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Steer clear of surprising your hematopoietic stem cells to ensure they are youthful as well as increasing.
tivity of CRC cells via autophagy and apoptosis and suggested a new mechanism of miR-126-mTOR interaction in CRC pathogenesis. © 2020 Wei et al.Purpose To investigate the association between the lncRNA NEAT1 and breast cancer, and to determine the influence of NEAT1 on regulation of other signaling molecules in breast cancer. Methods In the present study, we measured levels of the lncRNA NEAT1 in 106 breast cancer patients and in a human breast cancer cell line by qRT-PCR. The correlation between NEAT1 expression and patients' clinical characteristics was analyzed with in-house and TCGA data. We used cellular functioning assays and cell immunofluorescence assay to evaluate the role of NEAT1 and its target molecules in proliferation, invasion and migration in breast cancer. We used Western blotting to explore possible targets of NEAT1 and a subcellular fractionation assay to locate NEAT1 expression. Results NEAT1 was overexpressed in breast cancer tissue and also closely related to advanced clinical stages and positive lymph node metastases. NEAT1 levels were also tightly correlated to prognosis for breast cancer patients in survival analyses. Cellular function assays revealed that downregulation of NEAT1 could inhibit breast cancer cell viability, invasion and migration. Western blotting revealed down-regulation of CBX7 and up-regulation of RTCB following NEAT1 inhibition. Based on the cytoplasmic and nuclear expression of NEAT1, we investigated the possible regulation of CBX7 and RTCB by NEAT1. Results showed that NEAT1 regulated the expression of CBX7 and RTCB, possibly by binding of NEAT1 to DNA in the nucleus, which facilitates cell proliferation, invasion and migration. Conclusion The current results suggest that the lncRNA NEAT1 is upregulated in breast cancer and facilitates tumor cell viability, invasion and migration via CBX7 and RTCB. © 2020 Yan et al.Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumor in the digestive tract. Tyrosine kinase inhibitors (TKIs), represented by imatinib, sunitinib, and regorafenib, have become the main treatment for recurrent and metastatic GISTs. With the wide application of mutation analysis and the precision medicine, molecular characteristics have been determined that not only predict the prognosis of patients with recurrent and metastatic GISTs, but also are closely related to the efficacy of first-, second- and third-line TKIs for GISTs, as well as other TKIs. Despite the significant effects of TKIs, the emergence of primary and secondary resistance ultimately leads to treatment failure and tumor progression. Currently, due to the signal transmission of KIT/PDGFRA during onset and tumor progression, strategies to counteract drug resistance include the replacement of TKIs and the development of new drugs that are directed towards carcinogenic mutations. In addition, it is also the embodiment of precision medicine for GISTs to explore new carcinogenic mechanisms and develop new drugs relying on new biotechnology. Surgery can benefit specific patients but its major purpose is to diminish the resistant clones. However, the prognosis of recurrent and metastatic patients is still unsatisfactory. Therefore, it is worth paying attention to how to maximize the benefits for patients. © 2020 Liu et al.Background Epithelial ovarian cancer (EOC) is the most common type of ovarian cancer and is the most lethal gynecologic malignancy. Cytokeratin 19 (CK19) is a small type I cytokeratin. The aim of this study is to explore the functional role of CK19 and its underlying mechanism in EOC. Methods The expression levels of CK19 in EOC tissues were identified by Western blotting and RT-PCR assay. Transwell assay and CCK-8 proliferation assay were used to assess the invasion, migration and proliferation abilities of overexpressed or knockdown CK19 of ovarian cancer cells. We also detected the related genes of Wnt/β-catenin signal pathway, including β-catenin, TCF7, LEF1, c-MYC and cyclin D1 in the transfected ovarian cancer cells by Western blotting and RT-PCR assay. Results The results demonstrated that CK19 was upregulated in EOC tissue. CK19 was verified to promote the invasion, proliferation and migration of ovarian cancer cells. Additionally, CK19 activates the Wnt/β-catenin signaling pathway by upregulated β-catenin, TCF7, LEF1, c-MYC and cyclin D1. Conclusions In summary, this is the first study to investigate the role of CK19 in EOC. These findings provide a potential new therapeutic target for the clinical diagnosis and treatment of ovarian cancer. © 2020 Lu et al.Background SPRR3, also known as esophagin, has been shown to be involved in the initiation and progression of numerous types of tumor. However, the biological function of SPRR3 that contributes to non-small-cell lung cancer (NSCLC) growth and migration is largely unknown. Methods The expression of SPRR3 and its association with EZH2 and miR-876-3p in NSCLC cells were determined by real-time PCR. Protein levels were measured by immunohistochemistry (IHC) and Western blot. Cell functions were studied by CCK-8, transwell assay, flow cytometry and dual-luciferase reporter assay. The effect of SPRR3 on tumor growth in vivo was evaluated in patient-derived xenograft (PDX) models. Results SPRR3 was up-regulated in most NSCLC cell lines and clinical tissues. Also, the correlation between SPRR3 expression and clinical features was significant. Functional studies confirmed that SPRR3 modulates cell proliferation, invasion and cell apoptosis in NSCLC via regulating EZH2, which is a well-known oncogene in NSCLC. Furthermore, SPRR3 was found to be a direct target of miR-876-3p that also plays a suppressor role in NSCLC. Conclusion These findings indicated that miR-876-3p/SPRR3/EZH2 signaling cascade exerts important roles in the regulation of NSCLC, suggesting that this pathway can serve as a potential therapeutic