Histone demethylase KDM2A has been reported to be dysregulated in lung cancer. However, its function in gastric cancer remains poorly understood. Here, it was found that the expression level of KDM2A was increased in gastric cancer tissues. Moreover, forced expression of KDM2A in gastric cancer cells promoted cell growth and migration, while the knockdown expression of KDM2A inhibited the tumorigenicity of gastric cancer cells. Mechanistically, KDM2A regulated the growth and motility of gastric cancer cells through downregulating the expression of programmed cell death 4 (PDCD4), a known tumor suppressor in the progression of gastric cancer. Taken together, our study suggested that upregulation of KDM2A was very important in the progression of gastric cancer, and KDM2A might be a promising therapeutic target.

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Background Long non-coding RNAs (lncRNAs) are essential regulators of tumorigenesis and the development of colorectal cancer (CRC). Here, we aimed to investigate the role of lncRNA GAS6-AS1 in CRC and its potential mechanisms. Methods Bioinformatics analyses evaluated the level of GAS6-AS1 in colon cancer, its correlation with clinicopathological factors, survival curve and diagnostic value. qRT-PCR were performed to detect the GAS6-AS1 level in CRC samples and cell lines. The CCK8, EdU, scratch healing, transwell assays and animal experiments were conducted to investigate the function of GAS6-AS1 in CRC. RNA immunoprecipitation (RIP) and dual-luciferase reporter gene analyses were carried out to reveal interaction between GAS6-AS1, TRIM14, FUS, and miR-370-3p/miR-1296-5p. Results GAS6-AS1 was greatly elevated in CRC and positively associated with unfavorable prognosis of CRC patients. Functionally, GAS6-AS1 positively regulates CRC proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro and induces CRC growth and metastasis in vivo. Moreover, GAS6-AS1 exerted oncogenic function by competitively binding to miR-370-3p and miR-1296-5p, thereby upregulating TRIM14. Furthermore, we verified that GAS6-AS1 and TRIM14 both interact with FUS and that GAS6-AS1 stabilized TRIM14 mRNA by recruiting FUS. Besides, rescue experiments furtherly demonstrated that GAS6-AS1 facilitate progression of CRC by regulating TRIM14. Conclusion Collectively, these findings demonstrate that GAS6-AS1 promotes TRIM14-mediated cell proliferation, migration, invasion, and EMT of CRC via ceRNA network and FUS-dependent manner, suggesting that GAS6-AS1 could be utilized as a novel biomarker and therapeutic target for CRC.

Background This study aims to investigate the effect of lipid metabolism disorder on liver function in patients with malignant tumors after chemotherapy. Method A total of 428 patients with malignant tumors with normal liver function in our hospital between May 2013 to June 2018 were divided into an observation group (lipid metabolism disorder, n = 265) and control group (normal lipid metabolism, n = 163). The lipid metabolism levels and liver damage of the two groups were compared before and after chemotherapy. Results No significant differences in age, gender, body mass index, tumor types, history of surgery, levels of alanine aminotransferase (ALT; an indicator of liver function), and chemotherapy regimen were observed between the two groups. However, the observation group showed increased levels of total cholesterol ( P = 0.000), triglycerides ( P = 0.000), and low-density lipoprotein ( P = 0.01), as well as decreased levels of high-density lipoprotein ( P = 0.000) before chemotherapy compared with the control group. Furthermore, patients with lipid metabolism disorders were more likely to develop abnormal liver function after chemotherapy. Moreover, mixed lipid metabolism disorder was more likely to cause severe liver damage after chemotherapy. Additionally, the number of patients with lipid metabolism disorders after chemotherapy ( n = 367) was significantly increased compared with before chemotherapy ( n = 265) ( P < 0.01), indicating that chemotherapy might induce or aggravate an abnormal lipid metabolism. Conclusions After receiving chemotherapy, patients with malignant tumors presenting lipid metabolism disorders are more prone to liver damage and lipid metabolism disorders than patients with a normal lipid metabolism.