Dihydroartemisinin enhances the radiosensitivity of breast cancer by targeting ferroptosis signaling pathway through hsa_circ_0001610.

Objective: This study aimed to elucidate how DHA enhances the radiosensitivity of BC and to explain its potential mechanisms of action.

Methods: The circular structure of hsa_circ_0001610 was confirmed by Sanger sequencing, RNase R treatment, RT-PCR analysis using gDNA or cDNA. Cellular localization of hsa_circ_0001610 and microRNA-139-5p (miR-139-5p) was detected by fluorescence in situ hybridization.

Selection criteria and method for deep inspiration breath-hold in patients with left breast cancer undergoing PMRT/IMRT.

Purpose: This study explored whether a free-breathing mean heart dose (FB-MHD) of 4 Gy is a reliable dose threshold for selecting left breast cancer patients after modified radical mastectomy suitable for deep inspiration breath-hold (DIBH) and developed anatomical indicators to predict FB-MHD for rapid selection.

Materials And Methods: Twenty-three patients with left breast cancer treated with DIBH were included to compare FB and DIBH plans. The patients were divided into the high-risk (FB-MHD ≥ 4 Gy) and low-risk (FB-MHD < 4 Gy) groups to compare dose difference, normal tissue complication probability (NTCP) and the DIBH benefits.

Rapid Selection of Patients Suitable for Deep Inspiration Breath-Hold Using an Automatic Delineating System and RapidPlan Model in Patients With Left Breast Cancer Undergoing Adjuvant Radiation Therapy With IMRT.

Purpose: This study aimed to determine whether radiation therapy plans created using an automatic delineating system and a RapidPlan (RP) module could rapidly and accurately predict heart doses and benefit from deep inspiratory breath-hold (DIBH) in patients with left breast cancer.

Methods And Materials: One hundred thirty-six clinically approved free breathing (FB) plans for patients with left breast cancer were included, defined as manual delineation-manual plan (MD-MP). A total of 104 of 136 plans were selected for RP model training.

GSTM3 enhances radiosensitivity of nasopharyngeal carcinoma by promoting radiation-induced ferroptosis through USP14/FASN axis and GPX4.

Background: Radiotherapy is a critical treatment modality for nasopharyngeal carcinoma (NPC). However, the mechanisms underlying radiation resistance and tumour recurrence in NPC remain incompletely understood.

Methods: Oxidised lipids were assessed through targeted metabolomics.

Senescence-Related lncRNA Signature Predicts Prognosis, Response to Immunotherapy and Chemotherapy in Skin Cutaneous Melanoma.

Skin cutaneous melanoma (SKCM) is a highly malignant and aggressive cancer. Previous studies have shown that cellular senescence is a promising therapeutic strategy to limit melanoma cell progression. However, models to predict the prognosis of melanoma based on senescence-related lncRNAs and the efficacy of immune checkpoint therapy remain undefined.

Case report: Abolishing primary resistance to PD-1 blockade by short-term treatment of lenvatinib in a patient with advanced metastatic renal cell carcinoma.

Anti-PD-1 immunotherapy has been extensively used in treatment of patients with advanced metastatic renal cell carcinoma (mRCC). Several prospective clinical trials showed that the combined treatment of anti-PD-1 antibody plus lenvatinib, a potent receptor tyrosine kinase inhibitor (TKI), exhibited high response rate compared with single-agent sunitinib. However, whether the patients with primary resistance to PD-1 blockade could benefit from the addition of lenvatinib is still unclear.

CYLD deficiency enhances metabolic reprogramming and tumor progression in nasopharyngeal carcinoma via PFKFB3.

Aberrant cancer metabolism contributes to cell proliferation and tumor progression. However, the contribution of enhanced glycolysis, observed during cancer metabolism, to the pathogenesis and progression of nasopharyngeal carcinoma (NPC) remains unclear. CYLD, an NF-κB inhibitor, is frequently deficient in NPC.

Protein tyrosine phosphatase receptor type D gene promotes radiosensitivity via STAT3 dephosphorylation in nasopharyngeal carcinoma.

