Cahilllewis3825

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. 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. Trichostatin A molecular weight 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.