The incidence and mortality rate of colorectal cancer (CRC) have been significantly increasing. However, mechanisms involved in CRC progression are still unclear. LncRNA ZFAS1 has been verified as oncogenic molecular in a series of tumors, including CRC. However, the underlying mechanism of ZFAS1 in CRC carcinogenesis remains unclear. In the present study, our data showed that ZFAS1 expression was significantly upregulated in CRC tissues and cell lines. Correlation analysis showed that high ZFAS1 expression was significantly associated with Helicobacter pylori infection, lymph nodes metastasis, advanced TNM stage and poor overall survival of CRC patients. Loss-of-function experiments revealed that ZFAS1 inhibition could markedly suppress CRC cells proliferation and invasion both in vitro and in vivo. Bioinformatics analysis and luciferase reporter assay revealed that ZFAS1 directly interacted with miR-484. Rescue experiments showed that miR-484 inhibitor reversed the tumor suppressing roles of ZFAS1 knockdown on CRC cells. Therefore, our study suggested that ZFAS1 could act as an oncogene in CRC tumorigenesis, and discovered the functional regulatory pathway of ZFAS1 sponging miR-484.

Background Long non-coding RNA Malat1 has been widely identified as an oncogene which shows a significant relationship with tumorigenesis in colorectal cancer (CRC). Nonetheless, whether Malat1 participates in the autophagy of colorectal cancer remains unclear. Materials and methods First, the expression level of Malat1 in 96 pairs of colorectal cancer tissues and four cell lines was detected by qRT-PCR. Subsequently, the autophagy activity in colorectal cancer tissues and cell lines was detected by western blot. Furthermore, the CCK-8 assay and flow cytometry (FCM) were performed to detect the role of autophagy activated by Malat1 in colorectal cancer cell lines. Results In this study, significantly increased Malat1 expression and autophagy activity were found in colorectal cancer tissues compared with the adjacent normal tissues. Also, the Malat1 level was positively correlated with the expression of LC3-II mRNA in vivo. Moreover, autophagy activation and cell proliferation were significantly facilitated by Malat1 in colorectal cancer cells, while apoptosis decreased. Above all, the inhibition of autophagy by 3-MA not only relieved the Malat1-induced cell proliferation but also promoted the Malat1-induced cell apoptosis. In addition, Malat1 was found to act as an endogenous sponge by directly binding to miR-101 to reduce miR-101. Furthermore, the suppressive effects of miR-101 on the autophagy, proliferation, and apoptosis of CRC were abolished by Malat1. Conclusion Long non-coding RNA Malat1 activated autophagy and promoted cell proliferation, yet inhibited apoptosis by sponging miR-101 in colorectal cancer cells.

Gastric cancer is one of the leading mortal causes. Targeted therapy is a new type of cancer treatment, which precisely identifies and attacks cancer cells and significantly reduces side effects. In this network meta-analysis, we focused on the efficacy and safety of 12 targeted agents on gastric cancer among a total of 8,405 patients from 24 trials. Hazard ratio (HR) with 95% credible interval (CrI) were calculated for primary outcomes, including overall survival (OS) and progression-free survival (PFS), while odds ratio (OR) with 95% CrI were calculated for secondary outcomes. Surface under the cumulative ranking curve (SUCRA) were calculated to illustrate the rank probability of various agents for different outcomes. Compared with other analyzed treatments, ramucirumab is outstanding in survival outcomes. However, higher risk of hematological events should be noted during its application. Lapatinib is also efficacious in progression reduction, while it is always combined with severe gastrointestinal events. Trastuzumab is proposed for its high efficacy in improving survival rate and safety, which is proper for most patients. In conclusion, trastuzumab was recommended as the optimal targeted agent combined with chemotherapy for gastric cancer patients.

The aim of this study was to investigate the clinical significances of the mRNA expression of survivin gene and its four splice variants in the pathogenesis of colorectal cancer (CRC). CRC samples, matched adjacent tissues, and normal tissues were collected from surgical resections of 39 patients with histologically confirmed diagnosis. The mRNA expression of survivin and its four splice variants, that is, survivin-△Ex3, survivin-2B, survivin-3B, and survivin-2α, was detected using semiquantitative PCR and RT-PCR. Carcinoembryonic antigen (CEA) CAM5 was determined as control. The mRNA expression rates of survivin, survivin-△Ex3, survivin-2B, survivin-3B, surviving-2α, and CEA CAM5 in CRC samples were significantly higher than those in adjacent tissues (P < 0.01) and those in normal tissues (P < 0.01). The mRNA levels of the above variants in CRC samples were also significantly higher than those in adjacent tissues (P < 0.01) and those in normal tissues (P < 0.01). The mRNA levels of survivin, survivin-2B, and survivin-2α were not associated with any clinical variable of patients, while the levels of survivin-△Ex3 and survivin-3B were associated with lymphoid metastasis and Dukes grade (P < 0.05), and survivin-△Ex3 was associated with invasiveness. We concluded that mRNA expression rates and levels of survivin and its four splice variants elevated in CRC tissues, and expression levels of survivin-△Ex3 and survivin-3B were positively associated with tumor aggression.

Aberrant expression of microRNAs (miRNAs) plays fundamental effect on the pathogenesis of hepatocellular carcinoma (HCC). MiR-27b was previously found to play important roles in human cancers. However, its expression status, clinical significance, and biological functions in HCC remain largely unclear. The expression status of miR-27b in HCC specimens and cells were determined with qRT-PCR. MTT, 5-bromodeoxyuridine (BrdU) proliferation assays, and flow cytometry analysis were carried out to assay proliferation, cell cycle, and apoptosis. A subcutaneous model was used to evaluated the HCC tumor growth in vivo. The putative target gene of miR-27b was disclosed by TargetScan and a luciferase reporter assay. The levels of miR-27b were overexpressed in HCC. Overexpression of miR-27b was correlated with adverse prognostic features and reduced survival rate. Inhibition of miR-27b in SMMC-7721 cells remarkably suppressed proliferative ability and cell-cycle progression while enhanced apoptosis. In contrast, miR-27b overexpression resulted in prominent increased proliferation and process of cell cycle and reduced apoptosis of Hep3B cells. In vivo studies showed that knockdown of miR-27b inhibited the in vivo growth of SMMC-7721 cells in mouse xenograft model. Furthermore, we confirmed that Fbxw7 was directly regulated by miR-27b and mediated the roles of miR-27b in HCC. We suggest that miR-27b serves as an oncogenic miRNA in HCC by modulating proliferation, cell-cycle progression, and apoptosis, and its oncogenic effect is mediated by its downstream target gene, Fbxw7.