target in NSCLC. © 2020 Li et al.Background Circular RNAs (circRNAs) and microRNAs (miRNAs) have been reported to act as the important regulators in nasopharyngeal carcinoma (NPC). CircRNA ZNF609 (circ-ANF609) and miR-188 have been, respectively, reported to play a pro-cancer and anti-cancer role in NPC. The purpose of this study is to reveal the functional relation of circ-ZNF609 and miR-188 in NPC development. Methods The transcription level and protein level of genes were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assay, respectively. Cell proliferation was analyzed using 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Furthermore, flow cytometry analysis was used to assess cell cycle transition and cell apoptosis rate. Besides, the interaction between miR-188 and circ-ZNF609 or E74-like factor 2 (ELF2) was predicted by starbase or microT-CDS, and then confirmed by the dual luciferase reporter assay and RIP assay. Results Circ-ZNF609 and ELF2 levels were increased and miR-188 level was decreased in NPC. Circ-ZNF609 knockdown significantly inhibited cell proliferation and cell cycle transition, as well as accelerated apoptosis in NPC cells. Interestingly, circ-ZNF609 directly bound to miR-188. Circ-ZNF609 regulated NPC cell growth through modulating miR-188 expression. In addition, miR-188 suppressed NPC cell growth via directly targeting ELF2. Finally, we confirmed that circ-ZNF609 mediated miR-188 level to modulate ELF2 expression. Conclusion Our findings demonstrated that circ-ZNF609 depletion-repressed proliferation and cell cycle transition, and induced apoptosis of NPC cells via modulation of miR-188/ELF2 axis, providing potential targets for the therapy of NPC. © 2020 Li et al.Purpose Recent studies have shown that noncoding RNAs (ncRNAs) play essential roles in the development of a number of cancers. read more Circular RNAs (circRNAs) have been shown to contribute to the progression of colorectal cancer (CRC). Methods In this study, the expression levels of circular RNA 0060745 (circ_0060745), and microRNA 4736 (miR-4736) were measured using qRT-PCR. Kaplan-Meier survival analysis and receiver operating characteristic (ROC) analysis were used to evaluate the diagnostic value of circ_0060745. Transwell assay and cell counting kit-8 (CCK8) assay were used to determine the metastatic and proliferative capacity of CRC cells. The expression of chromosome segregation one like (CSE1L) was measured using Western blotting and immunohistochemistry (IHC). In addition, RNA pull-down assay and luciferase assay were performed to verify the targeted binding between miR-473,6 and circ_0060745, and between as miR-4736 and CSE1L. Results We showed that circ_0060745 was upregulated in CRC, and was associated with unfavorable clinicopathological characteristics. We also showed that circ_0060745 acted as an oncogene and promoted CRC cell proliferation and metastasis. Circ_0060745 was primarily located in the cytoplasm. Furthermore, miR-4736 was downregulated in CRC, was a downstream target of circ_0060745, and mediated proliferation and metastasis. We showed that circ_0060745 sequestered miR-4736, which resulted in CRC cell proliferation and metastasis. Finally, we showed that CSE1L, a downstream target of miR-4736, was upregulated in CRC and mediated suppression of proliferation and metastasis in CRC. Conclusion The results of this study showed that circ_0060745 promoted CRC cell proliferation and metastasis via modulation of miR-4736/CSE1L signaling. The Circ_0060745/miR-4736/CSE1L axis might be a novel target for the treatment of CRC. © 2020 Wang et al.Purpose The population of elderly patients with epilepsy has been growing rapidly and the chances of referring older patients with refractory epilepsy for surgical options could be increasing. In general, epilepsy surgery at higher ages has been less likely to be performed, because little is known regarding the risks and benefits in elderly patients. We, therefore, investigated surgical outcomes and comorbidities in a population ≥50 years old who underwent epilepsy surgery. Methods Patients ≥50 years old who underwent epilepsy surgery were identified from the database of our epilepsy center for the period from 2009 to 2017. Surgical complications and seizure outcome were reviewed, and seizure outcomes were evaluated using the International League Against Epilepsy (ILAE) surgery outcome scale. Results The mean age of 32 patients at the time of surgery was 56.1±5.1 years. The mean duration of epilepsy was 23.4±18.5 years and mean follow-up was 2.7±2.0 years. As of the most recent visit, 56.3% of patients remained completely seizure-free (ILAE Class I). The surgery-related complication rate was 11.5%, comprising permanent deficits in 3.8% and transient deficits in 7.7%. Conclusion These results suggest that epilepsy surgery may represent a valuable approach in selected adult patients. © 2020 Ichikawa et al.Background Although complications have been associated with head clamp systems, few reports have described head slippage. The present study aimed to determine risk factors for head slippage and speculated that the position of head holder pins might be associated. Patients and Methods We reviewed medical records and compared the positions of the pinned heads of patients on fused preoperative and postoperative computerized tomography (CT) images. We measured the distance between corresponding head pins to determine head slippage. Age, sex, body weight, body mass index, surgical position, surgical duration, craniotomy volume, and the relationship between head pins and the nasion-inion (NI) line were statistically compared between patients with and without head slippage. Results Head slippage in 3 (10%) of 28 patients was significantly associated with the most caudal pin position (p less then 0.001) and craniotomy volume (p = 0.036). Receiver operator characteristics curves indicated a cutoff of 4.5 cm from the NI line (sensitivity and specificity, 1.
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