LINC02562 Promotes Progression of Lung Cancer by Regulating NTHL1 Dependent DNA Damage Repair Mechanisms.

Lung cancer poses a serious threat to public health due to its high morbidity and mortality rates. The mechanisms of lung cancer formation and progression are complex and involve regulation of various biomolecules. Long noncoding RNAs (lncRNAs) have emerged to be critical in tumorigenesis of various malignancies.

Analysis of the diagnostic and prognostic value of Peripheral blood mononuclear cell microRNA-9-5p in patients with sepsis in the intensive care unit.

Objective: To investigate the diagnostic and prognostic value of miR-9-5p in peripheral blood mononuclear cells in sepsis patients.

Methods: Differentially expressed miR-9-5p in sepsis were screened from a database and available literature. Subsequently, iBMDM cell validation was conducted and the expression level of miR-9-5p in peripheral blood mononuclear cells was determined using RT-qPCR in 69 sepsis patients and 30 non-sepsis patients with infections, 24 hours after ICU admission.

A pan-cancer analysis of small nucleolar RNA host gene 14 (SNHG14) in human tumors.

Long non-coding RNAs (lncRNAs) are associated with tumorigenesis and progression. One of these, short nucleolar RNA host gene 14 (SNHG14), has exhibited significant prognostic value due to its aberrant expression across various tumor types. This study investigates the expression patterns, survival outcomes, and tumor stages associated with SNHG14 across various cancers, employing data from the Genotype-Tissue Expression and The Cancer Genome Atlas databases.

Differential mRNA profiles reveal the potential roles of genes involved in lactate stimulation in mouse macrophages.

Lactate is a glycolysis end product, and its levels are markedly associated with disease severity, morbidity, and mortality in sepsis. It modulates key functions of immune cells, including macrophages. In this investigation, transcriptomic analysis was performed using lactic acid, sodium lactate, and hydrochloric acid-stimulated mouse bone marrow-derived macrophages (iBMDM), respectively, to identify lactate-associated signaling pathways.

Urchin-like FeO@BiS Nanospheres Enable the Destruction of Biofilm and Efficiently Antibacterial Activities.

Biofilm-associated infections (BAIs) have been considered a major threat to public health, which induce persistent infections and serious complications. The poor penetration of antibacterial agents in biofilm significantly limits the efficiency of combating BAIs. Magnetic urchin-like core-shell nanospheres of FeO@BiS were developed for physically destructing biofilm and inducing bacterial eradication via reactive oxygen species (ROS) generation and innate immunity regulation.

FIT links c-Myc and P53 acetylation by recruiting RBBP7 during colorectal carcinogenesis.

Colorectal cancer (CRC) poses one of the most serious threats to human health worldwide, and abnormally expressed c-Myc and p53 are deemed the pivotal driving forces of CRC progression. In this study, we discovered that the lncRNA FIT, which was downregulated in CRC clinical samples, was transcriptionally suppressed by c-Myc in vitro and promoted CRC cell apoptosis by inducing FAS expression. FAS is a p53 target gene, and we found that FIT formed a trimer with RBBP7 and p53 that facilitated p53 acetylation and p53-mediated FAS gene transcription.

The importance of serum LMAN2 level in septic shock and prognosis prediction in sepsis patients.

Objectives: To study the importance of LMAN2 in septic shock and prognosis prediction in sepsis patients.

Methods: Serum LMAN2 was measured by ELISA in 109 sepsis patients within 24 h after their admission to ICU. We also collected clinical and laboratory variables.

Targeting ferroptosis as a vulnerability in pulmonary diseases.

Ferroptosis is an iron-dependent regulated cell death marked by excessive oxidative phospholipids (PLs). The polyunsaturated fatty acids-containing phospholipids (PUFA-PLs) are highly susceptible to lipid peroxidation under oxidative stress. Numerous pulmonary diseases occurrences and degenerative pathologies are driven by ferroptosis.

The lncRNA Neat1 promotes activation of inflammasomes in macrophages.

The inflammasome has an essential function in innate immune, responding to a wide variety of stimuli. Here we show that the lncRNA Neat1 promotes the activation of several inflammasomes. Neat1 associates with the NLRP3, NLRC4, and AIM2 inflammasomes in mouse macrophages to enhance their assembly and subsequent pro-caspase-1 processing.

, a c-Myc-inducible long noncoding RNA, cooperates with CNBP to promote mRNA stability in human cells.

Cyclin D1 is a critical regulator of cell cycle progression and works at the G1 to S-phase transition. Here, we report the isolation and characterization of the novel c-Myc-regulated lncRNA (ncRNA-ssisted tabilization of ranscripts), which acts as a mRNA stabilizer. Mechanistically, was shown to cooperate with CNBP to bind to the 5'UTR of mRNA to protect against possible nuclease targeting.

LncRNA-MIF, a c-Myc-activated long non-coding RNA, suppresses glycolysis by promoting Fbxw7-mediated c-Myc degradation.

The c-Myc proto-oncogene is activated in more than half of all human cancers. However, the precise regulation of c-Myc protein stability is unknown. Here, we show that the lncRNA-MIF (c-Myc inhibitory factor), a c-Myc-induced long non-coding RNA, is a competing endogenous RNA for miR-586 and attenuates the inhibitory effect of miR-586 on Fbxw7, an E3 ligase for c-Myc, leading to increased Fbxw7 expression and subsequent c-Myc degradation.