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miR-let-7a-5p can inhibit proliferation, invasion, and migration as well as promote apoptosis of hepatoma cells by decreasing
expression.
miR-let-7a-5p can inhibit proliferation, invasion, and migration as well as promote apoptosis of hepatoma cells by decreasing BZW2 expression.
To study the expression of
in breast cancer tissues using TCGA database, analyze the correlation between the expression and clinicopathological characteristics of patients, and explore the role of
in the development of breast cancer (BC).
The BC mRNA data and clinical information were downloaded from TCGA database. The correlation between
expression and clinicopathological parameters was analyzed. Cox regression multivariate analysis was used to explore the factors affecting the prognosis of BC patients. The UALCAN database was used to analyze the expression level of
in BC and its relationship with clinical pathological factors. The GSEA method was used to predict the possible regulatory pathways of
. Donafenib inhibitor Immune responses of
expression were analyzed using TISIDB and CIBERSORT. Additionally, GEPIA, K-M survival analysis and data from the HPA were used to validate the outcomes.
The expression of
in BC tissues was significantly higher than normal counterparts, patients with low
expressio13 expression is a poor prognostic factor for BC, and it can be used as a molecular marker for prognosis judgment and as a potential therapeutic target.[This corrects the article DOI 10.2147/OTT.S262089.].Uveal melanoma is the most common malignant tumor in adult eyes, mostly in the choroid, but also in the iris and ciliary body. Distant metastasis is found in nearly half of the patients. Cancer stem cells are a kind of cells with the ability of self-renewal and multidirectional differentiation, which are related to tumor invasion and metastasis. Although the concept of cancer stem cells is relatively mature in other tumors, its existence and verification methods in uveal melanoma are still uncertain. A more in-depth understanding of cancer stem cells and their mechanism may reveal new strategies to treat uveal melanoma. This article reviews the concept of cancer stem cells and their research progress in uveal melanoma, including identification, probable markers, cancer stem cell targeted drug therapy and the controversies and prospects in this field.
Monoclonal antibodies (mAbs) that target the programmed cell death-1 (PD-1)/programmed death-ligand 1 (PD-L1) immune checkpoint have demonstrated substantial clinical benefit for a variety of solid tumors. However, their applications in patients with hepatocellular carcinoma (HCC) are reported with unclear molecular mechanisms. Here, we report a novel mouse anti-human PD-1 mAb that can reverse the immunosuppressive effect of HePG2 cells on Jurkat cells.
HepG2 liver cancer cells, which were induced to overexpress PD-L1 by IFN-γ, were co-cultured with PHA-activated Jurkat lymphocytic cells to investigate the immunostimulative effect and mechanisms of the 14 newly generated PD-1 mAbs. Multiple cellular and molecular biology experiments were performed in this study, such as CCK-8, ELISA, flow cytometry, immunofluorescence and Western blot.
We found that mAb B1C4 significantly enhanced the tumor-killing cytokine secretion level by Jurkat cells in the co-culture system and increased the killing ability of Jurvital basis for applying PD-1 monoclonal antibodies in the treatment of HCC and provides antibody selection for the development of novel PD-1 mAb with blocking activity.
Pancreatic cancer is one of the deadliest cancers in the world, and pancreatic ductal adenocarcinoma (PDAC) accounts for 90% of all cases. Human positive coactivator 4 (PC4) is a transcriptional coactivator that has been associated with the development and progression of several tumors. However, no studies investigated the potential role of PC4 in PDAC.
We investigated PC4 expression in 81 PDAC tissue samples using immunohistochemistry and studied the impact of PC4 expression and the molecular mechanisms of this altered expression on PDAC tumorigenesis and proliferation both in vitro and in vivo.
PC4 overexpression was correlated with a poor outcome in PDAC patients. The RNAi-mediated knockdown of PC4 expression in CFPAC-1 and AsPC-1 cell lines reduced cell proliferation and tumor growth. The loss of PC4 in PDAC inhibits cell growth by inducing cell cycle arrest at the G1/S transition and suppressing the mTOR/p70s6k pathway.
Our findings reveal for the first time that PC4 exerts oncogenic functions by activating mTOR/p70s6k signaling pathway-mediated cell proliferation, implying that PC4 is a promising therapeutic target for PDAC.
Our findings reveal for the first time that PC4 exerts oncogenic functions by activating mTOR/p70s6k signaling pathway-mediated cell proliferation, implying that PC4 is a promising therapeutic target for PDAC.
Gastric cancer (GC) is one of the most common and lethal malignancies worldwide. Therefore, a better understanding of the mechanism of its malignant progression and chemoresistance will be helpful for the treatment of patients with GC.
The gene expression profiles downloaded from GEO database and the TargetScan Human were used to identify the key regulation model based on miRNA by bioinformatics analyses. The regulation of miRNA to target was clarified by luciferase assay, qPCR, and Western blotting. Then, the in vitro and in vivo experiments were further conducted by overexpression or knockdown of miRNA and/or target to examine the regulation effects and clarify the mechanism.
In the present study, miR-424-3p was identified to be differentially expressed among normal gastric, GC, and chemoresistant GC tissues. Target analysis results indicated that ABCC2, a chemoresistance-related gene, was a regulated target of miR-424-3p. The in vitro and in vivo experiment results further demonstrated that miR-424-3p relied on ABCC2-induced chemoresistance to promote GC proliferation and metastasis.
Overall, this study revealed that miR-424-3p contributed to the malignant progression and chemoresistance of GC. Thus, miR-424-3p could be a potential target for the treatment of GC.
Overall, this study revealed that miR-424-3p contributed to the malignant progression and chemoresistance of GC. Thus, miR-424-3p could be a potential target for the treatment of GC.
Read More: https://www.selleckchem.com/products/donafenib-sorafenib-d3.html
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