Polydatin, a potential NOX5 agonist, synergistically enhances antitumor activity of cisplatin by stimulating oxidative stress in non‑small cell lung cancer.

Non‑small cell lung cancer (NSCLC) is one of the major causes of cancer‑related death worldwide. Cisplatin is a front‑line chemotherapeutic agent in NSCLC. Nevertheless, subsequent harsh side effects and drug resistance limit its further clinical application.

Investigation on the Epidemic Situation of Epidemic Hemorrhagic Fever in an Island Industrial Park in Zhoushan, China.

To investigate the epidemic factors of hemorrhagic fever with renal syndrome (HFRS) and compare the S and M gene sequences of hantavirus (HV) between rodents and the infected cases. Detailed epidemiological investigations were conducted on the cases' working and living areas. Captured rodents were classified by night trapping method, and their lungs and blood were collected for virus carriage detection after aseptic dissection.

Dihydroartemisinin, a potential PTGS1 inhibitor, potentiated cisplatin-induced cell death in non-small cell lung cancer through activating ROS-mediated multiple signaling pathways.

Dihydroartemisinin (DHA) exerts an anti-tumor effect in multiple cancers, however, the molecular mechanism of DHA and whether DHA facilitates the anti-tumor efficacy of cisplatin in non-small cell lung cancer (NSCLC) are unclear. Here, we found that DHA potentiated the anti-tumor effects of cisplatin in NSCLC cells by stimulating reactive oxygen species (ROS)-mediated endoplasmic reticulum (ER) stress, C-Jun-amino-terminal kinase (JNK) and p38 MAPK signaling pathways both in vitro and in vivo. Of note, we demonstrated for the first time that DHA inhibits prostaglandin G/H synthase 1 (PTGS1) expression, resulting in enhanced ROS production.

CDK5 destabilizes PD-L1 via chaperon-mediated autophagy to control cancer immune surveillance in hepatocellular carcinoma.

Background: In the past few years, immunotherapies of hepatocellular carcinoma (HCC) targeting programmed cell death protein 1 (PD-1) and its ligand programmed cell death ligand 1 (PD-L1), have achieved durable clinical benefits. However, only a fraction of HCC patients showed objective clinical response to PD-1/PD-L1 blockade alone. Despite the impact on post-translational modifications of PD-L1 being substantial, its significance in resistance to HCC immunotherapy remains poorly defined.

MiR-196b-5p activates NF-κB signaling in non-small cell lung cancer by directly targeting NFKBIA.

Background: Our recent study found that QKI-5 regulated miRNA, miR-196b-5p, promotes non-small cell lung cancer (NSCLC) progression by directly targeting GATA6, TSPAN12 and FAS. However, the biological functions of miR-196b-5p in NSCLC progression and metastasis still remain elusive.

Methods: Cell proliferation, migration, colony formation, cell cycle assays were used to investigate cellular phenotypic changes.

[Expression of Tyrosine Kinase Receptor 2 in Oral Squamous Cell Carcinoma and the Effect on Cell Proliferation and Migration and Epithelial-Mesenchymal Transition Process].

Objective: To study the expression of tyrosine kinase receptor 2 (Tie2) in oral squamous cell carcinoma (OSCC) and its effect on cell proliferation and migration and the epithelial-mesenchymal transition (EMT) process.

Methods: Immunohistochemistry (IHC) tests were conducted to examine the expression of Tie2 in OSCC tissues and normal oral mucosa tissues. Western blot was performed to examine the expression of Tie2 in dysplastic oral keratinocyte (DOK) cell line and OSCC cell lines, and the cell line with high Tie2 expression was selected as the experimental cell line.

miR-31/QKI-5 axis facilitates cell cycle progression of non-small-cell lung cancer cells by interacting and regulating p21 and CDK4/6 expressions.

Background: RNA-binding protein Quaking-5 (QKI-5), a major isoform of QKIs, inhibits tumor progression in non-small cell lung cancer (NSCLC). However, the underlying molecular mechanisms of QKI-5 in the cell cycle of NSCLC are still largely unknown.

Methods: MTT, flow cytometry, and colony formation assays were used to investigate cellular phenotypic changes.

Pulmonary MALT lymphoma: Imaging findings in 18 cases and the associated pathological correlations.

Background: Pulmonary MALT lymphoma is a rare disease that is easily misdiagnosed. The objective of this study was to improve the understanding of pulmonary MALT lymphoma for clinicians.

Methods: The computed tomography (CT) scans of 18 patients (13 males and 5 females), aged 41-70 years (mean=55.

