Jifu Song, Zhibin Guan, Maojiang Li, Sha Sha, Chao Song, Zhiwei Gao, Yongli Zhao

Oncology Research, Vol.26, No.6, pp. 847-856, 2018, DOI:10.3727/096504017X15016337254632

Abstract MicroRNAs (miRNAs) have emerged as pivotal regulators of the development and progression of gastric cancer. Studies have shown that miR-154 is a novel cancer-associated miRNA involved in various cancers. However, the role of miR-154 in gastric cancer remains unknown. Here we aimed to investigate the biological function and the potential molecular mechanism of miR-154 in gastric cancer. We found that miR-154 was significantly downregulated in gastric cancer tissues and cell lines. The overexpression of miR-154 significantly repressed the growth and invasion of gastric cancer cells. Bioinformatics analysis and Dual-Luciferase Reporter Assay data showed that miR-154… More >

Gong-Yi Lv, Jun Miao, Xiao-Lin Zhang

Oncology Research, Vol.26, No.6, pp. 837-846, 2018, DOI:10.3727/096504017X14920318811721

Abstract Abnormal expression of long noncoding RNAs (lncRNAs) often contributes to the unrestricted growth and invasion of cancer cells. lncRNA X-inactive specific transcript (XIST) expression is upregulated in several cancers; however, its underlying mechanism in osteosarcoma (OS) has not been elucidated. In the present study, we found that XIST expression was significantly increased in OS tissues and cell lines by LncRNA Profiler and qRT-PCR. The effects of XIST and miR-320b on OS cell proliferation and invasion were studied by MTT and Transwell invasion assays. The competing relationship between XIST and miR-320b was confirmed by luciferase reporter More >

Lili Lv^*, Xiaodong Wang^†

Oncology Research, Vol.26, No.5, pp. 775-783, 2018, DOI:10.3727/096504017X15132494420120

Abstract Cervical cancer is the third most commonly diagnosed malignancy and the fourth leading cause of cancer-related deaths in women worldwide. MicroRNA-296 (miR-296) is aberrantly expressed in a variety of human cancer types. However, the expression levels, biological roles, and underlying molecular mechanisms of miR-296 in cervical cancer remain unclear. This study aimed to detect miR-296 expression in cervical cancer and evaluate its roles and underlying mechanisms in cervical cancer. This study demonstrated that miR-296 was significantly downregulated in cervical cancer tissues and cell lines. Restoring the expression of miR-296 inhibited the proliferation and invasion of More >

Chao Ma, Jinfeng Han, Dong Dong, Nanya Wang

Oncology Research, Vol.26, No.5, pp. 765-773, 2018, DOI:10.3727/096504017X15021536183535

Abstract MicroRNA-152 (miR-152) expression has been reported to be downregulated in osteosarcoma (OS). However, the role of miR-152 in OS is not well documented. In the present study, we aimed to explore the function and underlying mechanism of miR-152 in OS. We found that miR-152 was underexpressed in OS tissues and cell lines. Decreased miR-152 was inversely correlated with lymph node metastasis and advanced clinical stage. Overexpression of miR-152 significantly inhibited cell proliferation, colony formation, migration, and invasion of OS cells. Bioinformatics analyses showed that miR-152 directly targeted E2F transcription factor 3 (E2F3), as further confirmed More >

Daofu Jia^*, Yanping Niu^†, Dongling Li^‡, Zhaorui Liu^§

Oncology Research, Vol.26, No.5, pp. 753-764, 2018, DOI:10.3727/096504017X15024946480113

Abstract Osteosarcoma is a highly aggressive malignant bone tumor with poor prognosis. Evidence has suggested that lncRNAs are deregulated in multiple cancers. In this study, we investigated the role of the lncRNA C2dat1 on the biological functions of osteosarcoma cells. The expressions of C2dat1, miR-34a-5p, and Sirt1 in human osteosarcoma cells were altered by transfection with their specific vectors/shRNA or mimic/inhibitor. Cell viability, migration, invasion, and apoptosis were assessed posttransfection. The mRNA and protein levels of C2dat1, miR-34a-5p, and Sirt1 were detected by qRT-PCR and Western blot. The results showed that C2dat1 suppression reduced cell viability, More >

