Function of microRNA‑124 in the pathogenesis of cancer (Review).

Non‑coding RNAs with a length of 22‑24 nt are known as microRNAs (miRNAs or miRs), which are critical regulators of protein translation. Over the past 10 years, the roles of miRNAs have been extensively investigated in several human cancer types. There is evidence to indicate that miRNAs regulate gene expression by concentrating on a number of substances that have an impact on the physiology and development of cancer cells.

Conditional Deletion of Delayed Myelination during Early Postnatal Brain Development.

(forkhead box G1) syndrome is a neurodevelopmental disorder caused by variants in the gene that affect brain structure and function. Individuals affected by syndrome frequently exhibit delayed myelination in neuroimaging studies, which may impair the rapid conduction of nerve impulses. To date, the specific effects of FOXG1 on oligodendrocyte lineage progression and myelination during early postnatal development remain unclear.

A predictive model of immune infiltration and prognosis of head and neck squamous cell carcinoma based on cell adhesion-related genes: including molecular biological validation.

Background: Focal adhesion serves as a bridge between tumour cells and the extracellular matrix (ECM) and has multiple roles in tumour invasion, migration, and therapeutic resistance. However, studies on focal adhesion-related genes (FARGs) in head and neck squamous cell carcinoma (HNSCC) are limited.

Methods: Data on HNSCC samples were obtained from The Cancer Genome Atlas and GSE41613 datasets, and 199 FARGs were obtained from the Molecular Signatures database.

An ion-channel-gene-based prediction model for head and neck squamous cell carcinoma: Prognostic assessment and treatment guidance.

Purpose: Head and neck squamous cell carcinoma (HNSCC) is a very diverse malignancy with a poor prognosis. The purpose of this study was to develop a new signature based on 12 ion channel genes to predict the outcome and immune status of HNSCC patients.

Methods: Clinicopathological information and gene sequencing data of HNSCC patients were generated from the Cancer Genome Atlas and Gene Expression Omnibus databases.

Comparison of various surgical incisions in parotidectomy: A systematic review and network meta-analysis.

Background: This network meta-analysis aimed to comprehensively compare the operative and postoperative outcomes of different parotidectomy incisions.

Methods: Embase, PubMed, Web of Science, and Cochrane Central Register of Controlled Trials were searched up to April 2022. A complete Bayesian network meta-analysis was performed using the Markov Monte Carlo method in OpenBUGS.

Correction to: Role of PUMA in the methamphetamine-induced migration of microglia.

In the original publication of this article, wrong western blot images were inadvertently included in Fig. 2 and Fig. 3.

Identification and validation of immune-related lncRNA prognostic signature for breast cancer.

The prognosis of patients with breast cancer is closely related to both the infiltration of immune cells and the expression of lncRNAs. In this study, we evaluated the infiltration of immune cells in 1109 breast cancer samples obtained from TCGA by applying the ssGSEA to the transcriptome of these samples, thereby generating high immune cell infiltration group and low immune cell infiltration group. On the basis of these groupings, we found 696 differentially expressed lncRNAs which were sequentially subjected to univariate Cox regression and stepwise multiple Cox regression analysis.

Impaired DNA double-strand breaks repair by kinesin family member 4A inhibition renders human H1299 non-small-cell lung cancer cells sensitive to cisplatin.

Patients with non-small-cell lung cancer (NSCLC) are routinely treated with the platinum-based chemotherapeutics such as cisplatin. The drug exerts anticancer effects via multiple mechanisms, including DNA double-strand breaks (DSBs). Enhanced DNA DSB repair capacity would be associated with innate or acquired drug resistance.

Role of PUMA in the methamphetamine-induced migration of microglia.

In this study, we demonstrated that PUMA was involved in the microglial migration induced by methamphetamine. PUMA expression was examined by western blotting and immunofluorescence staining. BV2 and HAPI cells were pretreated with a sigma-1R antagonist and extracellular signal-regulated kinase (ERK), mitogen-activated protein kinase (MAPK), c-Jun N-terminal protein kinase (JNK), and phosphatidylinositol-3 kinase (PI3K)/Akt inhibitors, and PUMA expression was detected by western blotting.

Up-regulation of OLR1 expression by TBC1D3 through activation of TNFα/NF-κB pathway promotes the migration of human breast cancer cells.

Metastatic spread of cancer cells is the most life-threatening aspect of breast cancer and involves multiple steps including cell migration. We recently found that the TBC1D3 oncogene promotes the migration of breast cancer cells, and its interaction with CaM enhances the effects of TBC1D3. However, little is known regarding the mechanism by which TBC1D3 induces the migration of cancer cells.

Calmodulin promotes matrix metalloproteinase 9 production and cell migration by inhibiting the ubiquitination and degradation of TBC1D3 oncoprotein in human breast cancer cells.

The hominoid oncoprotein TBC1D3 enhances growth factor (GF) signaling and GF signaling, conversely, induces the ubiquitination and subsequent degradation of TBC1D3. However, little is known regarding the regulation of this degradation, and the role of TBC1D3 in the progression of tumors has also not been defined. In the present study, we demonstrated that calmodulin (CaM), a ubiquitous cellular calcium sensor, specifically interacted with TBC1D3 in a Ca2+-dependent manner and inhibited GF signaling-induced ubiquitination and degradation of the oncoprotein in both cytoplasm and nucleus of human breast cancer cells.

Cytoplasmic retention of a nucleocytoplasmic protein TBC1D3 by microtubule network is required for enhanced EGFR signaling.

The hominoid oncogene TBC1D3 enhances epidermal growth factor receptor (EGFR) signaling and induces cell transformation. However, little is known regarding its spatio-temporal regulation and mechanism of tumorigenesis. In the current study, we identified the microtubule subunit β-tubulin as a potential interaction partner for TBC1D3 using affinity purification combined with mass spectrometry analysis.

Calcium/calmodulin regulates ubiquitination of the ubiquitin-specific protease TRE17/USP6.

The TRE17 (USP6/TRE-2) oncogene induces tumorigenesis in both humans and mice. However, little is known regarding its regulation or mechanism of transformation. TRE17 encodes a TBC (Tre-2/Bub2/Cdc16)/Rab GTPase-activating protein homology domain at its N terminus and a ubiquitin-specific protease at its C terminus.

Nonredundant antioxidant defense by multiple two-cysteine peroxiredoxins in human prostate cancer cells.

Background: Peroxiredoxins (Prxs) are antioxidant enzymes expressed by most free-living organisms, often in multiple isoforms. Because mammalian Prxs have not been experimentally deleted or inhibited, it is not known how much they contribute to antioxidant defense, nor whether the multiple isoforms afford redundant or additive protection.

Materials And Methods: Expression of the four members of the 2-Cys family of human Prxs was tested in human tumor cell lines.