NF90 stabilizes cyclin E1 mRNA through phosphorylation of NF90-Ser382 by CDK2.

Nuclear factor 90 (NF90), an RNA-binding protein, has been implicated in regulating interleukin-2 (IL-2) and the immune response. It was recently reported that NF90 is upregulated in hepatocellular carcinoma (HCC) tissues and promotes HCC proliferation through upregulating cyclin E1 at the posttranscription level. However, the regulation of NF90 in HCC remains unclear.

SPINK1 promotes cell growth and metastasis of lung adenocarcinoma and acts as a novel prognostic biomarker.

Serine protease inhibitor Kazal type 1 (SPINK1) plays a role in protecting the pancreas against premature activation of trypsinogen and is involved in cancer progression. SPINK1 promoted LAC cells growth, migration, and invasion. Mechanistically, we found that SPINK1 promoted LAC cells migration and invasion via up-regulating matrix metalloproteinase 12 (MMP12).

Calotropin regulates the apoptosis of non‑small cell cancer by regulating the cytotoxic T‑lymphocyte associated antigen 4‑mediated TGF‑β/ERK signaling pathway.

Non‑small‑cell lung cancer (NSCLC) is one of the most common malignancies that is responsible for a high level of cancer‑associated mortalities worldwide. Previous evidence has shown that Calotropin is an upstream activator of protein kinase B, which can further inhibit the growth and promote the apoptosis of NSCLC cells. In the present study, the efficacy of Calotropin on growth, aggressiveness and apoptosis of NSCLC cells was investigated, as well as the potential underlying mechanism.

Peripheral lung adenocarcinomas harboring epithelial growth factor receptor mutations with microRNA-135b overexpression are more likely to invade visceral pleura.

Lung adenocarcinoma, characterized by its early and aggressive local invasion and high metastatic potential, is the most frequently observed histological type of non-small-cell lung cancer (NSCLC). Visceral pleural invasion (VPI) caused by peripheral lung adenocarcinomas is closely associated with the poor prognosis of patients with NSCLC. The association between VPI and some clinicopathological characteristics has been observed in the past few decades.

A retrospective clinicopathological study of lung adenocarcinoma: Total tumor size can predict subtypes and lymph node involvement.

Purpose: To analyze the predictive ability of total tumor size in lung adenocarcinoma subtype and lymph node involvement.

Materials And Methods: 1018 patients, ≤3cm tumor, were enrolled. The maximum diameter and other variables of each tumor were measured.

[Establishment of A Clinical Prediction Model of Solid Solitary Pulmonary Nodules].

Background: The solitary pulmonary nodule (SPN) is a common and challenging clinical problem, especially solid SPN. The object of this study was to explore the predictive factors of SPN appearing as pure solid with malignance and to establish a clinical prediction model of solid SPNs.

Methods: We had a retrospective review of 317 solid SPNs (group A) having a final diagnosis in the department of thoracic surgery, Shanghai Chest Hospital from January 2015 to December 2015, and analyzed their clinical data and computed tomography (CT) images, including age, gender, smoking history, family history of cancer, previous cancer history, diameter of nodule, nodule location (upper lobe or non-upper lobe, left or right), clear border, smooth margin, lobulation, spiculation, vascular convergence, pleural retraction sign, air bronchogram sign, vocule sign, cavity and calcification.

[Study on the hemodynamic changes in solid thyroid nodules by ultrasound contrast quantitative analysis].

Objective: To compare the difference between the different perfusional regions in solid thyroid nodules.

Methods: From October 2013 to May 2015, CEUS was performed in 59 patients who hospitalizated in Zhoushan Hospital with solid thyroid nodules before operation. The time-intensity curve (TIC) of normal thyroid tissue, tumor edge and tumor center was drawn to collect perfusion index like the peak intensity (PI), time to peak (TP), area under the curve (AUC), mean transit time (MTT).

Increased Tim-3 expression in peripheral NK cells predicts a poorer prognosis and Tim-3 blockade improves NK cell-mediated cytotoxicity in human lung adenocarcinoma.

T cell immunoglobulin- and mucin-domain-containing molecule-3 (Tim-3) has been shown to play an important role in mediating NK-cell function in human diseases. However, the relationship between Tim-3 expression in natural killer (NK) cells and human lung adenocarcinoma remains unclear. We therefore investigated the expression of Tim-3 in NK cells and explored the effect of Tim-3 blockade on NK cell-mediated activity in human lung adenocarcinoma.