The combined use of radiotherapy and pembrolizumab may also be effective. However, the combination use of chemotherapy, radiotherapy and immunotherapy in advanced cancer has not been well studied, and there are still many unsolved queries.Background Apatinib showed promising efficacy in the treatment of advanced or metastatic gastric cancer (mGC) in previous clinical studies. However, the real-world data are limited, and this study aimed to assess the effectiveness and safety of apatinib for the treatment of advanced or mGC in this setting. Methods In this prospective observational study, progression-free survival (PFS), overall survival (OS), overall response rate (ORR), disease control rate (DCR) and treatment-related adverse events (AEs) were recorded and evaluated. Univariate and multivariate analyses were conducted to explore potential biomarkers which might be related to the effectiveness. Results A total of 321 mGC patients from 47 centers in China were enrolled between July 1, 2015, and March 1, 2018. Thirty-two patients achieved partial response, 155 patients achieved stable disease, and 115 patients had progressive disease, and no CR was achieved, illustrating an ORR of 10.60% and a DCR of 61.92%. The median PFS and OS were 4.0 and 8.2 months, respectively. Multivariate Cox analysis showed that the potential biomarkers associated with longer PFS were combination regimens plus taxel/docetaxel, and apatinib initial dosage ≥500mg, occurrence of AEs of leukopenia, and hand-foot syndrome. Main AEs were proteinuria (17.1%), hypertension (15.9%), and handfoot syndrome (8.7%). Conclusion The present prospective observational study showed favorable effectiveness and safety of apatinib in real-world patients with advanced or metastatic GC in China. (A prospective, multi-center, non-intervention study of apatinib in the treatment of advanced gastric cancer-Trial Registry Number ChiCTR-OPN-15006601).Background Metformin is the first-line blood sugar control drug for type 2 diabetes, but recent epidemiological studies have shown that it inhibits the growth of a variety of tumours. However, few studies have examined metformin effects on gastric cancer (GC), and the anticancer mechanism has not been fully elucidated. Materials and methods We examined the inhibitory effect of metformin on GC cells by cell proliferation, migration and invasion assay. Transmission electron microscopy, confocal microscopy and Western blotting confirmed that metformin enhanced beclin1-dependent autophagy in gastric cancer cells. TCGA database and tissue chip analysis confirmed the differential expression of beclin1 in GC and adjacent tissues. Relevant functional tests verified the role of beclin1 as a tumour suppressor gene in GC. https://www.selleckchem.com/products/blu-285.html Western blotting, cell proliferation, cell migration and invasion were used to verify that metformin enhances autophagy in GC cells through the AMPK-mTOR signalling pathway. Xenograft tumour models were constructed to explore the inhibitory effect of metformin and the role of beclin1 as a suppressor on GC in vivo. Results In this study, we observed that metformin inhibits proliferation, migration and invasion of GC cells. Metformin could also promote beclin1-dependent autophagy in GC cells. We further discovered that beclin1 expression was downregulated in GC and that its low expression was associated with poor prognosis. Beclin1 acts as a tumour suppressor that inhibits the malignant phenotypes of GC cells in vitro and in vivo. Furthermore, we verified that metformin can upregulate beclin1-mediated autophagy to inhibit GC cells through the AMPK-mTOR signalling pathway. Conclusion In summary, the results revealed the role of autophagy in metformin inhibition of gastric cancer and suggest that beclin1 may be a potential target for gastric cancer therapy.Background A long noncoding RNA (lncRNA), ZNFX1 antisense RNA 1 (ZFAS1), was increased in multiple cancers, including hepatocellular carcinoma (HCC), resulting in malignancy development and progression. However, the mechanisms involving the interaction between ZFAS1 and microRNA-624 (miRNA-624) remain largely unknown. Therefore, the goal of this study was to probe the functional role of ZFAS1 in the development of HCC and its underlying mechanism. Methods Firstly, differentially expressed lncRNAs in HCC tissues were screened out by microarray. Subsequently, the prognostic effect of ZFAS1 patients with HCC was analyzed by the Kaplan-Meier analysis and The Cancer Genome Atlas database. ZFAS1 regulation on miRNA-624 was determined after si-ZFAS1 and/or miRNA-624 inhibitor were transfected into HepG2 and SMMC7721 cell lines. Finally, the effects of ZFAS1 on the growth and metastasis of HCC were observed by in vivo tumorigenesis and metastasis tests. Results ZFAS1 was overexpressed in HCC tissues and cells and indicated worse prognosis and shorter survival in patients with HCC. Silencing of ZFAS1 inhibited the malignancy of HCC cells, but miR-624 inhibitor could partially reverse the repressive role of si-ZFAS1. Moreover, ZFAS1 induced the extracellular-regulated protein kinases/c-Jun N-terminal kinase (ERK/JNK)/P38 pathway by binding to midkine (MDK) through miR-624, thus promoting the occurrence of HCC. Conclusion Collectively, ZFAS1 depletion inhibited the occurrence of HCC by downregulating the MDK/ERK/JNK/P38 pathway through restoring miR-624 expression. Inhibition of ZFAS1 may act as an innovative target to suppress occurrence in HCC.Irisin is a newly discovered exercise-induced cytokine, produced by the proteolytic hydrolysis of fibronectin type III domain-containing protein 5 (FNDC5). Irisin is widely distributed in the human body and is involved in the browning of white adipose tissue, improving insulin resistance, improving cognitive function, and regulating bone metabolism. Recent studies have shown that irisin concentration is elevated in a variety of tumor tissues as compared with that in normal tissues. However, irisin has different effects on the proliferation and apoptosis of tumor cells in breast cancer, lung cancer, and liver cancer through various mechanisms. Irisin plays an important role in the occurrence, development, and metastasis of different tumors, suggesting that irisin can be used as a potential target for tumor diagnosis and treatment. Therefore, studying the expression and function of irisin in tumors may be of great significance for the prevention and treatment of tumors. This article reviews the research progress on the role of irisin in tumors.