Radiotherapy is essential to the treatment of nasopharyngeal carcinoma (NPC) and acquired or innate resistance to this therapeutic modality is a major clinical problem. However, the underlying molecular mechanisms in the radiation resistance in NPC are not fully understood. Here, we reanalyzed the microarray data from public databases and identified the protein tyrosine phosphatase receptor type D (PTPRD) as a candidate gene.

Multi-modal magnetic resonance imaging-based grading analysis for gliomas by integrating radiomics and deep features.

Background: To investigate the feasibility of integrating global radiomics and local deep features based on multi-modal magnetic resonance imaging (MRI) for developing a noninvasive glioma grading model.

Methods: In this study, 567 patients [211 patients with glioblastomas (GBMs) and 356 patients with low-grade gliomas (LGGs)] between May 2006 and September 2018, were enrolled and divided into training (n=186), validation (n=47), and testing cohorts (n=334), respectively. All patients underwent postcontrast enhanced T1-weighted and T2 fluid-attenuated inversion recovery MRI scanning.

Epstein-Barr virus (EBV) encoded microRNA BART8-3p drives radioresistance-associated metastasis in nasopharyngeal carcinoma.

Radiotherapy plays an important role in the treatment of nasopharyngeal carcinoma (NPC), however, 20% of patients with NPC exhibit unusual radioresistance. Patients with radioresistance are at risk of recurrence, so it is imperative to explore the mechanism of resistance to radiotherapy. In the past, studies on the mechanism of radioresistance have been restricted to DNA damage and related cell cycle remodeling or apoptosis.

CYLD Promotes Apoptosis of Nasopharyngeal Carcinoma Cells by Regulating NDRG1.

Purpose: Nasopharyngeal carcinoma (NPC) is among the most common malignancies derived from the epithelium of the nasopharynx. To date, the regulatory networks involved in NPC have not been fully identified. Previous studies revealed multiple loss-of-function mutations in NPC and specifically in cylindromatosis lysine 63 deubiquitinase (); however, the exact role of CYLD in NPC progression and its potential mechanism remains unclear.

Author Correction: Epstein-Barr virus-encoded microRNA BART1 induces tumour metastasis by regulating PTEN-dependent pathways in nasopharyngeal carcinoma.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

EBV-miR-BART7-3p Imposes Stemness in Nasopharyngeal Carcinoma Cells by Suppressing SMAD7.

Cancer stem-like cells, possessing "stemness" properties, play crucial roles in progression, metastasis, and drug resistance in various cancers. Viral microRNAs (such as EBV-miR-BART7-3p), as exogenous regulators, have been discovered to regulate malignant progression of nasopharyngeal carcinoma (NPC), suggesting a possible role of viral microRNAs in imposing stemness. In this study, we found that EBV-miR-BART7-3p induce stemness of NPC cells.

EBV encoded miRNA BART8-3p promotes radioresistance in nasopharyngeal carcinoma by regulating ATM/ATR signaling pathway.

Resistance to radiotherapy is one of the main causes of treatment failure in patients with nasopharyngeal carcinoma (NPC). Epstein-Barr virus (EBV) infection is an important factor in the pathogenesis of NPC, and EBV-encoded microRNAs (miRNAs) promote NPC progression. However, the role of EBV-encoded miRNAs in the radiosensitivity of NPC remains unclear.

S100A4 suppresses cancer stem cell proliferation via interaction with the IKK/NF-κB signaling pathway.

Background: Bladder cancer often recurs due to incomplete elimination of the cancer stem cells (CSCs). Therefore, new strategies targeting bladder CSCs are needed and the aim of this study was to investigate the effect of S100A4 on the proliferation capacity of MB49 bladder cancer stem cells (MCSCs).

Methods: MCSCs were established and validated.

Influence and mechanism of 5-aminolevulinic acid-photodynamic therapy on the metastasis of esophageal carcinoma.

Backgroud: Photodynamic therapy (PDT) for the treatment of esophageal cancer was more and more popularly used since it was approved for the treatment of advanced esophageal cancer in 1996. It has been reported to influence the tumor growth and metastasis via a variety of signaling pathways, but its mechanism remains to be further studied. This research studied the effects of ALA-PDT on esophageal carcinoma in vitro and in vivo, discovering its molecular regulating mechanism and the way to enhence the PDT effect.

