The aim of the present study was to investigate the effects and mechanisms of 17‑AAG combined with salinomycin treatment on proliferation and apoptosis of the SGC‑7901 gastric cancer cell line. An MTT assay was used to detect the proliferation of SGC‑7901 cells. Morphological alterations of cells were observed under inverted phase‑contrast and fluorescence microscopes. Cell cycle and apoptosis were assessed by flow cytometry analysis. The protein expression of nuclear factor (NF)‑κB p65 and Fas‑ligand (L) were evaluated by immunocytochemistry. Salinomycin with a concentration range of 1‑32 µmol/l was demonstrated to inhibit growth of SGC‑7901 cells effectively, affect the morphology and apoptosis rate of cells, and arrest SGC‑7901 cells in S phase. Furthermore, salinomycin significantly increased the protein expression of Fas‑L and decreased the protein expression of NF‑κB p65. The alterations in SGC‑7901 cells co‑treated with salinomycin and 17‑AAG were more significant compared with cells treated with one drug only. In conclusion, the individual use of salinomycin and combined use with 17‑AAG may significantly inhibit SGC‑7901 gastric cancer cell proliferation and induce cell apoptosis. The potential mechanisms may be associated with upregulation of Fas‑L and downregulation of NF‑κB. These results provide a basis for the potential use of salinomycin in gastric cancer treatment.
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http://dx.doi.org/10.3892/mmr.2017.6735 | DOI Listing |
World J Surg Oncol
January 2025
Colorectal Surgery Department, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University/ Hunan Cancer Hospital, No. 283 Tongzipo Road, Yuelu District, Changsha, Hunan, 410013, China.
Objective: The clinical benefits of neoadjuvant bevacizumab plus chemotherapy in locally advanced gastric cancer patients are controversial. This study intended to evaluate the efficacy and safety of neoadjuvant bevacizumab plus chemotherapy in these patients.
Methods: In this retrospective study, 71 locally advanced gastric cancer patients receiving neoadjuvant bevacizumab plus chemotherapy or neoadjuvant chemotherapy alone were divided into bevacizumab plus chemo group (N = 23) and chemo group (N = 48).
Gastric Cancer
January 2025
Department of Gastroenterological Surgery, Osaka Metropolitan University Graduate School of Medicine, Osaka, Japan.
Background: The aim of this study was to determine the differential impact of frailty on surgical site complications (SSCs) and non-surgical site complications (non-SSCs) in gastric cancer (GC) patients undergoing gastrectomy.
Methods: In this study, frailty was assessed preoperatively using a frailty index (FI) in 395 patients scheduled for gastrectomy for GC between January 2016 and December 2023. Patients were divided into two groups (high FI vs.
Sci Rep
January 2025
Department of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University of Chinese Medicine, Nanjing, 210000, Jiangsu, China.
Gastric cancer (GC) is a prevalent malignant tumor of the digestive system that is often diagnosed at advanced stages owing to inconspicuous early symptoms and a lack of specific examination methods. Effective treatment of advanced stages remains challenging, emphasizing the need for new therapeutic targets. Metabolic reprogramming, a hallmark of tumors, plays a pivotal role in tumor progression, immune evasion, and immune surveillance.
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January 2025
Department of Gastrointestinal Surgery, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan Province, China.
This study aimed to elucidate the potential causal relationship between 4,907 plasma proteins and the risk of gastric cancer using a two-sample Mendelian randomization approach. We utilized genome-wide association study (GWAS) data to perform two-sample Mendelian randomization analyses, treating the 4,907 plasma proteins as exposure factors and gastric cancer as the outcome. Instrumental variables for plasma proteins were selected based on strongly correlated SNPs identified through data processing and screening of the GWAS data provided by the deCode database.
View Article and Find Full Text PDFCommun Biol
January 2025
Department of Oncology, NHC Key Laboratory of Cancer Proteomics & State Local Joint Engineering Laboratory for Anticancer Drugs, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.
Hyperactive c-Met signaling pathway caused by altered MET is a common mechanism underlying gastric cancer and represents an attractive target for the treatment of gastric cancer with MET alterations. However, no c-Met kinase inhibitors are currently approved specifically for the treatment of c-Met-amplified gastric cancer. Recently, bozitinib, a highly selective c-Met kinase inhibitor, has shown remarkable potency in selectively inhibiting MET-altered non-small cell lung cancer and secondary glioblastoma.
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