Kisspeptin‑13 inhibits bleomycin‑induced pulmonary fibrosis through GPR54 in mice.

Kisspeptin (KP) is an amidated neurohormone that is encoded by the KiSS‑1 metastasis suppressor (KISS1) gene and serves as the endogenous ligand for G protein‑coupled receptor 54 (GPR54). KP is involved in the regulation of several biological functions, such as reproduction, cancer and atherogenesis. Recent data suggested that KP may induce atherosclerotic plaque progression and instability, which may be reversed by the GPR54 antagonist KP‑234.

pATM and γH2AX are effective radiation biomarkers in assessing the radiosensitivity of C in human tumor cells.

Background: Tumour radiosensitivity would be particularly useful in optimizing the radiation dose during radiotherapy. The aim of the current study was to evaluate the potential value of phosphorylated H2AX (γH2AX) and ATM (pATM) in assessing C radiosensitivity of tumour cells.

Methods: Human cervical carcinoma HeLa cells, hepatoma HepG2 cells, and mucoepidermoid carcinoma MEC-1 cells were irradiated with different doses of C.

Genetic variations in the PI3K/AKT pathway predict platinum-based neoadjuvant chemotherapeutic sensitivity in squamous cervical cancer.

Aims: Cervical cancer is one of the most frequent malignant tumours in women. The PI3K/Akt pathway plays a role in chemoresistance to platinum-based neoadjuvant chemotherapy (NAC). The objective of this study was to evaluate the association between genetic polymorphisms in the PI3K/Akt pathway and chemotherapeutic outcomes following platinum-based NAC in Northwestern Chinese Han patients with squamous cervical cancer (SCC).

Induction of H2AX phosphorylation in tumor cells by gossypol acetic acid is mediated by phosphatidylinositol 3-kinase (PI3K) family.

Background: H2AX is phosphorylated (γH2AX) by members of the phosphatidylinositol 3-kinase (PI3K) family, including Ataxia telangiectasia-mutated (ATM), ATM- and Rad3-related (ATR) and DNA-PK in response to DNA damage. Our study shows that gossypol acetic acid (GAA) alone can induce γH2AX in Human mucoepidermoid carcinoma cell line (MEC-1) in vitro. Thus, we further examined the possible mechanisms of GAA to induce γH2AX in tumor cells.

The potential value of the neutral comet assay and γH2AX foci assay in assessing the radiosensitivity of carbon beam in human tumor cell lines.

Background: Carbon ions ((12)C(6+)) are high linear energy transfer (LET) radiation characterized by higher relative biological effectiveness than low LET radiation. The assessment of tumour radiosensitivity would be particularly useful in optimizing the radiation dose during radiotherapy. The aim of the current study was to evaluate the potential value of the neutral comet assay and γH2AX foci assay in assessing (12)C(6+) radiosensitivity of tumour cells.

[Gossypol acetic acid induces DNA double-strand breaks in human mucoepidermoid carcinoma cell MEC-1].

The present study was conducted to investigate the effects of gossypol acetic acid (GAA) on the proliferation of human mucoepidermoid carcinoma cell line MEC-1 in vitro and its possible molecular mechanisms of DNA double-strand breaks (DSB). MTT assay was performed to test the inhibition of proliferation of MEC-1 cells by GAA. DSB and γH2AX foci formation induced by GAA were detected by neutral comet assay and immunostaining.

[Effects of matrine on airway inflammation and early airway remodeling in asthmatic mice].

Objective: To observe the influence of matrine on airway inflammation and early airway remodeling in asthmatic mice.

Methods: Fifty BALB/c mice were randomly divided into 5 groups: a normal control group (A), an asthmatic group (B), a dexamethasone (DXM) group (C, 2 mg/kg), a high-dose matrine group (D, 50 mg/kg) and a low-dose matrine group (E, 25 mg/kg). The mice model of asthma in the B, C, D, and E groups was established by ovalbumin (OVA) intraperitoneal injections and aerosolization.

NADPH oxidase-mediated generation of reactive oxygen species: A new mechanism for X-ray-induced HeLa cell death.

Oxidative damage is an important mechanism in X-ray-induced cell death. Radiolysis of water molecules is a source of reactive oxygen species (ROS) that contribute to X-ray-induced cell death. In this study, we showed by ROS detection and a cell survival assay that NADPH oxidase has a very important role in X-ray-induced cell death.