated that this miRNA was downregulated in transforming growth factor (TGF)‑β1‑treated human proximal tubular epithelial (HK‑2) cells. When miR‑101 was overexpressed, this was sufficient to reverse TGF‑β1‑induced EMT in HK‑2 cells, leading to the upregulation of the epithelial marker, E‑cadherin, and the downregulation of the mesenchymal marker, α‑smooth muscle actin. By contrast, the downregulation of miR‑101 using an inhibitor exerted the opposite effect. The overexpression of miR‑101 also suppressed the expression of the miR‑101 target gene, TGF‑β1 type I receptor (TβR‑I), and thereby impaired TGF‑β1/Smad3 signaling, while the opposite was observed upon miR‑101 inhibition. To further confirm the ability of miR‑101 to modulate EMT, the HK‑2 cells were treated with the TβR‑I inhibitor, SB‑431542, which significantly suppressed TGF‑β1‑induced EMT in these cells. Notably, miR‑101 inhibition exerted a less pronounced effect upon EMT‑related phenotypes in these TβR‑I inhibitor‑treated HK‑2 cells, supporting a model wherein miR‑101 inhibits TGF‑β1‑induced EMT by suppressing TβR‑I expression. On the whole, the present study demonstrates that miR‑101 is capable of inhibiting TGF‑β1‑induced tubular EMT by targeting TβR‑I, suggesting that it may be an important regulator of RIF.Kidins220 is a transmembrane scaffold protein involved in several types of cancer. The aim of the present study was to examine the role of Kidins220 in tumorigenesis and disease progression of pancreatic cancer. The relevant signalling pathways including EGFR, EMT, and MMP were also investigated. The expression of Kidins220 was examined at the transcript and protein level. The Kidins220 knockdown cell model was established and its influence on cellular functions was determined. Involvement of Kidins220 in tumorigenesis and metastasis was examined in CD1 mice, respectively. The results showed that, reduced Kidin220 expression was associated with tumorigenesis, metastasis, and overall survival of pancreatic cancer. Knockdown of Kidins220 promoted proliferation, colony formation and tumorigenic capacity of pancreatic cancer cells in vitro and in vivo, respectively. Kidins220 regulated pancreatic cancer cell migration through the EGFR/AKT/ERK signalling pathway. Furthermore, enhanced EMT was observed in the pancreatic cancer cell lines with the knockdown of Kidins220, underlying EGFR regulation. Kidins220 also affected cell invasion via MMP1. A reduced expression of Kidins220 was observed in pancreatic cancer, which is associated with disease progression, distant metastasis and poor prognosis. The loss of Kidins220 in pancreatic cancer may contribute to disease progression through the upregulation of EGFR and downstream signalling.Women experience cognitive decline as they age due to the decrease in estrogen levels following menopause. Currently, effective pharmaceutical treatments for age‑related cognitive decline are lacking; however, several Traditional Chinese medicines have shown promising effects. Lycium barbarum polysaccharides (LBPs) were found to exert a wide variety of biological activities, including anti‑inflammatory, antioxidant and anti‑aging effects. However, to the best of our knowledge, the neuroprotective actions of LBP on cognitive impairment induced by decreased levels of estrogen have not yet been determined. To evaluate the effects of LBP on learning and memory impairment in an animal model of menopause, 45 female ICR mice were randomly divided into the following three groups i) Sham; ii) ovariectomy (OVX); and iii) OVX + LBP treatment. The results of open‑field and novel object recognition tests revealed that mice in the OVX group had learning and memory impairments, and lacked the ability to recognize and remember new objects.
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