[Retracted] Long non‑coding RNA NEAT1 promotes the malignancy of laryngeal squamous cell carcinoma by regulating the microRNA‑204‑5p/SEMA4B axis.

[This retracts the article DOI: 10.3892/ol.2021.

Targeting EFNA1 suppresses tumor progression via the cMYC-modulated cell cycle and autophagy in esophageal squamous cell carcinoma.

Purpose: Esophageal squamous cell carcinoma (ESCC) remains one of the most common causes of cancer death due to the lack of effective therapeutic options. New targets and the targeted drugs are required to be identified and developed.

Methods: Highly expressed genes in ESCA were identified using the edgeR package from public datasets.

Long non-coding RNA NEAT1 promotes the malignancy of laryngeal squamous cell carcinoma by regulating the microRNA-204-5p/SEMA4B axis.

Laryngeal squamous cell carcinoma (LSCC) is a highly invasive malignant tumor in the head and neck area. As an oncogene, long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) promotes cell proliferation, migration and invasion several types of cancer. The present study aimed to reveal the effects of NEAT1 on the progression of LSCC.

A metabolic investigation of anticancer effect of G. glabra root extract on nasopharyngeal carcinoma cell line, C666-1.

Although a majority of nasopharyngeal carcinoma (NPC) are undifferentiated and strongly radiosensitive, many NPC patients still have troubles in recurrence. Traditional Chinese medicine (TCM) is considered as potential therapeutic drugs in NPC. However, the effect of Glycyrrhiza glabra on NPC is limited.

CircHIPK3 promotes proliferation and invasion in nasopharyngeal carcinoma by abrogating miR-4288-induced ELF3 inhibition.

Circular RNAs (circRNAs) are reported to regulate the development and progression of multiple cancers. However, the functions of circRNAs in nasopharyngeal carcinoma (NPC) are unclear. In this study, we identified that circular homeodomain interacting protein kinase 3 (circHIPK3) was highly expressed in NPC tissues and cell lines.

(3R)-5,6,7-trihydroxy-3-isopropyl-3-methylisochroman-1-one ameliorates retinal degeneration in Pde6b mice.

As a severe photoreceptor-degenerative disease, retinitis pigmentosa (RP) is currently incurable and eventually leads to partial or complete blindness. (3R)-5,6,7-trihydroxy-3-isopropyl-3-methylisochroman-1-one (TIM) is a novel antioxidant isolated from the plant of Alpinia katsumadai Hayata, with protective effects on photoreceptor cells against lipoteichoic acid-induced damage through inhibiting oxidative stress. The present study was to further demonstrate whether TIM could ameliorate retinal degeneration of Pde6b (rd10) mice, a mouse model of RP.

MicroRNA-9 suppresses the sensitivity of CNE2 cells to ultraviolet radiation.

MicroRNA (miR)-9 has been demonstrated to regulate the radiosensitivity of tumor cells. In the present study, the mechanism by which miR-9 modulates the sensitivity of nasopharyngeal carcinoma (NPC) cells to ultraviolet (UV) radiation was investigated. The results demonstrated that exposure of NPC cells to UV light resulted in a significant increase in the expression of miR-9, and that CNE2 cells overexpressing miR-9 exhibited reduced levels of DNA damage and increased levels of total glutathione upon UV exposure.

A bacterial extract of OM-85 Broncho-Vaxom prevents allergic rhinitis in mice.

Background: According to the hygiene hypothesis, bacterial infections during early life contribute to a reduced incidence of asthma in animals. However, the effects of microbial products at a safe dose and within a rational time course on the prevention of allergic rhinitis (AR) have been inconclusive. This study investigated the immunomodulatory effects of oral administration of a bacterial extract, OM-85 Broncho-Vaxom (BV), with a low dose and general time course, which is currently used for respiratory infections in humans, on AR inflammation in mice.

[Inhibition of micro RNA-9 expression promotes UV-induced ROS damage in nasopharyngeal carcinoma cells].

Objective: To investigate the effects of down-regulated miR-9 expression on ultraviolet rays (UV)-induced reactive oxygen species (ROS) damage in nasopharyngeal carcinoma (NPC) cells.

Methods: The NPC cells were transfected with inhibitors of miR-9 by lipofectamine to decrease the expression of miR-9, and the cells transfected with inhibitor control as the control. ROS levels following UV exposure were examined with DCF-DA method and the concentration of glutathione was analyzed via the benzoic acid method; DNA damage and apoptosis also were evaluated.