Prognostic impact of pretherapeutic gamma-glutamyltransferase on patients with nasopharyngeal carcinoma.

Background: Gamma-glutamyltransferase (GGT) is a membrane-bound enzyme involved in the metabolism of glutathione. Studies suggested that GGT played an important role in the tumor development, progression, invasion and drug resistance and prognosis. The association between GGT and prognosis of patients with nasopharyngeal carcinoma (NPC) was unknown.

Higher methylation intensity induced by EBV LMP1 via NF-κB/DNMT3b signaling contributes to silencing of PTEN gene.

Phosphatase and tensin homolog (PTEN) is a major tumor suppressor and usually silenced via the deletion, insertion and mutation. We previously discovered its inactivation via aberrant CpG island methylation. Here, we provide further evidence that EBV latent membrane protein 1(LMP1) can induce a higher intensity of DNA methylation at PTEN CpG islands, inactivating PTEN at the cellular and molecular level.

miR156a Mimic Represses the Epithelial-Mesenchymal Transition of Human Nasopharyngeal Cancer Cells by Targeting Junctional Adhesion Molecule A.

MicroRNAs (miRNAs) have been documented as having an important role in the development of cancer. Broccoli is very popular in large groups of the population and has anticancer properties. Junctional adhesion molecule A (JAMA) is preferentially concentrated at tight junctions and influences cell morphology and migration.

The important role of the receptor for activated C kinase 1 (RACK1) in nasopharyngeal carcinoma progression.

Background: The receptor for activated C kinase 1 (RACK1) is involved in various cancers, but its roles in nasopharyngeal carcinoma (NPC) have not yet been fully elucidated.

Methods: Initially, RACK1 expression was analyzed by immunohistochemistry in NPC and normal nasopharyngeal (NP) tissues. It was also detected by qPCR and Western blot in NPC cells.

Epstein-Barr virus-encoded microRNA BART1 induces tumour metastasis by regulating PTEN-dependent pathways in nasopharyngeal carcinoma.

Epstein-Barr virus (EBV), aetiologically linked to nasopharyngeal carcinoma (NPC), is the first human virus found to encode many miRNAs. However, how these viral miRNAs precisely regulate the tumour metastasis in NPC remains obscure. Here we report that EBV-miR-BART1 is highly expressed in NPC and closely associated with pathological and advanced clinical stages of NPC.

Gold nano-particles (AuNPs) carrying anti-EBV-miR-BART7-3p inhibit growth of EBV-positive nasopharyngeal carcinoma.

Epstein-Barr virus (EBV) infection is a major etiological factor for nasopharyngeal carcinoma (NPC). Several EBV-encoded BART miRNAs have been associated with viral latency, immune escape, cell survival, cell proliferation and apoptosis. Here, we report that EBV-miR-BART7-3p, an EBV-encoded BART miRNA highly expressed in NPC, was correlated with cell-cycle progression in vitro and increased tumor formation in vivo.

TGFβR2 is a major target of miR-93 in nasopharyngeal carcinoma aggressiveness.

Background: MiR-17-92 cluster and its paralogues have emerged as crucial regulators of many oncogenes and tumor suppressors. Transforming growth factor-β receptor II (TGFβR2), as an important tumor suppressor, is involved in various cancer types. However, it is in cancer that only two miRNAs of this cluster and its paralogues have been reported so far to regulate TGFβR2.

EBV-miR-BART1 is involved in regulating metabolism-associated genes in nasopharyngeal carcinoma.

EBV-miR-BART1 has been found to be highly expressed in some cancers including nasopharyngeal carcinoma (NPC), but its exact roles in the pathogenesis of NPC remain unclear. Here, we did RNA deep sequencing to compare the gene expression profile between EBV-miR-BART1-expressing CNE1 cells and the control cells to determine the possible effects of EBV-miR-BART1 in NPC. Gene expression profiling analysis unexpectedly showed a significant number of up- and down-modulated metabolism-associated genes, such as G6PD, SAT1, ASS1, PAST1, FUT1, SGPL1, DHRS3, B4GALT1, PHGDH, IDH2, PISD, UGT8, LDHB and GALNT1, in EBV-miR-BART1-expressing NPC cells, which were next confirmed by RT-qPCR.