A specific super-enhancer actuated by berberine regulates EGFR-mediated RAS-RAF1-MEK1/2-ERK1/2 pathway to induce nasopharyngeal carcinoma autophagy.

Nasopharyngeal carcinoma (NPC), primarily found in the southern region of China, is a malignant tumor known for its highly metastatic characteristics. The high mortality rates caused by the distant metastasis and disease recurrence remain unsolved clinical problems. In clinic, the berberine (BBR) compound has widely been in NPC therapy to decrease metastasis and disease recurrence, and BBR was documented as a main component with multiple anti-NPC effects.

Berberine-mediated Ferroptosis through System Xc/GSH/GPX4 Axis Inhibits Metastasis of Nasopharyngeal Carcinoma.

Nasopharyngeal carcinoma (NPC) is a malignant tumor that is highly prevalent in Southeast China, and its metastasis remains an unresolved clinical problem. Ferroptosis, a type of nonapoptotic cell death, is a critical pathway in tumor metastasis. Berberine (BBR), a plant alkaloid, has been explored as a potential anti-NPC metastatic agent; however, the underlying mechanisms are unknown.

Carcinogen-induced super-enhancer RNA promotes nasopharyngeal carcinoma metastasis through NPM1/c-Myc/NDRG1 axis.

Chemical carcinogen is one etiology of nasopharyngeal carcinoma (NPC) occurrence, N,N'-Dinitrosopiperazine (DNP) has been verified to cause NPC cell metastasis and generate induced pluripotent stem cells (iPSCs). To investigate the oncogenic mechanism of DNP, NPC cells were exposed to DNP, and subjected to RNA-seq, GRO-seq, ChIP-seq, and data analysis. The results showed that the super-enhancer RNA (seRNA) participates in DNP-mediated NPC metastasis through regulating N-myc downstream regulated gene 1 (NDRG1).

JUN-induced super-enhancer RNA forms R-loop to promote nasopharyngeal carcinoma metastasis.

Oncogenic super-enhancers (SEs) generate noncoding enhancer/SE RNAs (eRNAs/seRNAs) that exert a critical function in malignancy through powerful regulation of target gene expression. Herein, we show that a JUN-mediated seRNA can form R-loop to regulate target genes to promote metastasis of nasopharyngeal carcinoma (NPC). A combination of global run-on sequencing, chromatin-immunoprecipitation sequencing, and RNA sequencing was used to screen seRNAs.

Clinical performance of metagenomic next-generation sequencing for the rapid diagnosis of talaromycosis in HIV-infected patients.

Background: Talaromycosis is an invasive endemic mycosis caused by the dimorphic fungus (, TM). It mainly affects immunodeficient patients, especially HIV-infected individuals, which causes significant morbidity and mortality. Culture-based diagnosis takes a long turnaround time with low sensitivity, leading to treatment delay.

Transcriptional factor III A promotes colorectal cancer progression by upregulating cystatin A.

Background: Advanced colorectal cancer (CRC) generally has poor outcomes and high mortality rates. Clarifying the molecular mechanisms underlying CRC progression is necessary to develop new diagnostic and therapeutic strategies to improve CRC outcome and decrease mortality. Transcriptional factor III A (GTF3A), an RNA polymerase III transcriptional factor, is a critical driver of tumorgenesis and aggravates CRC cell growth.

A novel oncogenic seRNA promotes nasopharyngeal carcinoma metastasis.

Nasopharyngeal carcinoma (NPC) is a common malignant cancer in southern China that has highly invasive and metastatic features and causes high mortality, but the underlying mechanisms of this malignancy remain unclear. In this study, we utilized ChIP-Seq to identify metastasis-specific super enhancers (SEs) and found that the SE of LOC100506178 existed only in metastatic NPC cells and powerfully aggravated NPC metastasis. This metastatic SE transcribed into lncRNA LOC100506178, and it was verified as a seRNA through GRO-Seq.

Oncogenic super-enhancer formation in tumorigenesis and its molecular mechanisms.

Super-enhancers (SEs) consist of a cluster of many enhancers bound to a great number of transcription factors. They are critical cis-regulatory elements that determine the identity of various human cell types. During tumorigenesis, DNA mutations and indels, chromosomal rearrangements, three-dimensional chromatin structural changes, and viral infections mediate oncogenic SE activation, and activated SEs have been found to regulate the expression of oncogenic genes.

Antitumor activity of recombinant RGD-IFN-α2a-core fusion protein in vitro.

Interferon (IFN) regulates immune responses and antitumor activity. Arginine-glycine-aspartic acid (RGD) peptides can specifically bind to integrin αvβ3, a transmembrane receptor that is highly expressed on the surface of various cancer cells. In this study, we expressed recombinant RGD-IFN-α2a-core fusion proteins and assessed their antitumor activity in vitro.

Self-assembled HCV core virus-like particles targeted and inhibited tumor cell migration and invasion.

We used a baculovirus expression system to express fusion proteins of HCV core, RGD (Arg-Gly-Asp) peptide, and IFN-α2a fragments in Sf9 cells. Western blotting and electron microscopy demonstrate that HCV core, peptides RGD, and IFN-α2a fusion proteins assemble into 30 to 40 nm nano-particles (virus-like particles, VLPs). Xenograft assays show that VLPs greatly reduced tumor volume and weight with regard to a nontreated xenograft.