p21 promotes gemcitabine tolerance in A549 cells by inhibiting DNA damage and altering the cell cycle.

Gemcitabine is one of the most widely used chemotherapy drugs for advanced malignant tumors, including non-small cell lung cancer. However, the clinical efficacy of gemcitabine is limited due to drug resistance. The aim of the present study was to investigate the role of p21 in gemcitabine-resistant A549 (A549/G) lung cancer cells.

MiR-17- 5p/RRM2 regulated gemcitabine resistance in lung cancer A549 cells.

The main objective of this study is to investigate the regulatory roles of the miR-17-5p/RRM2 axis in A549/G+ cells' gemcitabine resistance. The cell viability was determined using CCK8 and clonogenic assays. Gene expression level analysis by RT-qPCR and Western blotting.

A novel gut-restricted RIPK1 inhibitor, SZ-15, ameliorates DSS-induced ulcerative colitis.

As a key mediator of cell death and inflammation, receptor-interacting protein kinase 1 (RIPK1) responds to a broad set of inflammatory and pro-death stimuli in human diseases. Inhibitors targeting RIPK1 are being investigated for the treatment of a wide range of human diseases, including ulcerative colitis. In the present study, we designed, synthesized, and investigated the anti-necroptosis and RIPK1-inhibition effects of SZ-15-a symmetrical high-molecular-weight (>500 Da) compound.

Chloroquine increases the anti-cancer activity of epirubicin in A549 lung cancer cells.

The present study investigated whether the autophagy inhibitor chloroquine (CQ) can improve the sensitivity of the A549 lung cancer cell line to epirubicin (EPI). The Cell Counting Kit 8 (CCK8) assay was used to determine the EPI IC in A549 cells treated for 72 h. A549 cells were treated with Western blot analysis was performed to detect the expression level of the autophagy-associated protein, microtubule associated protein 1 light chain 3 β (LC3B), and apoptosis-associated proteins such as cleaved caspase-9 and cleaved caspase-3.

An increase in alveolar fluid clearance induced by hyperinsulinemia in obese rats with LPS-induced acute lung injury.

A lower mortality rate is observed in obese patients with acute lung injury (ALI), which is referred to as the obesity paradox, in several studies and recent meta-analyses. Hyperinsulinemia is characterized as the primary effect of obesity, and exogenous insulin attenuates LPS-induced pulmonary edema. The detailed mechanism responsible for the effect of hyperinsulinemia on pulmonary edema and alveolar filling needs to be elucidated.

Research progress on the relationship between lung cancer drug-resistance and microRNAs.

Lung cancer, a malignant tumor with the highest death rate of cancer, seriously endangers human health. And its pathogenesis and mechanism of drug resistance has been partially clarified, especially for the signal pathway of epidermal growth factor receptor (EGFR). The targeting therapy of EGFR signaling pathway in non-small cell lung cancer (NSCLC) has achieved a certain effect, but the two mutation of EGFR and other mechanisms of lung cancer resistance still greatly reduce the therapeutic effect of chemotherapy on it.

Screening miRNAs associated with resistance gemcitabine from exosomes in A549 lung cancer cells.

Purpose: To establish a gemcitabine-resistant lung adenocarcinoma cell line, A549/G+, and to screen the differences of miRNA expression in exosomes from A549 and A549/G+ cells.

Methods: A549 cells were exposed in gemcitabine until they were resistant to gemcitabine, and extracted exosomes from A549 and A549/G+. The RNAs from exosomes were subjected to miRNA expression microarray experiments.

Effects of baicalin on alveolar fluid clearance and α-ENaC expression in rats with LPS-induced acute lung injury.

Baicalin has been reported to attenuate lung edema in the process of lung injury. However, the effect of baicalin on alveolar fluid clearance (AFC) and epithelial sodium channel (ENaC) expression has not been tested. Sprague-Dawley rats were anesthetized and intratracheally injected with either 1 mg/kg lipopolysaccharide (LPS) or saline vehicle.

MiRNA-10b sponge: An anti-breast cancer study in vitro.

Breast cancer is a malignant tumor with the highest incidence among women. Breast cancer metastasis is the major cause of treatment failure and mortality among such patients. MicroRNAs (miRNAs) are a class of small molecular non-coding regulatory RNAs, which act as oncogenes or tumor suppressors in breast cancer.

Bifunctional fused polypeptide inhibits the growth and metastasis of breast cancer.

Breast cancer is the most common cancer and the leading cause of cancer-related death among women worldwide, with urgent need to develop new therapeutics. Targeted therapy is a promising strategy for breast cancer therapy. Stromal-derived factor-1/CXC chemokine receptor 4 (CXCR4) has been implicated in the metastasis of breast cancer, which renders it to be therapeutic target.

Fused polypeptide with DEF induces apoptosis of lung adenocarcinoma cells.

To analyze the effects of a new unknown peptide DEF on the growth of tumor cells, a fused polypeptide TAT-DV1-DEF was designed and synthesized. The lung adenocarcinoma cell line GLC-82 treated with TAT- DV1-DEF was analyzed with a cell counting kit 8, and the location of polypeptides in cells was observed under laser confocal microscopy. The efficiency of polypeptide transfection and changes in nuclear morphology were analyzed by flow cytometry and fluorescence microscopy, respectively.

Protective effects of fucoxanthin against ferric nitrilotriacetate-induced oxidative stress in murine hepatic BNL CL.2 cells.

Fucoxanthin is a carotenoid that is rich in some seaweed. Although fucoxanthin has been reported to possess radical-scavenging activities in vitro, little is known whether it may protect against iron-induced oxidative stress in cultured cells. In this study, we examined the protection of fucoxanthin against oxidative damage in BNL CL.