Activity

RTKs are modulated by their N‑linked glycans, and inhibition of N‑glycan biosynthesis decreased the claudin‑3 levels; therefore, we evaluated the correlation between N‑glycogenes and CLDN3 expression levels in each of the CRC molecular subtypes. The CMS1 (MSI immune) subtype concomitantly exhibited low expression levels of CLDN3 and N‑glycogenes (MGAT5, ST6GAL1, and B3GNT8), whereas CMS2 (canonical) exhibited high gene expression levels of CLDN3 and N‑glycogenes (ST6GAL1 and B3GNT8). A robust positive correlation was also observed between CLDN3 and B3GNT8 expression levels in all CMSs. These results support the hypothesis of a mechanism integrating RTK signaling and N‑glycosylation for the regulation of claudin‑3 levels in CRC, and they suggest that CLDN3 expression can be used to predict the prognosis of patients identified as CMS2 or CMS3.The main active compound of Garcinia hanburyi (referred to as gamboge) is gambogic acid (GA), which has long been a Chinese herbal medicine for treating several types of cancer. However, the potential therapeutic role and mechanisms of GA in T‑cell acute lymphoblastic leukemia (T‑ALL) remain unclear. In the present study, the effects of GA on proliferation, cell cycle, apoptosis, and autophagy in T‑ALL cell lines were investigated. The possible mechanisms underlying GA activity were also examined. The results showed that GA inhibited proliferation, induced apoptosis, and activated autophagy in T‑ALL cell lines (Jurkat and Molt‑4 cells). Findings confirmed that GA has an antileukemia effect against peripheral blood lymphocyte cells in patients with ALL. GA inhibited phospho‑GSK3β S9 (p‑GSK3β S9) protein levels to inactivate Wnt signaling and suppress β‑catenin protein levels. In addition, the inhibitory effect of GA on T‑ALL was reversed by overexpression of β‑catenin. Thus, GA can inhibit the growth and survival of T‑ALL cells. GA also had antileukemic activity, at least in part, through the downregulation of the Wnt/β‑catenin signaling pathway.The high activation of protein kinase B (AKT)/nuclear factor‑κB (NF‑κB) signaling has often been associated with the induction of non‑small cell lung cancer (NSCLC) cell survival and resistance to cisplatin, which is one of the most widely used chemotherapeutic drugs in the treatment of NSCLC. Reversan The inhibition of AKT/NF‑κB can potentially be used as a molecular target for cancer therapy. Eurycomalactone (ECL), a quassinoid from Eurycoma longifolia Jack, has previously been revealed to exhibit strong cytotoxic activity against the human NSCLC A549 cell line, and can inhibit NF‑κB activity in TNF‑α‑activated 293 cells stably transfected with an NF‑κB luciferase reporter. The present study was the first to investigate whether ECL inhibits the activation of AKT/NF‑κB signaling, induces apoptosis and enhances chemosensitivity to cisplatin in human NSCLC cells. The anticancer activity of ECL was evaluated in two NSCLC cell lines, A549 and Calu‑1. ECL decreased the viability and colony formation ability of both cell lides a rationale for the combined use of chemotherapy drugs with ECL to improve their efficacy in NSCLC treatment.Breast cancer (BC) is the most commonly diagnosed malignant cancer in women. BC is the main cause of cancer‑related death in women and seriously threatens the life and health of women worldwide. MicroRNAs (miRNAs/miRs) have been reported to regulate the development and progression of different types of cancer. However, the regulatory functions of miR‑188‑5p in BC have not been thoroughly demonstrated. In this present research, we identified that miR‑188‑5p was downregulated in BC tissues and several BC cell lines. Downregulation of miR‑188‑5p was significantly associated with advanced TNM stage. Moreover, we identified that miR‑188‑5p mimics significantly inhibited proliferation using CCK‑8 assay, colony formation and xenograft animal model, suppressed invasion and migration detected by Transwell invasion assay, and increased the cellular apoptosis of BC cells as determined by cell apoptosis assay. Moreover miR‑188‑5p mimics also reduced the expression of NF‑κB p65(Rel). To further investigate its regulatory mechanism, transcription factor zinc finger protein 91 (ZFP91) was predicted as the targeted protein of miR‑188‑5p by bioinformatic method. We confirmed their specific binding by dual luciferase (DLR) assay. We demonstrated that the overexpression of miR‑188‑5p significantly inhibited the expression of ZFP91 in BC cell lines and reduced the expression of NF‑κB p65(Rel). An inverse correlation was found between the expression of miR‑188‑5p and ZFP91 in BC tissues. Importantly, we demonstrated that the restoration of ZFP91 was able to block the effect of miR‑188‑5p on the progression of MDA‑MB‑231 cells. Therefore, our study showed that miR‑188‑5p may be one of the important indicators and could inhibit the progression of human BC via targeting the ZFP91/NF‑κB p65(Rel) signaling pathway, suggesting that miR‑188‑5p may be a promising future target for BC treatment.Oral squamous cell carcinoma (OSCC) is a cancer with high morbidity and mortality. Research has demonstrated that long non‑coding RNAs (lncRNAs) are critical for tumor initiation and development. In the present study, we aimed to ascertain the functions and potential mechanisms of lncRNA plasmacytoma variant translocation 1 (PVT1) in OSCC. Firstly, we found that the expression of PVT1 was increased in human OSCC tumor tissues and it was related to reduced survival of the patients. Furthermore, miR‑150‑5p expression was downregulated in OSCC tumor tissues and it was negatively related with PVT1. Moreover, GLUT‑1 protein expression was upregulated in human OSCC tumor tissues. In addition, cell proliferation capacity was measured by CCK‑8 assay and cell invasion and migration were measured by Transwell assay. PVT1 overexpression promoted cell proliferation, invasion and migration, while these effects were abrogated by PVT1 downregulation. In addition, luciferase gene reporter assay verified the miR‑150‑5p directly binds with PVT1, which regulates the biological functions of OSCC.