Shanhong Duan^*, Ali Wu^†, Zhengyu Chen^‡, Yarong Yang^*, Liying Liu^*, Qi Shu^*

Oncology Research, Vol.26, No.5, pp. 713-723, 2018, DOI:10.3727/096504017X15016337254641

Abstract MicroRNAs (miRNAs) are small noncoding RNAs that are involved in human carcinogenesis and progression. miR-204 has been reported to be a tumor suppressor in several cancer types. However, the function and underlying molecular mechanism of miR-204 in cervical cancer (CC) are still unclear. In the present study, the expression level of miR-204 was measured using the qRT-PCR method in 30 paired CC clinical samples and in 6 CC cell lines. We found that the expression of miR-204 was significantly downregulated in CC tissues and cell lines compared to normal cervical tissues and cell line. miR-204… More >

Meng Yang^*, Xu Zhai^†, Tingting Ge^*, Chang Yang^*, Ge Lou^*

Oncology Research, Vol.26, No.5, pp. 703-712, 2018, DOI:10.3727/096504017X14982569377511

Abstract Expression of miR-181a-5p associates with the proliferation and progression of cancer cells via its targets. This study was designed to investigate the effect of miR-181a-5p and its target inositol polyphosphate-5- phosphatase A (INPP5A) on the progression of cervical cancers. Upregulation of miR-181a-5p was revealed in the cervical cancer cell lines HeLa and SiHa in comparison with a normal cervical epithelium cell line End1/ E6E7 (p<0.001). The inhibition and upregulation of miR-181a-5p in cervical cancer cell lines significantly reduced or increased cell proliferation and invasion capacity, accompanied with enhanced or reduced apoptosis (p<0.05). Moreover, INPP5A overexpression significantly More >

Shidan Liu¹, Jiaxi Luan¹, Yan Ding

Oncology Research, Vol.26, No.5, pp. 683-690, 2018, DOI:10.3727/096504017X14982585511252

Abstract This study aimed to investigate the role of miR-144-3p in pancreatic cancer (PC) carcinogenesis and to explore the mechanism of its function in PC. miR-144-3p was downregulated in PC tissues and cells. miR-144-3p overexpression significantly inhibited PC cell proliferation, migration, and invasion. FosB proto-oncogene, AP-1 transcription factor subunit (FOSB) was a target gene of miR-144-3p. miR-144-3p could repress PC cell proliferation, migration, and invasion by inhibiting the expression of FOSB. In conclusion, miR-144-3p plays an important role in PC cell proliferation, migration, and invasion by targeting FOSB. miR-144-3p may provide a new target for the More >

Heping Wang^*, Yanzhang Yu^†, Shuxin Fan^*, Leifeng Luo^*

Oncology Research, Vol.26, No.5, pp. 665-673, 2018, DOI:10.3727/096504017X14908298412505

Abstract Long noncoding RNA (lncRNA) taurine-upregulated gene 1 (TUG1) has been confirmed to be involved in the progression of various cancers; however, its mechanism of action in osteosarcoma has not been well addressed. In our study, TUG1 was overexpressed and miR-153 was downregulated in osteosarcoma tissues and cell lines. A loss-of-function assay showed that TUG1 knockdown suppressed the viability, colony formation, and invasion of osteosarcoma cells in vitro. Moreover, TUG1 was confirmed to be an miR-153 sponge. Ectopic expression of TUG1 reversed the inhibitory effect of miR-153 on the proliferation and invasion of osteosarcoma cells. Further More >

Yi Long Wan^*, Han Jue Dai^†, Wei Liu^‡, Hai Tao Ma^*

Oncology Research, Vol.26, No.4, pp. 637-644, 2018, DOI:10.3727/096504017X15112639918174

Abstract Claudin18 (CLDN18) is necessary for intercellular junctions and is reported to be involved in cell migration and metastasis, making it like an oncogene in various cancer types. However, the biological function and regulatory mechanisms of CLDN18 in lung adenocarcinoma are not yet clear. In this study, we found downregulation of miR-767-3p and upregulation of CLDN18 in lung adenocarcinoma tissue and cell lines. In addition, there was a negative correlation between the expression of miR-767-3p and CLDN18 in lung adenocarcinoma. Double luciferase reporter gene analysis showed that miR-767-3p modulates the expression of CLDN18 by binding its More >